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Novel recovery strategies for elite athletic performance Buschmann, Lauren Kathryn 2015

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	  NOVEL RECOVERY STRATEGIES FOR ELITE ATHLETIC PERFORMANCE    by    Lauren Kathryn Buschmann     B.Sc., University of Vermont, 2013      A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF  THE REQUIREMENTS FOR THE DEGREE OF   Master of Science    in  THE FACULTY OF GRADUATE AND POSTDOCTORAL STUDIES  (Kinesiology)      THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver)   September 2015    © Lauren Kathryn Buschmann, 2015   	  	  	   ii	  Abstract Background: Recovery strategies aim to reduce the inflammatory response that occurs following exercise induced muscle damage (EIMD) by compressing the vasculature, and subsequently facilitating increased venous return.  Hot and cold-water immersion (contrast water therapy, CWT) alternates vasoconstriction (during cold-water immersion) and vasodilatation (during hot-water immersion), and consequently reducing the localized oedema that occurs following high-intensity exercise The NormaTec MVP compression device mimics the body’s venous return via the musculoskeletal pump, by pumping blood from the extremities, where oedema pools following strenuous exercise, back towards the heart. Variable intermittent pressure is a novel technique that aims to promote venous return and stimulate parasympathetic reactivation. Available research is contradictory as to whether these recovery strategies are effective in reducing recovery time and improving subsequent athletic performance. As a result, further research into this area is warranted. Purpose: To determine which recovery application is an effective means of promoting and accelerating recovery for highly trained athletes following heavy eccentric exercise, and therefore maintaining subsequent athletic performance. Hypothesis: We hypothesize that the VIP and CWT will be most effective in maintaining performance and reducing muscle soreness and swelling following the fatiguing exercise protocol, compared to placebo (passive recovery) and NormaTec conditions. Methods: A RCT was employed to investigate 24 highly trained participants. Testing occurred over five test sessions (Day 1-5). At baseline, participants underwent measures of VJ, 10m and 30m sprints, HRV, VAS and Leg Girth (Sub-gluteal, mid-thigh, above-the-knee). Following baseline measures, participants underwent 10 x 10 repetitions of a plyometric drop jump from a 0.6m box. Participants had 10 sec rest between repetitions, and 1 min rest between sets. Participants were randomly assigned into four conditions: 1) Contrast water therapy (CWT, n=6), 2) Variable intermittent pressure (VIP, n=6), 3) NormaTec IPC (NormaTec, n= 6), 4) Passive Recovery/ Placebo (Placebo, n=6). Perception of recovery was analyzed following recovery application using a Likert Recovery Questionnaire. Follow-up measures of outcome variables occurred at 24, 48 and 72 hr post-exercise. Data Analysis: Two-way mixed model ANOVA was used to assess between groups (CWT, VIP, NormaTec, Placebo) and repeated measures (baseline, 24 hr, 48 hr, 72 hr) effects. Tukey’s HSD was used when necessary. Results: CWT demonstrated 4.36% increase in mean VJ @ 72 hr (p > 0.05). VIP demonstrated performance maintenance for VJ and sprint measures (p > 0.05). VIP demonstrated significantly (p < 0.05) increased VAS scores compared to CWT during the stand to sit movement, maximal quadriceps contraction (right leg only), and passive quadriceps stretch (right and left leg) and for total pain scores at 72 hr post-exercise. VIP VAS scores were also significantly (p < 0.05) increased for the NormaTec (Stand to Sit) and Placebo (Stand to Sit, Total Pain) at 72 hr post-exercise. No other statistically significant differences (p > 0.05) was evident between groups at any time point for measures of HRV, VJ, 10m and 30m sprint, or leg girth. Trend approaching significance (p=0.058) for an interaction effect between CWT(1.38%) and VIP (0.46%) for increases in sub-gluteal leg girth at 24 hr. Conclusion: The CWT and VIP appear to be beneficial in facilitating recovery and the maintenance of performance during a high intensity training program compared to placebo 	  	  	   iii	  and NormaTec conditions. There appear to be differences in subjective perceptions of muscle soreness reflecting the differences in recovery strategy methodologies.  Further research appears to be warranted to determine the underlying mechanisms responsible for facilitating recovery and maintaining physical performance.                                      	  	  	   iv	  Preface   The research detailed in this thesis investigation took place at the Cardiovascular Physiology and Rehabilitation (CPR) laboratory at the University of British Columbia, Vancouver Campus, by Dr. Darren Warburton, Dr. Shannon Bredin, Dr. Don McKenzie, and Lauren Buschmann. Dr. Darren Warburton and myself collaborated to create the research project and design. Drs. Warburton, Bredin, and McKenzie all contributed towards the refinement of the project. I was responsible for participant recruitment, data collection of all measurements (Heart Rate Variability, Leg Girth, Muscle Soreness, Vertical Jump and 30m Sprint), and data analysis. Andrew Perrotta, a PhD. student in the Cardiovascular Physiology and Rehabilitation laboratory assisted with the analysis of heart rate variability. I conducted all testing sessions with participants, as well as wrote the manuscript. I conducted all data analyses independently of all inventors of the devices/protocols examined in this study.   The research project, Novel Recovery Strategies for Elite Athletic Performance, received ethics approval through the University of British Columbia Clinical Research Ethics Board. The ethics approval certificate number is: H14-00899.                	  	  	   v	  Table	  of	  Contents	  Abstract	  .............................................................................................................................................	  ii	  Preface	  ..............................................................................................................................................	  iv	  List	  of	  Tables	  .................................................................................................................................	  vii	  List	  of	  Figures	  ...............................................................................................................................	  viii	  List	  of	  Abbreviations	  ...................................................................................................................	  ix	  Glossary	  .............................................................................................................................................	  x	  Acknowledgments	  ........................................................................................................................	  xi	  Dedication	  ......................................................................................................................................	  xii	  Chapter	  1:	  Introduction	  ...............................................................................................................	  1	  1.1 Introduction	  ..........................................................................................................................................	  1	  1.2 Research Questions and Hypothesis	  ................................................................................................	  2	  Primary Question	  .......................................................................................................................................................	  2	  Secondary Questions	  ................................................................................................................................................	  2	  Hypotheses	  ..................................................................................................................................................................	  2	  Chapter	  2:	  Literature	  Review	  ....................................................................................................	  3	  2.1 Eccentric Exercise	  ................................................................................................................................	  3	  2.2 Recovery	  ................................................................................................................................................	  4	  2.3 Hydrotherapy	  .......................................................................................................................................	  6	  Contrast Water Therapy	  .......................................................................................................................................	  10	  2.3 Variable Intermittent Pressure System	  ........................................................................................	  16	  Lower Body Negative Pressure	  .........................................................................................................................	  18	  Lower Body Positive Pressure	  ...........................................................................................................................	  19	  2.4 Intermittent Pneumatic Compression	  ..........................................................................................	  21	  NormaTec MVP Recovery Device	  ...................................................................................................................	  24	  Chapter	  3:	  Methodology	  ............................................................................................................	  30	  3.1 Study Design	  ......................................................................................................................................	  30	  3.2 Study Location	  ...................................................................................................................................	  30	  3.3 Recruitment	  .......................................................................................................................................	  30	  3.4 Procedures	  ..........................................................................................................................................	  31	  Recovery Procedures	  .............................................................................................................................................	  33	  3.5 Measures	  .............................................................................................................................................	  34	  Resting Blood Pressure	  ........................................................................................................................................	  34	  Anthropometric Measures	  ...................................................................................................................................	  35	  Grip Strength	  ...........................................................................................................................................................	  35	  Heart Rate Variability	  ...........................................................................................................................................	  36	  Leg Girth Measurements	  .....................................................................................................................................	  37	  Muscle Soreness	  .....................................................................................................................................................	  37	  Vertical Jump	  ...........................................................................................................................................................	  38	  Speed (30m sprint)	  .................................................................................................................................................	  39	  Likert Recovery Questionnaire	  ..........................................................................................................................	  39	  3.6 Statistical Analysis	  ............................................................................................................................	  40	  	  	  	   vi	  3.7 Ethical considerations	  ......................................................................................................................	  40	  Chapter	  4:	  Results	  ........................................................................................................................	  42	  4.1 Participants	  ........................................................................................................................................	  42	  4.2 Heart Rate Variability	  .....................................................................................................................	  43	  4.3 Muscle Soreness (Visual Analog Scale)	  ........................................................................................	  45	  Stand to Sit	  ................................................................................................................................................................	  45	  Sit to Stand	  ................................................................................................................................................................	  47	  Passive Quadriceps Stretch	  ................................................................................................................................	  48	  Passive Hamstrings Stretch	  ................................................................................................................................	  51	  Maximal Quadriceps Contraction	  ....................................................................................................................	  53	  Maximal Hamstrings Contraction	  ....................................................................................................................	  55	  Total Pain	  .................................................................................................................................................................	  57	  4.4 Vertical Jump	  ....................................................................................................................................	  59	  4.5 10m and 30m Sprint	  .........................................................................................................................	  62	  4.6 Limb Circumference	  ........................................................................................................................	  67	  4.7 Likert Recovery Questionnaire	  .....................................................................................................	  71	  Chapter	  5:	  Discussion	  .................................................................................................................	  73	  5.1 Heart Rate Variability	  .....................................................................................................................	  73	  5.2 Muscle Soreness	  ................................................................................................................................	  76	  5.3 Vertical Jump	  ....................................................................................................................................	  81	  5.4 10m and 30m Sprint	  .........................................................................................................................	  83	  5.5 Limb Circumference	  ........................................................................................................................	  89	  5.6 Likert Recovery Questionnaire	  .....................................................................................................	  93	  5.7 Training Status	  ..................................................................................................................................	  94	  5.8 Protocols	  .............................................................................................................................................	  96	  5.9 Conclusion	  ..........................................................................................................................................	  97	  5.10 Limitations	  .......................................................................................................................................	  99	  Bibliography	  ...............................................................................................................................	  100	  Appendices	  .................................................................................................................................	  110	  Appendix A: Recruitment Notice	  ......................................................................................................	  110	  Appendix B: Consent Form	  ................................................................................................................	  111	  Appendix C: The Physical Activity Readiness Questionnaire (PAR-Q+).	  ...............................	  118	  Appendix D: Training and Health History Questionnaire	  ..........................................................	  122	  Appendix E: Likert Recovery Questionnaire	  ..................................................................................	  124	  Appendix F: Randomization of Recovery Applications	  ...............................................................	  125	  Appendix G: Grip Strength Categorizations	  ..................................................................................	  126	  Appendix I: Visual Analog Scale 	  ......................................................................................................	  127	          	  	  	   vii	  List of Tables TABLE 1: DESCRIPTION OF PARTICIPANT CHARACTERISTICS (MEAN ± SD) *.	  ..................................................................	  43	  TABLE 2: MEAN RMSSD (± S.D.) VALUES AT EACH TEST SESSION (MEAN ± SD).	  .........................................................	  44	  TABLE 3: MEAN SITTING AND STANDING VISUAL ANALOG SCALE SCORES (CM) (MEAN)	  ...........................................	  48	  TABLE 4: MEAN VAS SCORES: PASSIVE QUADRICEPS STRETCH [CM] (MEAN ± S.D.)	  ..................................................	  50	  TABLE 5: RIGHT AND LEFT LEG PASSIVE HAMSTRING STRETCH MEAN VISUAL ANALOG SCALE SCORES (MEAN ± S.D.)	  ...............................................................................................................................................................................................	  52	  TABLE 6: LEFT AND RIGHT LEG - MAXIMAL QUADRICEPS CONTRACTION MEAN VISUAL ANALOG SCALE SCORES (MEAN ± S.D.)	  ............................................................................................................................................................................	  54	  TABLE 7: RIGHT AND LEFT LEG - MAXIMAL HAMSTRING CONTRACTION MEAN VAS SCORES (MEAN ± S.D.)	  ....	  56	  TABLE 8: MEAN LIMB CIRCUMFERENCE MEASUREMENTS – THREE LOCATION SITES [CM] (MEAN ± SD).	  ................	  69	                   	  	  	  	  	  	  	  	   viii	  List of Figures  FIGURE 1: SCHEDULE AND CONTENT OF TESTING SESSIONS	  ...................................................................................................	  33	  FIGURE 2 MEAN STAND TO SIT VAS SCORES (MEAN ± SD).	  ..................................................................................................	  46	  FIGURE 3: 72 HR POST-EXERCISE STAND TO SIT VISUAL ANALOG SCALE MEAN SCORES (MEAN ± SD).	  ................	  47	  FIGURE 4: PASSIVE QUADRICEPS STRETCH VAS SCORES AT 72 HR POST-EXERCISE (MEAN ± S.D.)	  .........................	  51	  FIGURE 5: THE 72 HR MAX. QUAD. CONTRACTION MEAN VAS SCORES (RIGHT LEG ONLY) (MEAN ± S.D.)	  ........	  55	  FIGURE 6: TOTAL PAIN VISUAL ANALOG SCALE MEAN SCORES (ALL TIME POINTS) (MEAN ± SD).	  .........................	  58	  FIGURE 7:  PEAK VERTICAL JUMP [CM] (MEAN ± SD).	  .............................................................................................................	  60	  FIGURE 8: MEAN VERTICAL JUMP SCORES [CM] (MEAN ± SD).	  ............................................................................................	  61	  FIGURE 9: MEAN 10M SPRINT TIMES [SEC] (MEAN ± SD).	  .......................................................................................................	  63	  FIGURE 10: PEAK 10M SPRINT SPLIT TIMES [SEC] (MEAN ± SD).	  ...........................................................................................	  64	  FIGURE 11: MEAN 30M SPRINT TIMES [SEC] (MEAN ± SD).	  ....................................................................................................	  66	  FIGURE 12: PEAK 30M SPRINT TIMES [SEC] (MEAN ± SD).	  ......................................................................................................	  67	  FIGURE 13: SUB-GLUTEAL LIMB CIRCUMFERENCE MEASUREMENTS - RIGHT LEG ONLY [CM] (MEAN ± SD).	  ......	  68	  FIGURE 14: MEAN LIKERT SCALE RECOVERY QUESTIONNAIRE (MEAN ± SD).	  ................................................................	  71	                         	  	  	   ix	  List of Abbreviations  CWT – Contrast Water Therapy  CWI – Cold Water Immersion  HWI – Hot Water Immersion   TWI – Thermoneutral Water Immersion  IPC – Intermittent Pneumatic Compression  EIMD – Exercise Induced Muscle Damage  DOMS – Delayed Onset Muscle Soreness  VJ – Vertical jump  VAS - Visual Analog Scale  HRV - Heart Rate Variability   RMSSD – Root Mean Square of Successive Differences   PAR-Q+ - Physical Activity Readiness Questionnaire for Everyone                    	  	  	   x	  Glossary  Eccentric muscle contractions  The lengthening of the muscle while performing an exercise or physical movement.                            	  	   	  	  	  	   xi	  Acknowledgments   I am very thankful to my thesis supervisor, Dr. Darren Warburton, for providing me the opportunity to learn and immerse myself in the research process over the past two years. I am very appreciative of the opportunity to be involved in this research project, and am grateful to you for making this possible.   To my committee members, Dr. Don McKenzie and Dr. Shannon Bredin, thank you for your assistance and advisement during my two years at UBC. I appreciate the time and effort that was invested into this project, and I am extremely grateful for the opportunity to learn from each of your expertise.   I would also like to thank my lab mates from both the CPR and LEARN labs for all of their support and assistance on various projects. Particularly, I owe a big debt of gratitude to Andrew Perrotta, for his extensive support, guidance, and answering each of my millions of questions. Thank you to Andrew, David Kim, Jean Burrows, and Anne Lasinsky for assisting with set-up during the data collection process, you made my life much easier as a result.  Special thanks are required for my parents and my brother, as they emotionally, and financially, supported me during my post-graduate career. Also, for fielding each one of my countless phone calls and e-mails when I was most stressed. Your unrelenting support means the world to me.   Final thank you to the faculty, and staff at UBC for guiding me through during my time here, and assisting with this research in immeasurable ways that I am truly appreciative and grateful for.                   	  	  	   xii	  Dedication                To Mom, Dad, and Nathan	  	  	   1	  Chapter 1: Introduction  1.1 Introduction  Elite athletes follow extensive training programs and are exposed to excessive levels of fatigue (both physiologically and psychologically) on a regular basis. The need to constantly train in order to continually progress and improve their performance can result in these individuals never fully recovering. Athletes and their support staff are actively investigating various methodologies that can provide any increased advantage over their competitors (Halson, 2013). This research often focuses on advancements in training regimens. However, athletes and their support staff may overlook the effects that a carefully constructed recovery regimen can have on minimizing fatigue following training sessions, and subsequently improving athletic performance. By addressing the need for recovery strategies, the athletes may be able to minimize the excessive fatigue that accumulates following high intensity exercise allowing for more effective training (i.e. the ability to train at exercise intensities associated with optimal performance) and a reduction in the risk of injury in future competitions and training sessions (Barnett, 2006). In order to mitigate the risks of injury and optimize training, it is critical to investigate the role that various recovery applications can play in this process.   Studies that have investigated recovery mechanisms report extremely conflicting findings regarding effective options for facilitating recovery following a fatiguing event. As such, while many athletes are currently engaging in post-exercise recovery regimens, they are doing so based on anecdotal support rather than empirical evidence. Investigation into effective recovery mechanisms has demonstrated conflicting results based on inconsistent protocols and methodology (Versey et al., 2013). Investigation of novel recovery strategies for elite athletes could result in accelerated recovery time, optimization of training sessions, reduced risk of injury, and improved athletic performance.    	  	  	   2	  1.2 Research Questions and Hypothesis Primary Question 1. Do current novel recovery strategies used in elite athletics enhance the recovery from high intensity exercise training and subsequent performance? Secondary Questions 1. Is there a recovery protocol that demonstrates an optimal effectiveness in the ability to facilitate recovery and subsequent performance following high intensity eccentric exercise?  2. Is there a direct relationship between athletes’ perception of recovery/performance and their actual physiological recovery/performance? Hypotheses  We hypothesize that novel recovery strategies used in elite athletics (that elicit phasic changes in blood volume/flow) will enhance the recovery and subsequent performance from high intensity exercise. We also hypothesize that there will be differences between recovery strategies with the Variable Intermittent Pressure (VIP) and Contrast Water Therapy Strategies being the most effective strategies.               	  	  	   3	  Chapter 2: Literature Review 2.1 Eccentric Exercise  The repetitive stress placed on the body through subsequent high-intensity training sessions can lead to inflammation and exercise induced muscle damage (Barnett, 2006; Connolly et al., 2003). It is widely understood that exercise results in damage to the skeletal muscle fibres, characterized by micro tears in the skeletal muscle, particularly the sarcolemma and sarcomeres (Higgins et al., 2013; McHugh et al.,1999). The micro tears in the musculature results in a localized inflammatory response at the site of injury. This inflammatory response is characterized by the increase in circulating inflammatory biomarkers [Creatine Kinase (CK), Interleukin-6 (IL-6)], and muscle proteins [C- Reactive Protein (CRP), myoglobin (Mb)] (Kanda et al., 2013; McHugh et al., 1999; Nédélec et al., 2012). Furthermore, strenuous high-intensity exercise is responsible for promoting an influx of hydrogen ions in the muscle cells, which is characterized by acidosis within the muscle (Barnett, 2006). This metabolic acidosis is believed to be the result of ATP demand exceeding the possible production of the energy compound, which consequently results in the increased ion concentration mentioned earlier (Robergs et al., 2004). Concurrently, extracellular fluid shuttles to the site of exercise-induced muscle damage and tissue injury due to an increase in vascular permeability caused by the release of leukotrienes (Connolly et al., 2003). This results in localized oedema at the site of muscular injury. The increased permeability also results in the localization of neutrophils, and subsequently free radical production, at the site of muscle damage (Pizza et al., 2001). This indicates that there are considerable metabolic waste products produced within the muscle following an exercise session, specifically involving high intensity eccentric movements.   Eccentric muscle contractions have been associated with the production of these metabolic waste products, which often result in delayed onset muscle soreness and muscle stiffness (Chleboun et al., 1995; Cleak & Eston, 1992; McHugh et al., 1999). Eccentric contractions during exercise cause excessive lengthening of the sarcomeres that can cause disruptions in the fibres (Connolly et al., 2003; McHugh et al., 1999; Proske & Morgan, 2001). The disruption may lead to an excessive stretch, which ultimately results in sarcomere failure (McHugh et al., 1999). The sarcomere failure leads to overreliance on secondary structures, known as the intermediate filaments, which appears to be the root location of 	  	  	   4	  exercise induced muscle damage (McHugh et al., 1999). This disruption also leads to the inflammatory process as mentioned previously, but also may cause damage to the excitation- contraction coupling (Proske & Morgan, 2001). Damage to the excitation-contraction coupling process can result in diminished ability to generate maximal muscle force, as the body’s inability to process calcium ions would minimize the overall magnitude of the muscle contraction (Proske & Morgan, 2001). The increased reliance on the intermediate filaments following sarcomere disruption for force production is what can inevitably cause said filaments to structurally fail, resulting in further muscular damage (McHugh et al., 1999). Consequently, the mechanisms of repeated eccentric muscle contractions indicate athletes that experience these repeated contractions in training will be exposed to an increased inflammatory response, delayed onset muscle soreness, and reduced force production (Cleak & Eston, 1992; Nédélec et al., 2012). Specifically, sports that involve significant deceleration, jumping, landing and changing of direction (high eccentric components) are at a increased risk of exposure to these negative side effects resulting from heavy repetitive bouts of eccentric contractions (Cochrane et al., 2013). With a build up of metabolic waste products, reduced force production and increased muscle soreness, an athlete’s training performance and event performance can be severely diminished. It is thought that an effective recovery strategy would be able to mitigate or blunt the inflammatory response resulting from eccentric movements, and would subsequently facilitate an athlete’s ability to recover. 2.2 Recovery  It has been widely suggested that the need for recovery strategies is due to the considerable muscle damage caused by strenuous eccentric activities (Cleak & Eston, 1992; Gill et al., 2006; McHugh et al., 1999). The need for an effective recovery program is applicable to all sports involving decelerating or braking, change of direction, and explosive movements (such as jumping) due to the heavy eccentric component involved in each of these movements (Cochrane et al., 2013). This classification of eccentric activities presented by Cochrane et al. (2013) encompasses components of most Olympic events, ranging from team sports to Olympic weightlifting. Elite athletes devote their lives to improving their sport specific skills and overall athletic performance, and as such would benefit from any aspect of improved performance, or at the very least, maintenance of performance. Many studies have 	  	  	   5	  looked at the maintenance of performance in repeated or successive exercise sessions following strenuous eccentric exercise (Vaile et al., 2008a, 2011). Vaile et al. (2008a) reported that two variations of hydrotherapy (cold water immersion and contrast water therapy) were effective in maintaining performance in comparison to the control (passive recovery), with the cold water immersion participants demonstrating a performance difference of 0.1-1.0%, and the contrast water immersion participants demonstrating a performance difference of 0.0-1.7%. In contrast, the control group demonstrated a 2.6-3.8% decrease in performance (Vaile et al., 2008a). Being able to maintain or even improve performance during multiple repeated maximal efforts, commonly seen during world championship competitions and the Olympics, is critical for elite athletes (Higgins et al., 2002). The ability to address this issue, without affecting the athlete’s physical training, is a unique and exciting opportunity that sport scientists and exercise professionals are being faced with today. A broad spectrum of recovery methods have been suggested to be effective in promoting recovery; however there is very little scientific evidence supporting one method as opposed to another. Investigations have tested pain perception, blood biomarkers and performance measures (Bahnert et al., 2013; Gill et al., 2006) to determine the efficacy of recovery strategies on elite athletes. The Australian Institute of Sport (Australian Institute of Sport website, n.d.) has identified several strategies that may be useful for athletes including: 1) Hydrotherapy, 2) Compression, 3) Active Recovery, 4) Stretching, 5) Cryotherapy, 6) Carbohydrate Ingestion, and 7) Massage (Bahnert et al., 2013; Barnett, 2006; Gill et al., 2006; Higgins et al., 2002; Mika et al., 2007; Montgomery et al., 2008). Within those methods there are a variety of alternatives that can be utilized, and many of these alternative strategies have been investigated. Each of these strategies use different proposed mechanisms in an attempt to explain their impact on accelerating recovery following an exercise session.   	  	  	   6	  2.3 Hydrotherapy  One of the most commonly used recovery mechanisms in recent years has various forms of hydrotherapy. Hydrotherapy refers to the immersion of an area of the body in water for the purpose of altering circulation and improving venous return as a means of recovery. This grouping of recovery strategies consists of cold water immersion (CWI), hot water immersion (HWI), thermoneutral water immersion (TWI), and contrast water therapy (CWT). Cold water immersion is the immersion of the body in temperatures typically ranging from 10-15oC, but is open to any water immersion <20 oC (Versey et al., 2013). Hot water immersion is the immersion of the body in temperatures exceeding 36 oC, but typically ranging from 38-42 oC (Versey et al., 2013; Wilcock et al.,2006). Thermoneutral water immersion is considered to be any water immersion that exceeds 20 oC, but is less than 36 oC (Versey et al., 2013). Contrast water therapy is the alternating of the body in cold water immersion and hot water immersion (Wilcock et al., 2006). Durations of treatment vary greatly, but largely range between 5 – 20 min, depending on the temperature of the water (Wilcock et al., 2006). As with most recovery mechanisms, that literature is largely conflicting on the length of treatment, most effective temperature, and the underlying mechanism that facilitates recovery. In fact, most studies do not take a mechanistic approach to the examination of the recovery protocol owing to the practical limitations associated with high performance sport testing.    For all temperatures of hydrotherapy, the proposed mechanism of action is the presence of hydrostatic pressure (Bieuzen et al., 2013; Vaile et al., 2008a; Vaile et al., 2008b; Versey et al., 2013; Wilcock et al., 2006). Hydrostatic pressure acts on the body when it becomes immersed in water, and the degree of pressure intensity depends on the depth of the immersion and depth of the water level (Wilcock et al., 2006). The various levels of water immersion used in the literature regarding accelerating recovery consist of hip level immersion (immersed to the superior aspect of the iliac crest), xiphoid process immersion, and full-body immersion (head and neck out of water) (Wilcock et al., 2006). The pressure that is acting on the body when it is immersed in the water is thought to act as a compressive force on both the muscular and vascular structures submerged in water (Pournot et al., 2011). This compressive force is believed to blunt the pooling of oedema and reduce the 	  	  	   7	  inflammatory response that occurs following high intensity exercise, and subsequent exercise induced muscle damage (Pournot et al., 2011). While anecdotally most hydrotherapy occurs at the hip level (superior aspect of the iliac crest), full body (head and neck out only) is reported to be most beneficial for promoting the clearance of metabolites due to the demonstration of larger increase of central blood volume compared to other immersion levels (Vaile et al., 2008b). Hydrostatic pressure acts on the body when it is immersed in water and causes a change in the osmotic pressure gradient, which moves fluids from an area of high pressure to an area of lower pressure, redistributing fluids from the interstitial space into the intravascular space (Vaile et al., 2008b; Wilcock et al., 2006). This redistribution of fluids into the intravascular space moves tissue fluids and metabolites into circulation, and they are cleared through venous return, back towards the heart (Vaile et al., 2008b). Hydrotherapy has been chosen for investigation to determine if varying temperatures are effective in facilitating recovery, owing to the hydrostatic pressure mechanism present, or if it is the temperature that is the primary mechanism resulting in accelerated recovery. It appears as though hydrostatic pressure may be the primary mechanism acting on the body, and temperature is a secondary mechanism, as studies that have used hot showers for HWI or cold showers for CWI do not appear to be as effective (Versey et al., 2013). The use of showers instead of water immersion removes the possibility for hydrostatic pressure to act on the body and aid in compression of the affected limbs (Versey et al., 2013). Hydrostatic pressure appears to be the primary underlying mechanism that aids the body in clearing excess oedema and metabolites from the musculature and redistributes the fluid and by-products back into circulation (Montgomery et al., 2008; Versey et al., 2013). It also appears that using showers instead of water immersion decreases the surface area that temperature of water could potentially influence, and therefore, showers may negate the effects of temperature on the body as well (Versey et al., 2013).  The displacement of fluids from the interstitial space into the intravascular space has been reported by several studies (Bieuzen et al., 2013; Montgomery et al., 2008; Pournot et al., 2011; Versey et al., 2013; Versey et al, 2011). This fluid shift results in a wide variety of physiological responses that occur following increased compression and subsequent increase in venous return. As previously mentioned, the compression to the submerged portion of the body aids in metabolite transport through the pressure gradient and ultimately via venous 	  	  	   8	  return (Bieuzen et al., 2013). This increase in venous return is caused by an increase in blood flow to the central cavity (Bieuzen et al., 2013; Vaile et al., 2008a). This fluid shift from the periphery of the extremities to the central cavity has two primary physiological outcomes. The increased blood flow leads to an increase in central blood volume (Schaal et al., 2013; Vaile et al., 2008a), which also results in decreased peripheral resistance in the peripheral blood vessels, and extracellular fluid due to the changes in the intracellular-intravascular osmotic gradients (Bieuzen et al., 2013). Increased blood volume is demonstrated by two mechanisms 1) haemodilution 2) blood displacement (Wilcock et al., 2006). Haemodilution is the increased diffusion of fluids that results from the hydrostatic pressure acting on the submerged portion of the body, while blood displacement is caused by the haemodilution and leads to relocation of fluids through an osmotic pressure gradient (Wilcock et al., 2006). This is believed to be a key underlying mechanism aiding in the removal of excess oedema and metabolites that pool in the limbs following high intensity eccentric muscle contractions. The increase in central cavity blood volume causes the activation of arterial and cardiopulmonary baroreceptors, which subsequently reduce sympathetic activity and increase parasympathetic activity (Schaal et al., 2013). Furthermore, an increased central blood volume has important effects on cardiac pre-load and ventricular filling (Wilcock et al., 2006; Krip et al., 1997; Bieuzen et al., 2013; Schaal et al., 2013). It has been demonstrated previously (Krip et al., 1997) that increases in blood volume can result in immediate changes in diastole function (ie. the amount of blood filling in the heart between heart beats). An increased cardiac output is important for athletes as it would aid in the clearance of the metabolites from venous blood returning to the heart and increase oxygen transport to the musculature facilitating recovery following exercise. The increase in central blood volume and resulting cardiac changes are affected directly by the depth of immersion, particularly stroke volume. Stroke volume increases drastically as hydrostatic pressure, and depth of immersion increases, as demonstrated by increases of 12-37% (hip level immersion), 38-67% (xiphoid process immersion), 28-95% (head out only immersion) (Wilcock et al., 2006).   Another important aspect of hydrotherapy for improving recovery that has been investigated is the effect hydrostatic pressure can have on the sympathetic and parasympathetic systems. The sympathetic and parasympathetic systems are indicators of recovery, as sympathetic activity is increased following exercise, while parasympathetic 	  	  	   9	  activity has been found to decrease (Cochrane, 2004). With adequate rest and recovery, an athlete’s sympathetic nervous system activity should return to resting levels (Cochrane, 2004; Schaal et al., 2013), however, as mentioned previously, elite athletes rarely are exposed to the recommended amount of recovery time for this return to baseline levels to occur. Without the adequate rest period, sympathetic activity remains high (subsequently maintaining parasympathetic activity), and this can lead to the signs/symptoms demonstrated by overtraining/overreaching (Cochrane, 2004). Furthermore, with increased sympathetic activity, the body is unable to return to homoeostasis and normal levels of parasympathetic activity. It has been suggested that the measurements of sympathetic/parasympathetic activity via heart rate variability is a possible useful tool for measuring recovery (Urhausen & Kindermann, 2002). Furthermore, cardiac parasympathetic dominance is related to the maintenance of exercise performance, and ability to maintain desired exercise intensity, as it is a measure of an individual’s ability to fully recover to resting levels of sympathetic/ parasympathetic resting levels (Stanley et al, 2012). As a result, any recovery mechanism that was found to improve parasympathetic activity would be beneficial for athletes maintaining performance throughout a training macrocycle (Schaal et al., 2013).  In a study investigating the effects of parasympathetic/sympathetic reactivation following CWI, CWT, or passive recovery using HRV, Stanley et al. (Stanley et al., 2012) found that both methods of hydrotherapy (CWI and CWT) demonstrated higher reactivation of parasympathetic activity compared to the passive recovery group. A possible reason for the increase in parasympathetic reactivation could be due to the hydrostatic pressure that stimulates the cardiovascular system as explained previously via increased venous return, stroke volume and cardiac output. Moreover, the parasympathetic reactivation could be the result of the stimulation from cold-water immersion that is included in both methods of hydrotherapy (CWI and CWT). While there was no statistically significant increase in performance for the hydrotherapy methods, it was demonstrated that both CWT and CWI groups experienced increased perception of recovery, as well as cardiac parasympathetic reactivation. Both mechanisms are feasible, as another study has demonstrated that Whole Body Cryotherapy (“dry” cryotherapy that involves no water immersion) was also effective in improving cardiac parasympathetic activity (Schaal et al., 2013). However, there are contradictions in the literature regarding whether it is the temperature (more specifically, 	  	  	   10	  cold) that is influencing parasympathetic reactivation, or the act of hydrostatic pressure on the body. While Stanley et al. (Stanley et al., 2012) demonstrated that both CWT and CWI exhibited increased parasympathetic reactivation compared to the control group, they still suggest that CWT may not expose the body to cold temperature change for long enough to truly stimulate the autonomic nervous system (ANS), which consists of the parasympathetic system.  Contrast Water Therapy Contrast water therapy (CWT) is the combination of HWI and CWI. Similarly to the previously mentioned hydrotherapies, CWT is hypothesized as an effective recovery method due to the use of water immersion to elicit hydrostatic pressure on the muscular and vascular structures (Vaile et al., 2008a). Furthermore, it is reasonable to suggest that CWT elicits the benefits of both HWI and CWI within one treatment. It has been reported that CWT could potentially be an effective recovery mechanism, as the vasodilation that results from exposure to HWI and the vasoconstriction that results from CWI resembles a “pumping” action within the blood vessels (Cochrane, 2004; Crampton et al., 2013; Hamlin, 2007; Pournot et al., 2011). The alternating HWI and CWI are hypothesized to mimic the skeletal muscle pump, a naturally occurring mechanism within the musculature that aids in venous return (Cochrane, 2004). By mimicking the skeletal muscle pump, the alternating vasodilation and vasoconstriction is believed to aid in the removal of oedema and metabolites (Cochrane, 2004; Hamlin, 2007). There has been much debate over whether this mechanism of action is in fact occurring, while some critics suggest that CWT may not expose the vessels to enough hot/cold temperature in order to elicit circulatory changes (Cochrane, 2004). Also, it has been suggested that the removal of tissue debris from muscle damage and metabolic by-products is facilitated by the lymphatic system, and therefore would not be altered by changes in circulation elicited by hydrotherapy, specially CWT (Cochrane, 2004; Myrer et al., 1997) However, due to the inconsistency in protocols and methodology, it is difficult to make generalizations from these reports (Bieuzen et al., 2013; Cochrane, 2004; Pournot et al., 2011).    Due to the considerable contradiction in literature, studies have been done in an attempt to demonstrate a dose-response in regards to the length of treatment and ratio of HWI to CWI (Versey et al., 2011). While there does not appear to be a dose response (i.e., benefits 	  	  	   11	  increase with an increase in treatment length), it does appear that CWT treatments ranging between 6 and 12 min are effective in maintaining performance, whereas CWT of 18 min did not demonstrate performance maintenance (Versey et al., 2011). Furthermore, it appears that the ratio of HWI to CWI is critical to the effectiveness of performance improvement or at the very least, maintenance (Vaile et al., 2008a; Vaile et al., 2008b; Versey et al., 2011). Most of the literature surrounding CWT uses protocols including ratios of HWI to CWI of 4:1 or 3:1, implying that HWI is the more critical immersion required to elicit benefits for recovery. While some researchers indicate that these ratios are indeed the most effective (Cochrane, 2004), the most consistent reports include protocols of equal, brief, immersions 1.5:1.5 (Pournot et al., 2011) or 1:1 (Vaile et al., 2008a; Vaile et al., 2008b). Furthermore, it has been suggested that CWT with high HWI treatment length compared to CWI treatment length is ineffective in facilitating recovery, and therefore studies that investigate these treatment ratios are counterproductive to advancing the literature in the field (Versey et al., 2011). Moreover, the majority of studies that have reported CWT to be an ineffective recovery strategy have used varying, and inconsistent levels of water immersion/depth of immersion (Versey et al., 2011). Full body water immersion during CWT (head and neck out only) has been demonstrated to be effective for up to 12 min (Versey et al., 2011). This is likely due to the increased hydrostatic pressure acting on a greater surface area of the body (Versey et al., 2011). It has largely been demonstrated that CWI and CWT are the most effective hydrotherapy methods, as studies have demonstrated performance maintenance in these two conditions compared to HWI and TWI. CWI and CWT have been found to improve performance in regards to average power output on a cycle ergometer by 0.5-2.2% (CWT) and 0.1-1.4% (CWI), where HWI showed a decrease in performance (-0.6-3.7%), as did passive recovery (-1.7-4.9%) (Vaile et al., 2008a). The benefits of CWT have been demonstrated in highly eccentric contraction based protocols as well. Minimal changes in peak power for weighted jump squats were demonstrated at 48-72 hr post- heavy eccentric protocol for CWT and at 24-72 hr for CWI (Vaile et al., 2008b). Moreover, following the same protocol mid-thigh girth was reduced for both CWI and CWT compared to HWI (Vaile et al., 2008b). These findings indicate that CWT may be effective in reducing oedema that results from exercise induced muscle damage, as well as maintaining performance following 	  	  	   12	  eccentric heavy exercise protocols. CWT was found to have minimal changes from baseline performance in regards to 1 hr and 24 hr post-exercise measurements of maximal voluntary contraction (MVC) of the knee extensors and vertical jump (Pournot et al., 2011). These findings reiterate that CWT may be effective in maintaining subsequent exercise performances in comparison to baseline values. This is critical because if athletes are able to perform at the same level after multiple games/matches, they are at an advantage over their competitors. Moreover, if athletes are able to maintain their performance in subsequent training sessions (following highly fatiguing training sessions) they will be able to maximize each session. A return to baseline would indicate recovery (Pournot et al., 2011; Tomlin & Wenger, 2001), and therefore indicate that CWT may be effective in minimizing the risk of overreaching/overtraining syndrome.  Studies have also investigated CWT as a mechanism for removing metabolic waste products and inflammatory biomarkers such as Creatine Kinase [CK], Lactate Dehydrogenase [LDH], Interleukin-6 [IL-6], Myoglobin [Mb], and C-Reactive Protein [CRP] that result from eccentric muscle contractions (Barnett, 2006; Bieuzen et al., 2013; Kanda et al., 2013; McHugh et al., 1999; Nédélec et al., 2012). Increased blood plasma concentrations of these metabolites have been associated with performance decrements at 48 hr post-exercise, which is consistent with research regarding exercise induced muscle damage and delayed onset muscle soreness (Pournot et al., 2011). It has been demonstrated that CK and Mb were reduced in CWT groups compared to passive recovery groups (Bieuzen et al., 2013), demonstrating that CWT may be, at the very least, more effective than no recovery treatment at all. CWT has resulted in 85% recovery of CK levels to baseline after 84 hr, compared to 88.2% recovery from active recovery, 84.4% recovery from compression garments and merely 29% recovery from passive recovery (Gill et al., 2006). This reiterates that CWT may be effective in improving the clearance rate of CK and other metabolites following strenuous exercise, especially when compared to passive recovery. When compared to CWI, CWT was found to have no statistically significant difference in serum CK levels compared to the CWI (Bieuzen et al., 2013), although there appear to be trends that CK levels were lower for CWI. Moreover, another study indicated that CWI, when compared to CWT, TWI, and passive recovery, was the only experimental condition that resulted in significantly lowered CK levels following high- intensity circuit training (Pournot 	  	  	   13	  et al., 2011). Furthermore, there did not appear to be significant differences between CWI and CWT in regards to clearance rate of LDH (Bieuzen et al., 2013). In fact, Pournot et al. (2011), reported that when compared to TWI, CWI and passive recovery, CWT was the only method that exhibited increases in LDH. One study reported no reductions in measures of CRP or CK for three treatment conditions (CWI, CWT, passive), as all groups demonstrated a marked increase of CK and CRP 48 hr following game-like performances (Ingram et al., 2009). All of these results further indicate the contradictions and inconsistencies in the available scientific evidence regarding CWT and other methods of hydrotherapy.  It is believed that the benefits demonstrated by CWI and CWT appear to be linked to the hydrostatic pressure exhibited from water immersion, but also the exposure to extreme temperature changes that results in increased perception of recovery and reduced feelings of muscle soreness (Ingram et al., 2009). It has been suggested that the localized cooling effect demonstrated with CWI may blunt the diffusion rate of inflammation markers, via compression from hydrostatic pressure and vasoconstriction from the cold temperature (Stanley et al., 2012), while subsequently reducing the inflammatory response and the occurrence of exercise induced muscle damage (Pournot et al., 2011). This reduced inflammatory response has been demonstrated by decreased leukotriene and neutrophil concentrations 1-hr post exercise (Pournot et al., 2011). As such, it is possible that the cold water immersion portion of CWT may also elicit similar benefits, which are maximized by the “vaso-pumping” mechanism resulting from alternating HWI and CWI (Pournot et al., 2011). This exposure to cold water is thought to stimulate the nervous system and reactivate the parasympathetic system that is blunted during and following exercise (Cochrane, 2004; Schaal et al., 2013). This is critical to the recovery process, as once parasympathetic reactivation occurs, heart rate variability begins to normalize, which ultimately leads to increased recovery and return to optimal resting levels (Schaal et al., 2013). It has been suggested that the stimulation of the nervous system that results from exposure to cold temperatures (from CWI or CWT) results in vasoconstriction, which results in increased blood volume in the central cavity due to increased venous return (Schaal et al., 2013). As mentioned earlier, increases in central blood volume leads to cardiovascular changes such as increased stroke volume, increased cardiac output, and increased arterial pressure (Schaal et al., 2013; Vaile et al., 2008a; Wilcock et al., 2006). The cardiovascular changes demonstrated 	  	  	   14	  by increased central blood volume subsequently lead to activation of baroreceptors, which aid in the reduction of sympathetic activity and increased parasympathetic activity (Schaal et al., 2013). This is a very important finding, as it has been demonstrated and mentioned previously that by facilitating reactivation of parasympathetic activity, it is feasible to suggest that recovery time would be reduced, as heart rate variability would normalize faster than if parasympathetic activity needed to reactivate at a normal rate. Furthermore, it has been suggested that hydrostatic pressure may also activate parasympathetic activity via baroreceptor activation, due to the increased venous return demonstrated by the changes in the osmotic pressure gradient (Schaal et al., 2013). However, some researchers believe the CWT may not expose the body to cold stimulation for enough time to cause this parasympathetic reactivation (Schaal et al., 2013). In a study investigating the effects of hydrotherapies on parasympathetic activity reactivation, it was determined that CWI and CWT both demonstrated increased cardiac parasympathetic reactivation and increased activity when compared to passive recovery, during a 90 min recovery session following supramaximal activity (Stanley et al., 2012). Due to the contradictions in the literature, more research into the effects of CWT on parasympathetic activity is needed to establish a better understanding regarding this phenomenon. It is also very important to tailor recovery mechanisms towards parasympathetic reactivation, as when parasympathetic activity is blunted following exercise and sympathetic activity remains high, it can lead to the signs and symptoms typically associated with overreaching/overtraining (Cochrane, 2004).  Finally, another key outcome measure used in studies investigating CWT appears to be perception of recovery and/or muscle soreness. It is hypothesized by researchers that recovery strategies that aim to blunt the inflammatory response and subsequent exercise induced muscle damage can minimize muscle soreness, as the influx of prostaglandins that result from muscle damage is what causes muscle soreness (Connolly et al., 2003). This has been demonstrated by a variety of tools; however the most commonly used measures are a Visual Analog Scale (Bieuzen et al., 2013; Vaile et al., 2008b), TQR Recovery Scale (Kinugasa & Kilding, 2009), or a Likert Scale (Bieuzen et al., 2013). In a review of studies that used CWT (Bieuzen et al., 2013), pooled results from all studies indicated that CWT significantly reduced reports of muscle soreness, as reported by mean standard differences (MSD): 24 hr post-exercise (-0.51 MSD), 48 hr (-0.58 MSD), 72 hr (-0.40 MSD), and >96 hr 	  	  	   15	  (-1.21 MSD). This same study (Bieuzen et al., 2013) indicated that compared to CWI, CWT did not demonstrate significant differences in regards to perception of muscle soreness, suggesting that both hydrotherapy methods are effective at improving perception of recovery and muscle soreness. Furthermore, it was determined that the minimal important difference for changes in muscle soreness resulting from CWT is a range from 14-25% from baseline measures (Bieuzen et al., 2013). Studies demonstrated this minimal important difference between 24-72 hr post-exercise in the studies included in the review, however there was not standardization for the VAS used (Bieuzen et al., 2013). As such, when all pooled results were measured on a 10 cm VAS, the minimal important difference was not met (Bieuzen et al., 2013). Furthermore, another study (Higgins et al., 2013) found that passive recovery demonstrated lower pain scores at 24 hr, and CWI demonstrated lower pain scores at 48 hr post-exercise when compared to CWT. This further substantiates that there are considerable inconsistencies in protocols and methodology that must be addressed if researchers hope to progress in the field of recovery and recovery applications.  Several studies have investigated the difference between CWI and CWT (as well as CWT and other recovery mechanisms) in regards to muscle soreness perception. Researchers have suggested that CWI is more effective than CWT in minimizing muscle soreness (Halson, 2013; Ingram et al., 2009), while both CWI and CWT demonstrated large effect sizes in regards to perception of muscle soreness (1.48 and 0.81, respectively) The main effect in regards to CWT did show improvements in muscle soreness and pain perception at 24 hr, demonstrating it can, in fact, be effective for this outcome measure (Halson, 2013; Ingram et al., 2009). Conversely, one study reported that CWT was the only hydrotherapy (HWI, CWI) to reduce perception of pain significantly (p < 0.01) at time points of 24,48 and 72 hr following highly eccentric exercise protocol (Vaile et al., 2008b). It is hypothesized that the thermal sensation is reduced following CWI (Kinugasa & Kilding, 2009), which could help to explain the improvements in perceived recovery following treatment. Furthermore, it has been reported that CWI reduces nerve conduction velocity and, therefore, reduces pain sensations (Bahnert et al., 2013). Reduced pain perception ultimately leads to lower reports of muscle soreness and improved perceptions of recovery. It is reasonable to consider, that this may be one of the underlying mechanisms for CWT being an effective treatment, as CWT exposes individuals to CWI during its protocol and, as such, likely 	  	  	   16	  exhibits several similar benefits as CWI. Furthermore, it is suggested that ending CWT treatment on CWI will elicit these analgesic benefits, similar to that demonstrated by solely CWI (Bieuzen et al., 2013). Also, as described earlier, the buoyancy that occurs during hydrotherapy may also cause reduced perception of fatigue, as the immersed portion of the body is not being acted on by gravitational forces (Montgomery et al., 2008; Wilcock et al., 2006). As with many studies in the field of recovery mechanisms, there are studies that have suggested CWT does not improve perception of recovery and muscle soreness. One study reported that muscle soreness was not reduced 24 hr following an eccentric exercise protocol, but rather, was significantly increased following CWT, CWI, TWI and passive recovery (Pournot et al., 2011). However, the majority of scientific evidence indicates that CWT and CWI are capable of improving an individual’s perception of recovery (Stanley et al., 2012). Furthermore, it has been demonstrated that there may be a moderate correlation between the perception of muscle soreness and rMSSD, a common measurement observed through heart rate variability (Stanley et al., 2012). This finding suggests that a greater increase in parasympathetic activity (which has been observed following CWI and CWT) may result in a reduced perception of muscle soreness. Again, further research is required to determine the specific underlying mechanisms that drive CWT as a potentially effective recovery strategy, while also establishing a better understanding of the specific protocol required to elicit the benefits believed to be associated with the use of CWT.  2.3 Variable Intermittent Pressure System The variable intermittent pressure (VIP) device was invented by Dr. Darren Warburton for usage with clinical and high performance populations. The VIP consists of a differential pressure system that alternates positive and negative pressure on the lower limbs in an attempt to facilitate cardiovascular changes that may potentially facilitate the removal of oedema and metabolites. The VIP device also contains a customized and integrated cycle ergometer for active recovery during the treatment, in an attempt to elicit the improved clearance of metabolites typically associated with active recovery (Spencer et al.,2006). Owing to the proprietary nature of this methodology, there are currently no published studies using this recovery application. However, there is considerable evidence regarding the specific changes elicited from negative or positive pressure application separately to the limbs. The investigations that have been undertaken with the use of this device have 	  	  	   17	  demonstrated significant reductions in pain and improved performance in a wide range of athletes including Olympic athletes (Warburton et al; unpublished observations). Also, elite athletes that have utilized the VIP system have reported improved perception of recovery following treatments and they believe this improved recovery benefitted their subsequent performance (Warburton et al; unpublished observations). The use of this device in comparison to other slightly more established recovery applications would allow us to further develop the understanding of the effects of this device while also establishing scientific evidence on this novel recovery strategy. The theory behind the use of positive and negative pressures originates from the clinical use for their technologies as a method for wound healing following injury and/or surgery. Similar to IPC treatment and compression garments, the origins of the VIP recovery application stems from the clinical use of negative and positive pressure as a method for facilitating circulation. The benefits of negative pressure as a method for stimulating blood flow to enhance wound healing have been studied extensively in the clinical setting (Thompson & Marks, 2007). Furthermore, it has been reported that acute wound recovery is effectively enhanced due to the application of negative pressure, and the facilitation of oedema and metabolite removal from the wound site (Thompson & Marks, 2009). The process of wound healing is comparable to that of recovery from EIMD, as both represent the presence of inflammation, and the subsequent inflammatory process. Furthermore, it has been reported that alternating normal pressure and negative pressure has been effective in improving circulation, as well as venous return and removal of waste products via the lymphatic system (Orletskiy & Timtchenko, 2009). Consequently, the benefits observed through the alternation of normal pressure and negative pressure in regards to improving circulation from the lower body to the central cavity would, theoretically, be enhanced by the replacement of positive pressure in place of normal pressure. Positive pressure enhances skin blood flow through compression of the endothelial cells, increasing shear and strain forces in the vessels and ultimately promoting increased venous return (Liu et al., 1999; Journeay et al., 2004). The alternation of negative and positive pressure provides a passive and/or indirect pressure application that mimics a massaging technique (common mechanism to promote lymphatic return), and facilitates the lymphatic return (Orletskiy &Timtchenko, 2009; Fonda & Sarabon, 2015). Studies have reported that intermittent application of negative pressure 	  	  	   18	  and normobaric conditions have been effective in promoting blood flow and lymphatic drainage (Orletskiy &Timtchenko, 2009; Fonda & Sarabon, 2015). Theoretically, the addition of positive pressure intermittently applied with negative pressure would amplify the benefits observed during the normal pressure phases of treatment.  Lower Body Negative Pressure There is evidence that indicates the use of negative pressure in facilitating cyclic changes. It has been reported that negative pressure application results in increased blood flow towards the area of decreased pressure, which causes pooling of blood at the limbs affected by the negative pressure (Murray et al., 1968). This is characteristic of the law of fluid dynamics, in which fluids shift from an area of higher pressure through an osmotic pressure gradient to an area of lower pressure (Esch et al., 2007). This exposure to negative pressure has been demonstrated to increase leg circumference (Murray et al., 1968), which demonstrates the increased blood flow and subsequent pooling that occurs in the limbs affected by negative pressure (Journeay et al., 2004). Exposing the body to negative pressures initially causes dilation of the blood vessels at the areas of pressure application (Murray et al., 1968). This shift in blood flow causes a drop in blood pressure that leads to hypovolemia (Murray et al., 1968) or syncope (Esch et al., 2007). When the body is exposed to hypovolemia, the natural response of the vessels is to vasoconstrict in an attempt to restore homoeostasis (Murray et al., 1968) which ultimately leads to increases in heart rate (Esch et al., 2007). Increases in heart rate response are characteristic of increases in sympathetic activity, which further facilitates the vasodilation response to the negative pressure being applied on the lower body (Cochrane, 2004). Skin blood flow during negative pressure has been reported to reduce (Journeay et al., 2004), which suggests that the baroreceptors are not stimulated. Subsequently, lower body negative pressure application has been found to reduce stroke volume and increase heart rate when compared with lower body positive pressure (Journeay et al., 2004). Furthermore, it has been suggested that prolonged exposure to negative pressure, and subsequent venous pooling to the lower body, results in reduced skin blood flow (Journeay et al., 2004). One study (Fonda & Sarabon, 2015) investigated the effect of intermittent lower body negative pressure and normobaric conditions compared to passive recovery, and demonstrated reduced pain perceptions, reduced explosive power loss following a plyometric 	  	  	   19	  eccentric protocol, compared to a control/passive recovery condition. This suggests that the negative pressure application was effective in promoting blood flow changes that reduced the occurrence of oedema and improved perception of recovery (Fonda & Sarabon, 2015). This study indicated that it was the first published study to investigate the effects of negative pressure application following strenuous plyometric exercise. As a result, it is clear that further research is warranted to understand the effects of lower body negative pressure on the facilitation of recovery or impact on physical performance following strenuous exercise.  Lower Body Positive Pressure  Positive pressure has been found to increase tissue pressure, through a reduced pressure gradient that subsequently results in increased venous pressure (Nishiyasu et al., 1998). The occurrence of increased venous pressure results in increased venous return towards the core of the body, ultimately leading to increased central blood volume (Nishiyasu et al., 1998). It has been postulated that increases in central blood volume may lead to increases in parasympathetic activity, which have been found to normalize heart rate variability, and subsequently results in an improved rate of recovery from exercise (Schaal et al., 2013). As mentioned previously, increased central blood volume leads to increased stroke volume and subsequently, increased cardiac output (Schaal et al., 2013). Furthermore, dominant parasympathetic activity is associated with maintenance of exercise performance (Stanley et al., 2012), so, as a result, if positive pressure is able to elicit increases in parasympathetic activity, it is possible that it may benefit in the maintenance of subsequent athletic performance for individuals. It has been demonstrated that increases in central blood volume result in the activation of baroreceptors that decrease sympathetic activity, and increase parasympathetic activity (Stanley et al., 2012), which allows the athlete to return to resting levels. It appears that by alternating between applications of both positive and negative pressure, substantial changes in cyclic blood flow can occur, which will aid in the removal of oedema and metabolites that result from high intensity exercise, and therefore facilitate the recovery from exercise for athletes. As a result, it appears that these cyclic changes in circulation are more substantial than other mechanisms relying strictly on hydrostatic pressure and/or compression application to facilitate venous return, indicating that the VIP device may demonstrate significant clinical and practical significance in the 	  	  	   20	  field of recovery. However, there is conflicting literature regarding the ability of lower body positive pressure to facilitate an increase in cardiac output (Williamson et al., 1994). It has been reported that body posture may influence the extent to which fluids shift towards the central cavity, and subsequently increasing cardiac output (Williamson et al., 1994). A semi-recumbent posture position may not be as effective as a completely supine posture for maximizing the cardiac output increase during, and following, the application of lower body positive pressure (Williamson et al., 1994). Further research should investigate the efficacy of different recovery strategies to determine the ideal position to facilitate the shift in fluids towards the central cavity, and thereby increasing cardiac output. This report (Williamson et al., 1994), however, only focused on lower body positive pressure, and not the combination of negative/positive as demonstrated with the VIP system. As a result, it is possible that the alternation of negative/positive pressure applied during the VIP treatment protocol could elicit greater mobilization of pooled metabolites and oedema, and subsequently result in enhanced venous return, as opposed to the application of positive pressure alone.  Positive pressure application has been reported to reduce HR following exercise (Journeay et al., 2004), which would indicate an increase in parasympathetic activity or a return to a resting state. Furthermore, previous literature (Journeay et al., 2004) has demonstrated significant increases in skin blood flow from the lower limbs to the central cavity following the application of positive pressure (+45mmHg). This increase in blood flow to the central compartment is believed to be due to an increase in baroreceptor stimulation (Journeay et al., 2004). Baroreceptor stimulation is a key function that precipitates parasympathetic reactivation (Schaal et al., 2013), and is a crucial step towards recovery following strenuous exercise.  Most of the literature available regarding the theoretical benefit of lower body positive pressure and/or lower body negative pressure focuses exclusively on one mechanism or the other. It is clear that further research into the combination of lower body positive and negative pressure applied in combination is needed to further understand the impact that the VIP system may have on enhancing recovery from strenuous athletics. As mentioned previously, negative pressure and normobaric conditions demonstrated an ability to reduce pain perceptions and facilitate performance maintenance following strenuous plyometric exercise (Fonda & Sarabon, 2015). In theory, the combination of increased positive pressure 	  	  	   21	  in place of normobaric conditions should enhance the performance and physiological responses following intermittent pressure application. 2.4 Intermittent Pneumatic Compression   Compression garments have been demonstrated to be effective in maintaining performance, minimizing perception of fatigue and muscle soreness, as well as aiding in the removal of metabolites and oedema from the limbs (Gill et al., 2006; Hanson et al., 2013; Montgomery et al., 2008). Consequently, researchers have hypothesized that by applying higher intensity of compression to the limbs, this will further enhance an athlete’s ability to recover and subsequently, positively impact performance. The mechanism proposed to do so is intermittent pneumatic compression devices (IPC). IPC has widely been used as a mechanism for facilitating haemodynamics changes that improve circulation for patients with vascular disorders (Chen et al., 2001). The circulatory changes that result from IPC are similar to those reported from hydrotherapy, as pressure/compression is applied to the limbs, in an attempt to facilitate venous return, improve clearance of metabolites and oedema, and increase central blood volume (Chen et al., 2001; Liu et al., 1999). As mentioned previously increases in central blood volume results in increased stroke volume and ultimately increased cardiac output. It has been reported that the application of IPC devices results in two specific forces occurring within the vessels, 1) strain 2) shear (Chen et al., 2001; Liu et al., 1999). The strain force that occurs within the endothelial cells is a consequence of the vasodilatation that occurs proximally from the point of compression application (Chen et al., 2001). This vasodilation has demonstrated an increase of 20% strain forces acting on the endothelial cells when 50 mm Hg is applied to the limb, due to the increase of blood flow being pushed through the vessels and back towards the heart via venous return (Chen et al., 2001). Furthermore, the intensity of pressure and inflation rate can influence blood flow velocity within the vessels, which can cause increases in shear forces acting on the endothelial cells as well (Chen et al., 2001; Liu et al., 1999). When pressure is applied sequentially, as is the case with sequential pneumatic compression devices such as the NormaTec MVP/PRO recovery device, an increase in blood flow velocity of approximately 200% has been reported to occur, which causes excessive shear stress on the same cells experiencing strain forces from vasodilation (Chen et al., 2001). The shear stress that is occurring within the cells causes the body to release the vasodilator, nitric oxide (Liu et al., 1999). As such, it is suggested that the 	  	  	   22	  most beneficial form of IPC would be a device that has a high inflation rate, that subsequently causes a large shear stress on the endothelial cells, resulting in the release of nitric oxide (Liu et al., 1999). This release of nitric oxide is believed to be the primary cause of vasodilation towards the proximal end of the limbs that aids in venous return, and therefore facilitates the removal of metabolic waste products and excess oedema (Liu et al., 1999).    The speculation of IPC as an effective mechanism for athletes has taken root in the theory that IPC improves venous return, and would therefore remove the metabolites that occur following exercise induced muscle damage resulting from highly eccentric muscle contractions (Gill et al., 2006). Studies regarding IPC have largely focused on improving circulation in patients with deep vein thrombosis, peripheral artery disease, and other vascular disorders (Chen et al., 2001; de Haro et al., 2010; Liu et al., 1999; Talbot et al.,2012). Studies that have investigated pneumatic compression in clinical populations have used the ankle-brachial index as the primary outcome measure, which is calculated from the larger measure of systolic pressures measured in the dorsalis pedia artery and the posterior tibial artery of the limb in which pressure is applied, divided by the larger measure of systolic pressures in the brachial arteries of the arms (de Haro et al., 2010). It has been demonstrated that ankle-brachial index post-exercise steadily increases with respect to the length of a treatment program, as ankle brachial index post exercise increased by 42% from baseline after one month of treatment and 97% above baseline after 3 months of treatment (de Haro et al., 2010). This is a significant finding, as this study also demonstrated that ABI at rest did not change, suggesting that IPC treatment may be effective in improving oxygenation and circulation during exercise (de Haro et al., 2010). Furthermore, this change in ABI has been suggested to aid in blood flow for patients suffering from peripheral arterial obstruction disorder (Chang et al., 2012). This has been demonstrated by improvements in both initial claudication distance (onset of pain during a 6 min walk test) and absolute claudication distance (distance patients could walk before cessation of the test due to claudication pain) (Chang et al., 2012). Following three months of IPC treatment, patients demonstrated improved initial claudication distance of 146% from baseline values, and absolute claudication distance of 94% from baseline values (Chang et al., 2012). This indicates that 	  	  	   23	  the changes in limb haemodynamics are evident following IPC treatment, which could potentially be translated towards healthy populations, particularly athletes.   IPC treatment has been reported to facilitate the removal of oedema and metabolites, as indicated by decreasing arm volume by 25% in participants with lymphatic disorders (Chen et al., 2001). Furthermore, the increase in interstitial pressure that results from the application of compression to the limbs causes fluids within the vessels to re-enter circulation, suggesting that IPC is in fact effective in facilitating the clearance of metabolites and oedema that occur following surgery and/or following high-intensity eccentric exercise (Chen et al., 2001). This effect however, may be time dependent, as IPC has shown to be most effective on day 2 and 3 following a heavy eccentric exercise protocol, in regards to both reduction in the occurrence of oedema and muscle stiffness (Chleboun et al., 1995). This reduction in swelling on day 2 and 3 post-exercise is interesting, as this is consistent with the time frame demonstrated for the occurrence of delayed onset muscle soreness (Chleboun et al., 1995). This finding indicates that the use of IPC may help reduce the amount of oedema and muscle stiffness that results in delayed onset muscle soreness, suggesting that IPC may be effective in influencing perception of recovery, due to the lower incidence of delayed onset muscle soreness (Chleboun et al., 1995). However, it is important to note that while IPC was effective in minimizing swelling and stiffness, the treatment did not reduce the documented 5-day course of recovery and return to baseline levels (Chleboun et al., 1995). Furthermore, as mentioned previously, IPC may be effective in minimizing markers of muscle damage due to this reduction in swelling and stiffness, such as the clearance of metabolites, such as CK (Gill et al., 2006).    There does not appear to be an abundance of literature regarding the use of IPC devices as a tool for maintaining or improving performance following high intensity exercise, as this use of IPC devices has not become widespread until only recently. As with most of the literature regarding other recovery strategies, the information regarding IPC use is inconsistent due to the varying types of IPC devices, length of treatment, intensity of treatment, and underlying mechanisms occurring from use of the device. Contrary to what some research studies have indicated, it has been suggested by one study that IPC may not be effective as a recovery strategy, as it may not impact haemodynamic changes in healthy populations as it does in vascular disorders (Cochrane et al., 2013). Furthermore, there is 	  	  	   24	  conflicting evidence that reports intermittent sequential pneumatic compression devices did not reduce circulating metabolites following a maximal aerobic capacity test (VO2 Max test) (Zelikovski et al., 1993). However, these findings also demonstrated a 45% increase in aerobic capacity (VO2 Max test) (Zelikovski et al., 1993) suggesting that there may be alternative underlying mechanisms resulting in the effectiveness of pneumatic compression devices as a recovery application. It is important to note, however, that this study (Zelikovski et al., 1993) used aerobic capacity tests as an outcome variable, whereas the vast majority of studies regarding recovery and circulating metabolites have addressed pneumatic compression devices’ effectiveness following high intensity, eccentric muscle contractions such as resistance training protocols or sports that involving significant jumping, decelerating or change of direction (Cochrane et al., 2013).  Due to the inconsistency in the literature, the findings presented here are from a variety of types of intermittent pneumatic compression. As technology has developed in recent years, the type of compression application has changed. Types of compression application include: 1) intermittent mechanical compression (de Haro et al., 2010) 2) intermittent pneumatic compression with uniform compression (non-sequential) (Chang et al., 2012; NormaTec Science Website, n.d.) 3) sequential (pressure applies sequentially up the limb at the same pressure, holds, and full release of compression at the same time) 4) sequential gradient: pressure applies sequentially up the limb at different pressures, in which the pressure in the proximal chambers must be less than the previous and more distal chamber 5) sequential pulse technology: which will be explained in next chapter (NormaTec Science Website, n.d.). Sequential pulse technology is the technology currently utilized by the leading intermittent pneumatic compression recovery device, the NormaTec MVP/PRO (NormaTec Science Website, n.d.).  NormaTec MVP Recovery Device The NormaTec MVP is a pneumatic compression device that has gained popularity and anecdotal support from athletes as a post-exercise recovery strategy in recent years. Similar to other IPC devices, there is little scientific evidence to support the NormaTec as a post-exercise strategy, as it has previously been used as a treatment method for vascular disorders (Talbot et al., 2012). The evidence is inconsistent, and largely anecdotal, but the NormaTec has become an increasingly popular recovery strategy for elite level athletes 	  	  	   25	  across all sports (NormaTec Science Website, n.d.). The standard NormaTec device is comprised of two leg sleeves for lower body recovery treatment, or two arm/shoulder sleeves for upper body recovery treatment. The key difference separating the NormaTec recovery device from other pneumatic compression devices is that the NormaTec uses a patented sequential pulse technology for its pressure application (NormaTec Science Website, n.d.). The components of sequential pulse technology consist of a five-chamber inflation system, in which the chambers inflate distally to proximally with varying intensity of pressures (Normatec Science Website, n.d.; Cochrane et al., 2013; Hanson et al., 2013). NormaTec refers to this system as a six-phase process, in which: 1) phase 1 the chamber begins to inflate and pulse in chamber one (the most distal end of the limb), 2) chamber one (distal chamber) holds pressure, and chamber two (next sequential chamber) begins inflating and pulsing, 3) chamber three begins to inflate and pulse, while chamber one and chamber two hold pressure, 4) chamber four begins to inflate and pulse, chamber two and chamber three hold pressure, and chamber one releases pressure, 5) chamber five begins to inflate and pulse, chamber three and four hold pressure, and chamber two releases pressure, 6) chamber five and chamber four hold pressure, while chamber 3 releases. (NormaTec Science Website, n.d.). At the end of this sequence the two most proximal chambers (chamber four and chamber five) release pressure, and the sequence begins again at the distal end of the limb, in chamber one (NormaTec Science Website, n.d.). The device comes programmed with three options for recovery programs: recovery flush, customized and pre-programmed options. There are a wide variety of pressure intensities that can be applied during treatment options, but the manufacturer’s default for the most common option, the recovery flush, consists of pressures ranging from 60-80 mm Hg (Cochrane et al., 2013; Hanson et al., 2013). This equates to 70 mm Hg applied in chamber one (distal end chamber), 80 mm Hg in chambers two-four (middle three chambers), and 60 mm Hg in chamber five (proximal end chamber) (Cochrane et al., 2013; Hanson et al., 2013).  The gradual and sequential pressure application is believed to mimic two naturally occurring mechanisms in the body, the skeletal muscle pump (Cochrane et al., 2013; Hanson et al., 2013) and the peristaltic compression waves of the lymphatic vessels (Sands et al., 2014a; Talbot et al., 2012). Similarly to the other recovery mechanisms discussed previously, the application of pressure is thought to aid in venous return, which is accomplished naturally 	  	  	   26	  via the skeletal muscle pump. Furthermore, sequential compression has been demonstrated to be the most effective for emptying the veins, thereby facilitating venous return, and is the method of application the NormaTec device utilizes (Chen et al., 2001). The use of sequential pressure mimics the skeletal muscle pump by pushing the fluids away from the distal end of the limb and back through the veins. As such, when the presence of compression is applied sequentially rather than uniformly (as is demonstrated by many of the IPC devices in previous studies) the greatest increases in blood flow velocity occur (Chen et al., 2001). As mentioned previously, by increasing blood flow velocity by nearly 200% (as has been demonstrated with sequential pneumatic pressure), shear stress occurs (Chen et al., 2001; Liu et al., 1999). This increase in venous return accomplished by both the shear and strain forces occurring in the vessels, as well as the compression causing fluids from the interstitial space to re-enter circulation (Chen et al., 2001), suggest that the NormaTec may in fact be beneficial in accelerating the removal of exercise induced oedema and metabolic waste products. This has been demonstrated by some studies as the possible underlying mechanism owing to the anecdotal reports from elite athletes all over the world.  As previous compression literature has suggested, swelling, and muscle stiffness resulting from exercise induced muscle damage may be blunted by the compression, as well as less available space for the oedema and metabolites to pool (Halson, 2013). By facilitating the removal of oedema and metabolites that pool around the muscle from exercise induced muscle damage by applying increased pressure to the affected limbs and muscles, the NormaTec may also be able to blunt the inflammatory response (as other compression methods are believed to do) (Halson, 2013) that results following high-intensity eccentric exercise (Connolly et al., 2003; McHugh et al., 1999). During muscle damage, the presence of biomarkers of muscle damage concentrate near the damaged muscle, which initiates an inflammatory response leading to an increase in leukotrienes that then increase the vascular permeability of the vessels (Connolly et al., 2003). This increase in vascular permeability leads to the excessive build-up of oedema in the affected limbs, which ultimately leads to stiffness, and range of motion decrements (Chleboun et al., 1995; Connolly et al., 2003; McHugh et al., 1999). Therefore, by mimicking the skeletal muscle pump, the NormaTec would be able to blunt this inflammatory response and subsequently minimize the effects of exercise induced muscle damage and delayed onset muscle soreness.  	  	  	   27	  The patented sequential pulse technology that NormaTec utilizes is thought to mimic the peristaltic compression waves exhibited in the lymphatic vessels (Sands et al., 2014a; Talbot et al., 2012). The contraction phase of peristalsis is demonstrated by the compression of the various chambers during the sequential pressure application, while the relaxation phase occurs when a distal chamber releases following inflation of two more proximal chambers (Cochrane et al., 2013; Talbot et al., 2012). This mimicking of peristaltic compression waves may aid in the mobilizing and removal of fluids and metabolites that have pooled around the muscle, creating stiffness characteristic of exercise induced muscle damage (Chleboun et al., 1995). Furthermore, by removing the debris near the muscles via smooth muscle contractions characteristic of peristalsis, it is thought that obstructions to the lymphatic vessels will be reduced (Sands et al., 2014a). Obstructions are caused by the accumulation of biomarkers of inflammation and muscle damage, and without the accelerated removal of them with the aid of an external force, it is suggested that recovery will be delayed due to prolonged inflammation (Sands et al., 2014a). It appears that there are minor smooth muscle contractions occurring in the lymphatic vessel during exercise, but not to the extent that the NormaTec is reported to facilitate (Sands et al., 2014a). The ability of the NormaTec to mimic two naturally occurring biological mechanisms may strengthen the anecdotal support for athletes to use this device as a means of accelerating their recovery prior to subsequent training sessions.  There are very few studies that have specifically investigated the NormaTec as a means of facilitating recovery or maintaining/improving subsequent athletic performances. To our knowledge there appear to be four studies specifically addressing the NormaTec as a post-exercise recovery device, and all four used vastly different protocols and measurements to assess effectiveness.  The use of the NormaTec in regards to metabolite clearance has been demonstrated by two studies (Cochrane et al., 2013; Hanson et al., 2013). One of the studies, however, (Hanson et al., 2013), used blood lactate levels as a measure of recovery, which is a highly controversial and increasingly unsupported method for investigating recovery (Robergs et al., 2004). This further adds to the contradictions of the literature regarding this specific recovery strategy, as the results of the study (Hanson et al., 2013) indicate that the group using the NormaTec compared to passive recovery was effective in clearing blood lactate during a 20-	  	  	   28	  min recovery session between Wingate Tests. As this study did not investigate any other blood biomarkers, it is difficult to make any conclusions based off of these findings. Another study (Cochrane et al., 2013) investigated a variety of outcome measures following an exercise induced muscle damage inducing protocol, but specifically focused on Creatine Kinase (CK) levels as a measure of muscle damage. The findings demonstrate that both groups (NormaTec and Control) showed significant increases in CK levels, and therefore the NormaTec was unable to facilitate recovery from exercise (Cochrane et al., 2013). The literature is significantly lacking on the NormaTec in general and, as a result, it is difficult to conclude as to whether these findings should be supported. Cochrane et al. (2013) also looked at the impact the NormaTec had on maximal voluntary contraction (muscular strength) and vertical jump (lower body explosive power). However, the conclusions remained the same as there was no significant difference between maximal vertical jump and/or maximal voluntary contraction via muscle dynamometry (Cochrane et al., 2013). This appears to be the most comprehensive study regarding the NormaTec MVP recovery device, and the results indicate the device may not be effective in facilitating recovery following strenuous eccentric muscle contractions. Owing to the novelty of this device and the lack of depth in the literature, further research is warranted to substantiate or refute these findings.  Adding to the inconsistency of the available literature is a study that was performed on athletes at the United States Olympic Training Center (Sands et al., 2014a). This study is unique as it did in fact use elite athletes, as few studies have demonstrated, however, they did not standardize the exercise protocol of the athletes. Rather, they permitted the athletes to undergo their typical training. This poses significant issues as there can be considerable confounding variables acting on the athlete during these training sessions that may influence the results. Furthermore, this study (Sands et al., 2014a) investigated the athletes’ response to a pain to pressure threshold test after training and after using the NormaTec device, which is a completely unique outcome measure in regards to the previous literature regarding the NormaTec device. This makes the findings significantly difficult to compare and interpret. It was demonstrated in this study (Sands et al., 2014a) that participants in the NormaTec experimental condition required increased pressure to elicit pain via algometer when compared to baseline values. This suggests that the NormaTec is effective in reducing muscle soreness following high intensity training sessions in elite athletes. In a study done by the 	  	  	   29	  same authors (Sands et al., 2014b) that also used the NormaTec to investigate the effects of pneumatic compression devices on lower body flexibility. This study used experienced dancers to determine whether the NormaTec was able to elicit improvements in flexibility during a traditional forward split test (Sands et al., 2014b). The NormaTec group demonstrated absolute changes for flexibility of 25.3% in the right leg, and 33.3% in the left leg, compared to the control group that demonstrated absolute changes for flexibility of 12.2% in the right leg and 1.0% in the left leg (Sands et al., 2014b). There are many possible mechanisms suggested for why such a rapid change in flexibility was observed, but one possible explanation is due to the pulsing mechanism provided by the NormaTec, as it is believed that vibration/pulsing treatments can improve flexibility (Sands et al., 2014b). It can be hypothesized that if the NormaTec improves flexibility it may reduce muscle stiffness brought on by exercise induced muscle damage, as demonstrated by previous studies (Chleboun et al., 1995). There is very little scientific evidence available involving the NormaTec as a means of recovery from exercise, from the available scientific literature, there is a high degree of inconsistency making conclusions extremely difficult. Furthermore, only one of the studies used an intentional high volume eccentric contraction protocol to elicit and investigate the NormaTec’s impact on exercise induced muscle damage (Cochrane et al., 2013). Clearly, further research into the NormaTec as a recovery application and specifically the impact it has on exercise induced muscle damage caused by eccentric muscle contractions is warranted to develop further understanding of this device.               	  	  	   30	  Chapter 3: Methodology  3.1 Study Design This research utilized a randomized controlled trial experimental design, with participants randomly assigned to one of four possible groups (CWT, IPC, VIP, CON). The study utilized both between group and within group (repeated measures) for comparisons. The study took place over 10 weeks (January- April 2015) and received ethics approval from the University of British Columbia Clinical Research Ethics Board (CREB).  3.2 Study Location The study took place at the University of British Columbia (Vancouver campus), within the Cardiovascular Physiology and Rehabilitation (CPR) laboratory, in Osborne Centre Unit II. All outcome measures were taken in the Osborne Centre Unit II. Speed testing (30m sprint) was measured in Gym F of Osborne Centre Unit II, and is directly adjacent to the CPR lab. On days when Gym F of Osborne Centre Unit II was unavailable, speed testing took place between Osborne Centre Unit II and the UBC Tennis Bubble. The remainder of testing (consent forms, questionnaires, anthropometric measures, grip strength, HRV, leg girth, VAS, and VJ) occurred in the CPR lab. These locations were chosen due to ease and availability of use, and based on the ability to properly execute all outcome measurements.  3.3 Recruitment Students at the University of British Columbia were recruited to participate in the research study through two methods. Email correspondence was utilized to make contact with varsity head coaches at UBC, including a recruitment notice (Appendix A) for their athletes. This initial contact was followed up with in-person meetings to further discuss and explain the research project to the coaches. The coaches then provided their athletes with the recruitment notice. Participants then contacted the primary contact and arranged a meeting. Participants were also recruited through knowledge of individuals in the Kinesiology department that would meet the inclusion criteria. Participants were contacted through email, and provided with a recruitment notice. Participants then arranged a meeting to have the study explained in further detail. When all participants arrived at the meeting, participants were provided with a formal invitation letter, the study was explained in full detail and each participant was then asked if they wanted to participate in the study. Participants were 	  	  	   31	  provided with comprehensive detail regarding the study so that they could formally consent to participating. Participants filled out informed consent forms, and then underwent baseline testing (testing day 1).  Contact was made with participants from January – March 2015. Both female and male participants were recruited to participate in the study if the minimum physical activity requirements were met, indicating they were highly trained. Highly trained was defined as participating in at least four days per week of moderate to vigorous physical activity. Both males and females were recruited in order to achieve a satisfactory sample size. Previous research has utilized men and women during eccentric exercise induced DOMS (Vaile et al., 2008b), and suggested both genders demonstrate comparable physiological responses to eccentric loading and subsequently EIMD (Brown et al., 1997; Vaile et al., 2008b). Furthermore, participants were included if they had no severe orthopaedic injuries that would inhibit their ability to participate in the eccentric exercise protocol, particularly of the back and knee (herniated disk, patellar tendinopathy, etc.). Participants were included in the study if they were within the prospective age range (18-35 years old), and free of known cardiovascular and respiratory diseases that could be exacerbated during exercise testing. Lastly, participants were included if they had 2 years of resistance training experience.  3.4 Procedures  Testing took place on five test sessions. When possible, participants were tested on five consecutive days. Due to participants work and school schedules it was difficult to schedule testing on five consecutive days for some participants. In this instance, participants baseline testing occurred at the same time of day as the subsequent four testing sessions, but occurred the week prior. There was no more than five days between baseline testing and subsequent test sessions. Test sessions 2-5 occurred on four consecutive days for all participants. Testing took place at the same time of day for all participants, with mean test times occurring at 24.10, 47.98, and 71.77 hr post-intervention. A detailed schedule of test sessions is included in Figure 1.  Informed consent from the participants was obtained prior to the start of baseline testing (testing session 1). Testing session 1 initiated with participants signing and completing informed consent forms (Appendix B), the Physical Activity Readiness 	  	  	   32	  Questionnaire for Everyone (PAR-Q+)(Warburton et al., 2014) (Appendix C), and a Training and Health History Questionnaire (Appendix D).  Following the completion of the health and safety forms, participants’ basic anthropometric measurements were taken, followed by grip strength measurements, and resting blood pressure measurements. Lastly, once basic health measures were obtained, participants underwent the fully battery of baseline testing, consisting of Heart Rate Variability (HRV), leg girth, Visual Analog Scale (VAS), vertical jump (VJ), and speed tests.  Testing session 2 consisted of the eccentric exercise protocol. Participants were instructed to warm-up at a self-selected pace on a Monark cycle ergometer (Model: Ergomedic 828e, Vansbro, Sweden) for 10 min. The protocol consisted of 10 sets of 10 repetitions (100 total repetitions) of a plyometric drop jump. The plyometric drop jump occurred from a 24-in (60.96 cm) plyometric box. Participants had 10 secs rest between each repetition, and 1-min rest between each set (Jakeman et al., 2010). Following the eccentric exercise protocol, participants had 5 min of standardized rest to allow for explanation and set-up of the recovery applications. Participants were randomly assigned to one of four recovery applications: CWT, VIP, NormaTec, Placebo (Control). Following the completion of the 20 min recovery, participants filled out a Likert Scale Recovery Questionnaire (Appendix E). Random assignment occurred using a random numbers website (random.org), and consisted of the random generation of integer sets. Integer sets were designed to include sets of four assignments, with each set containing a random allocation of each of the 4 recovery applications (Appendix F). An allocation of 1 indicated an assignment to CWT, 2 to VIP, 3 to Placebo and 4 to NormaTec (Appendix F). Testing sessions 3-5 consisted of follow-up measurements of the outcome variables (HRV, leg girth, VAS, VJ and speed) at 24, 48 and 72 hr post-exercise.         	  	  	   33	  Figure 1: Schedule and Content of Testing Sessions 	  Recovery Procedures   Participants assigned to the VIP system underwent a 20 min proprietary protocol applying low levels of negative and positive pressure with concurrent exercise. The protocol was invented/designed by Dr. Darren Warburton. Participants assigned to the NormaTec MVP Recovery device (Newton Center, Massachusetts, USA) underwent a 20 min recovery flush using the lower limb sleeves. The participant underwent a standardized, manufacturer’s default recovery flush, selected from a pre-programmed list. Pressure throughout the five sleeve chambers ranged from 60-80 mmHg. The proximal chamber exhibited 60 mmHg, the central three chambers exhibited 70 mmHg, and the distal chamber operated at 80 mmHg throughout the treatment (Cochrane et al., 2013). The entire recovery protocol lasted 20 min, with each sequential chamber inflating for 30 sec, and then pulsing for 30 sec, before deflating. Participants lay supine on a cushion table, while the NormaTec sleeves were positioned up to their hips. Headphones were placed on the participants so as to mimic the conditions of the placebo/sham condition.  Participants assigned to the CWT intervention underwent 12 min of CWT. Prior to the start of the CWT; participants underwent 8 min of supine, passive recovery to standardize for the length of time all other participants experienced with the varying protocols. The Day 1: Baseline Testing  • HRV • Leg Girth • VAS • VJ • 30m sprint Day 2: Eccentric Exercise Protocol • Plyometric drop jumps • 10 sets x 10 repetitions • 10 seconds between repetitions • 1 minute between sets • Assigned recovery method • Likert Recovery Questionnaire Day 3,4,5: Follow-up measurements • Measures taken at 24, 48 and 72 hr post-exercise. • HRV • Leg girth • VAS • VJ • 30m sprint 	  	  	   34	  protocol for CWT consisted of 1 min of HWI (38 °C) followed by 1 min of CWI (15°C) for 12 min total (6 cycles) (Vaile et al., 2008a). Due to difficulty maintaining temperature, the mean temperature for participants assigned to CWT was 36.31°C for HWI and 14.22°C for CWI. Temperature was measured every 2 min cycle with a hand held thermometer to ensure accurate recording of temperature. The participants entered the immersion baths (Intex Pure Spas, Model: SSP-H-10, Long Beach, California, USA) beginning in the HWI for one min, followed by CWI for one min. This cycle was repeated for a total of 6 cycles. Participants ended the 12-min protocol with CWI. The immersion baths were equipped with jets that were activated during the water immersion treatment, so as to maximize relative temperature, as well as disrupt any boundary layer (French et al., 2008) that can occur during immersion. The participants were instructed to submerge themselves to their shoulders, with only their head and neck protruding from the water. Hydrostatic pressure was calculated to be approximately 36.37 mmHg, based on the fact that hydrostatic pressure increased by 0.74 mmHg for ever 1cm of immersion (Paddon-Jones & Quigley, 1997). Depth of immersion was measured to be 19.35 in (49.1 cm).  Participants assigned to the placebo/sham condition were instructed to lay supine on a cushioned table with the NormaTec sleeves placed on the lower limbs, however the sleeves were not inflated. Participants were instructed that the recovery protocol would last 20 min. Participants were not informed that there was a sham/placebo condition and participants that received this application assignment thought they were receiving the NormaTec condition. Participants were debriefed after the completion of all data collection regarding their true recovery application assignment. Participants were instructed to wear headphones so as to mitigate the possibility of them noticing the sleeves were not inflating (the NormaTec MVP recovery device is quite audible when actively inflating).  3.5 Measures  Resting Blood Pressure Participants’ resting blood pressure was measured using an electronic blood pressure monitor (BPM-200, BpTRU Medical Devices, Coquitlam, British Columbia).   Three measures of resting blood pressure were taken after 5 min of seated rest. Participants were instructed to have their feet flat on the floor, while they were seated upright in a chair. 	  	  	   35	  Measurements were taken from the left arm of participants, with their palm facing upwards, in correct anatomical position. Participants were instructed not to talk during the duration of the measurements. Blood pressure measurements were averaged and were utilized solely to ensure participants were fit to undergo a strenuous exercise protocol. Blood pressure measurements were only taken at baseline (test session 1).  Anthropometric Measures Participants’ height, weight, and waist circumference were measured and recorded during baseline testing (test session 1). Height was measured using a standard portable stadiometer (Seca, Chino, USA), and was measured to the nearest 0.1 cm. Weight was measured using an electronic scale (TANITA BC-534 InnerScan Body Composition Monitor, Tokyo, Japan), and was measured to the nearest 0.1 kg. Waist circumference was measured using a standard Gulick Tape Measure, and was measured to the nearest 0.1 cm. Height, weight, and waist circumference were used to determine similarities or differences between each of the four groups. Anthropometric measures were only taken at baseline (test session 1). Grip Strength  Grip strength was measured using a hand-grip dynamometer (Almedic, Saint-Laurent, Quebec). Two measures per hand were taken, with the participant alternating the dynamometer between hands to allow sufficient rest of the hand between repetitions. Participants were instructed to hold the dynamometer 45 degrees abducted from the torso, arm fully extended, and with the dial facing downwards. Participants were then instructed to maximally squeeze the hand-grip dynamometer without moving their body from this position. This process was repeated for both hands, twice each, while alternating between hands to allow for rest. This measurement was utilized to assess overall musculoskeletal health, as grip strength has been found to be a valid and reliable tool for assessing overall muscle strength (Kallman et al., 1990; Rantanen, 2003). Grip strength was only assessed at baseline (test session 1). Mean grip strength for each hand was combined to assess a categorization (poor, fair, good, very good, excellent) of overall musculoskeletal strength (Appendix G) (Jamnik & Gledhill, 2014). 	  	  	   36	  Heart Rate Variability  Heart rate variability was measured using infrared heart rate monitors (Polar RS800cx Multi RS800, Polar Electro Canada, Inc., Lachine, Quebec) and supporting infrared heart rate monitor computer watch. This device is an effective and reliable tool for measuring beat-by-beat analysis during rest and exercise (Essner et al., 2013). The devices were programmed to collect beat-by-beat analysis, so as to collect R-to-R interval data for later analysis. The polar heart rate monitor strap was prepared for use (strap was dampened with water at the electrode site, and heart rate monitor was securely fastened to strap) and provided to the participant. Participant placed the strap at the mid-line (sternum) of the chest. Participants were instructed to have the strap be tight fitting and secure against their chest, but not uncomfortable. A check of the heart rate monitor system was performed once attached to the participant to ensure adequate reading of the participants’ heart rate was occurring. Participants were then instructed to lay supine on a cushion table, with a sleep mask and noise cancelling headphones on. The mask and headphones were provided to minimize any extraneous sensory input that could occur from the surrounding laboratories. This was required to ensure participants reached an optimal resting state for the HRV reading. Participants lay still for 10 min while HRV was measured. After test sessions, data was transferred from the heart rate monitor computer watch via infrared technology to a computer, utilizing Polar ProTrainer 5 software (Polar Electro Canada, Inc., Lachine, Quebec). Data was then labeled with participant number and converted from beats per min to milliseconds. After conversion to milliseconds, data was exported from Polar ProTrainer 5 software as a text file and downloaded in Kubios HRV software (Version 2.2, University of Eastern Finland) for analysis of HRV. Through Kubios HRV analysis, participants’ root mean square of successive differences (RMSSD) was calculated.  RMSSD values were utilized for assessing participants’ heart rate variability as well as the development of recovery profiles for each participant. Recovery profiles were provided to participants as a benefit for participating in the study, and served as a brief analysis of an individual’s baseline RMSSD, as well as how their nervous system reacts to and subsequently recovers from, a strenuous training session. RMSSD is considered to be an adequate measure of parasympathetic reactivation (Aubert et al., 2003; Stanley et al., 2012). 	  	  	   37	  Leg Girth Measurements  Leg girth measurements were taken using a Gulick tape measure. Measurements were taken on both the right and left leg for each participant. Measurements were taken at three landmarks on each leg: Above-the-knee, Mid-thigh, and Sub-gluteal (Vaile et al., 2008b). Above-the-knee was determined from palpation at the top of the patella. Mid-thigh was determined to be equal distance between the greater trochanter and the lateral epicondyle. Sub-gluteal was measured and marked at the sub-gluteal fold. All three landmarks were marked on both the right and left leg using a permanent marker to ensure for accurate and repeatable measurements through the course of the testing sessions. Leg girth measurements were utilized to determine changes in leg circumference due to swelling following EIMD. Muscle Soreness  Muscle soreness was assessed using a Visual Analog Scale (VAS) (Appendix H). The VAS is a clinically validated and reliable measure for accurately assessing a participant’s muscle soreness (Hawker et al., 2011). The VAS is a continuum scale that is 10cm (100mm) in length with written descriptors at each end of the scale (No pain, to pain as bad as it could possibly be). Participants were instructed to mark a straight line along the scale indicating where their pain rated following a particular movement. Participants were put through 6 different movements to assess their lower body muscle soreness: sit to stand, stand to sit, passive quadriceps stretch, passive hamstrings stretch, maximal quadriceps contraction, maximal hamstrings contraction. For each unilateral movement (passive quadriceps stretch, passive hamstrings stretch, maximal quadriceps contraction, maximal hamstrings contraction) the movement was performed and measured individually on each leg.  The sit to stand movement consisted of participants standing from a seated position in a chair, without the use of their hands and arms for assistance. The stand to sit movement consisted of participants sitting down into a chair from a standing position without the use of their hands and arms for assistance. The passive quadriceps stretch consisted of the participant lying prone on a cushioned table while the research assistant fully flexed the knee (bringing the heel towards the gluteus muscles). The passive hamstring stretch consisted of the participant lying supine on a cushioned table while the research assistant flexed the hip 	  	  	   38	  (bringing the toes towards the central cavity) with a fully extended leg. The research assistant continued with the movement until the participant experienced a deep (comfortable) stretch. The maximal quadriceps contraction consisted of the participant sitting upright on the cushion table with their legs hanging off of the side (knees flexed at 90 degrees). The research assistant instructed the participant to resist the research assistant’s force. The research assistant was trying to flex the knee while the participant was instructed to attempt to extend their knee. This isolated the quadriceps muscle during a maximal contraction. The maximal hamstrings contraction consisted of the participant lying supine on a cushioned table. The research assistant moved the participant’s leg into hip flexion (with their leg fully extended), similar to the movement demonstrated during the passive hamstrings stretch. Once the hip was flexed and the participant experienced a deep stretch, the research assistant instructed the participant to attempt to fully extend their hip against the force being applied by the research assistant. This movement isolated the hamstring muscle while establishing a maximal contraction of the hamstrings muscle group. Immediately following each movement, the participant was instructed to rate their level of pain or muscle soreness experienced during the individual movement. Scores were then calculated by measuring (to the nearest 0.05cm) using a ruler, from the starting point (0cm; No pain) to the mark indicated by the participant. Scores were analyzed as individual movement scores, as well as a total movement score (sum of all individual movement scores for that testing session). These two methods were utilized to determine if there was significant changes for each individual movement, and if their overall muscle soreness significantly changed throughout the course of testing. Vertical Jump Vertical jump was measured using a VerTec vertical jump measuring device (Gill Athletic, PowerMax Equipment, Champaign, Illinois, USA) (Rowsell et al., 2009). VJ was utilized to assess an individual’s lower body anaerobic power (Bieuzen et al., 2013). Each participant performed 3 repetitions during the session, with 30 sec rest between repetitions. A participant’s standing reach was determined prior to the start of jumping. A participant’s standing reach was determined by the participant walking through the plastic slides on the VerTec device with their arm raised over their head. The amount of plastic slides pushed forward was combined with the height indicated on the VerTec device to calculate standing 	  	  	   39	  reach. Participants were then instructed to perform a three-quarter squat, with their arms extended behind them. When participants reached the desired depth of the squat, they were instructed to hold the position while a research assistant counted a 3 second pause. After holding the static position for 3 sec, participants were then instructed to jump. Participants were instructed to maximally jump, swinging their arm forward to make contact with the plastic slides of the VerTec device. The number of plastic slides pushed forward was added to the standing height of the device, and then the participant’s standing reach was subtracted from this number. The remaining value was determined to be the participant’s vertical jump. This process follows the guidelines put forth by the National Strength and Conditioning Association (NSCA) in regards to maximal vertical jump testing (Baechle & Earle, 2008). Speed (30m sprint) Speed was measured using electronic speed gates (TC-timing system, Brower Timing Systems, Draper, Utah, USA). Repeated sprint ability and speed was assessed via 4 repetitions of 30m sprints. Speed gates were set up at the start (0m), 10m and 30m. Participants were instructed to start with their foot 6 in behind the start (0m), so as to not trip the speed gates early by leaning forward. Participants were then instructed to run at maximal speed past the 30m speed gates, and decelerate only after passing the 30m gates. Participants were instructed to walk back to the starting line (0m), and this walk would serve as their rest period between repetitions. Once participants reached the starting line, they were instructed to position themselves in a starting position and repeat the 30m sprint. This process was repeated until the participant had completed 4 repetitions of 30m sprints. Sprints took place in an adjacent indoor gym facility from the CPR lab in Osborne Centre Unit II. 30m sprints were utilized, as it is the maximal length that could be achieved in the indoor gym facility provided. Also, previous literature has utilized this sprint length (French et al., 2008). Repeated sprint ability was measured by calculating the mean sprint time for 10m and 30m sprints over the 4 repetitions.  Likert Recovery Questionnaire  A 10-question Likert recovery questionnaire (Appendix F) was utilized to determine participants’ perception of recovery following the use of their assigned recovery application. Participants were provided with a questionnaire immediately following the conclusion of 	  	  	   40	  their assigned recovery application, with possible answers ranging from: Strongly Disagree, Disagree, Undecided, Agree, Strongly Agree. Questions were scored based on the direction of the scale, with positive questions awarded values of 1-5, and reverse questions (questions that contradicted the benefits of recovery applications awarded values of 5-1. Participants were given a total score out of a possible 50 points. This score was then converted to a percentage (%), and utilized as a percentage of a participant’s perception of recovery. Participants scoring >90% were considered to feel completely recovered, >80% were considered to feel well recovered, >70% were considered moderately recovered, >60% were considered somewhat recovered and <60% were considered not recovered.  3.6 Statistical Analysis All statistical analysis was done using IBM SPSS Version 21. A mixed model two-way ANOVA was performed to determine if there was any interaction effect between group x time. The between groups variable analyzed was type of recovery application (CWT, VIP, Placebo, NormaTec). The repeated measures (within groups) variable was time (baseline, 24 hr post-exercise, 48 hr post-exercise, 72 hr post-exercise). ANOVA was performed for each of the dependent variables (HRV, 30m sprint, VJ, VAS, leg girth). Effect size was calculated to determine differences between physical and physiological measures between groups. Pearson correlation coefficient was performed to determine the relationship between physical recovery measures (total pain VAS score at 24 hr; mean vertical jump at 24 hr) and perception of recovery (Likert recovery questionnaire). Group differences were analyzed utilizing height, weight, waist circumference, and grip strength (left and right hand) to determine if there were any significant differences between the four groups. When necessary, Tukey’s HSD was utilized to determine where statistically significant differences may have occurred.  3.7 Ethical considerations  Ethical approval for this research investigation was obtained through the University of British Columbia Clinical Research Ethics Board. All electronically stored data was stored on a computer encrypted with McAfee drive encryption software. The computer was password protected. Hardcopy data was stored in a locked cabinet. Both hardcopy and electronic copy data was stored in a locked laboratory. The laboratory was also alarmed, with 	  	  	   41	  only students and faculty working in the laboratory having access. All data was coded with a participant number to ensure confidentiality of participant information and identification.                                        	  	  	   42	  Chapter 4: Results 4.1 Participants  Participants ranged in age from 18-33 yr old. All participants were highly trained (4 or more days of moderate to vigorous physical activity per week). A total of 24 athletes participated in the study, with six participants assigned to each recovery strategy. A one-way analysis of variance (ANOVA) was performed to determine if there were any between group differences for height, weight, waist circumference, and grip strength (left and right hand). Descriptive statistics were calculated and are listed included in Table 1. There were no statistically significant differences between groups for any of the dependent measures (p > 0.05). Mean height for the 24 participants was 172.04 ± 10.78 cm, F(3,20) = 0.134, p = 0.939. Mean weight for all participants was 72.07 ± 15.16 kg, F(3,20) = 0.658, p = 0.587. Mean waist circumference of all participants was found to be 80.56 ± 8.3 cm, F(3,20) = 0.647, p = 0.594. Grip strength means were assessed for both hands. Mean grip strength of the left hand was found to be 39.96 ± 11.85 kg, F(3,20) = 0.419, p = 0.742. Mean grip strength of the right hand was determined to be 42.77 ±13.42 kg, F(3,20) = 0.791, p = 0.513. Participants were categorized into poor (0), fair (4), good (3), very good (6) and excellent (11), relative to normative data (Jamnik & Gledhill, 2014) on combined grip strength (both hands). Each group’s means and standard deviations for the anthropometric measurements are included in Table 1.                  	  	  	   43	  Table 1: Description of Participant Characteristics (Mean ±  SD) *.  Recovery Strategy Height (± S.D.) [cm] Weight (± S.D.) [kg] Waist Circumference (± S.D.) [cm] Grip Strength-Left (± S.D.) [kg] Grip Strength- Right (± S.D.) [kg] CWT 172.1 (± 14.2) 71.3 (± 14.2) 81.0 (± 8.4) 41.7 (± 10.2) 43.1 (± 15.6) VIP 171.4 (± 10.6) 73.2 (± 15.2) 80.9 (± 8.4) 41.8 (± 14.1) 44.8 (± 15.9) Placebo 170.3 (± 8.7) 65.7 (± 11.6) 76.8 (± 6.9) 35.1 (± 12.3) 35.8 (± 7.1) NormaTec 174.4 (± 11.7) 78.1 (± 20.6) 83.6 (± 10.1) 41.3 (± 12.4) 47.8 (± 13.4) Total Mean 172.0 (± 10.8) 72.1 (± 15.2) 80.6 (± 8.3) 40.0 (± 11.9) 42.8 (± 13.4) *There were no statistical differences between groups indicating appropriate matching and random assignment.  4.2 Heart Rate Variability   A two-way mixed model ANOVA was performed to analyze the two independent variables group (4) x time (4). Descriptive statistics for RMSSD measurements for each group and each time point are included in Table 2. The between groups analysis focused on the recovery interventions, whereas the within groups analysis focused on the repeated measures (baseline, 24, 48 and 72 hr test sessions). Heart Rate Variability was assessed using the RMSSD. A between groups analysis was performed to determine any significant changes between the four recovery strategies. Across all time points (Baseline, 24, 48, and 72 hr) there was no statistically significant difference in RMSSD values between any of the recovery strategies. Baseline RMSSD values demonstrated a mean across all groups of 86.9 (± 65.0) RMSSD, F(3,20) = 0.836, p = 0.490. Partial-eta squared was calculated (0.111), as well as observed power (0.198). At 24 hr post-exercise, a grand mean of RMSSD values was 	  	  	   44	  calculated to be 63.4 (± 55.2) RMSSD, F(3,20) =0.210, p = 0.888. Partial eta-squared was calculated (0.030), as well as observed power (0.083). The remaining test sessions demonstrated no statistical significance at 48 hr post-exercise [Mean = 73.3(± 55.2) RMSSD; F(3,20) = 0.206, p = 0.891; partial eta-squared = 0.030; observed power = 0.082] and 72 hr post-exercise [Mean = 75.0 (± 49.4); F(3,20) = 0.409, p = 0.748; partial-eta squared = 0.058; observed power = 0.117]. Peak parasympathetic decrease (RMSSD decrements) occurred at 24 hr post- eccentric exercise in VIP (12.45%), placebo (26.68%), and NormaTec (41.22%) groups. Peak parasympathetic decrease for the CWT groups occurred at 72 hr post-exercise (23.39%). The placebo group was the only group to return to baseline values by 72 hr post-eccentric exercise (0.86% increase from baseline values). CWT (23.39%), VIP (2.32%) and NormaTec (20.87%) were all below baseline values at the 72 hr test session.    Table 2: Mean RMSSD (± S.D.) values at each test session (Mean ±  SD).  Recovery Strategy   Test Session CWT VIP Placebo NormaTec Grand Mean Significance Baseline 90.2 (± 43.3) 70.9 (± 73.1) 66.2 (± 24.8) 120.2 (± 97.1) 86.9 (± 65.0) p = 0.490 24 hr 72.3 (± 54.4) 62.1 (± 71.9) 48.5 (± 26.2) 70.6 (± 69.0) 63.4 (± 55.2) p = 0.888 48 hr 71.9 (± 24.3) 72.1 (± 79.0) 61.6 (± 34.7) 87.7 (± 74.5) 73.3 (± 55.2) p = 0.891 72 hr 69.1 (± 40.9) 69.3 (± 67.0) 66.7 (± 26.3) 95.1 (± 60.8) 75.0 (± 49.4) p = 0.748  A repeated measures ANOVA was also performed to investigate the within groups changes over the four test sessions (baseline, 24, 48, 72 hr). There was no significant group x time interaction effect  [Greenhosue-Geisser adjustment: F(6.588, 43.921] = 1.226, p = 0.310; Partial Eta-Squared = 0.155; Observed Power = 0.450]. A significant main effect for within groups repeated measures was observed [Greenhouse-Geisser adjustment: F(2.196, 43.921) = 5.730, p = 0.005]. Bonferroni pairwise comparisons were performed to determine where the significant main effect differences occurred. The only significant difference observed between test sessions occurred between baseline and 24 hr post-exercise, with a significant decrease from baseline values [24 hr mean difference = 23.47 RMSSD, p = 	  	  	   45	  0.017]. There was no statistically significant difference between baseline and 48 hr post-exercise [48 hr mean difference = 13.53 RMSSD, p = 0.088], or between baseline and 72 hr post-exercise [72 hr mean difference = 11.81 RMSSD, p= 0.625]. None of the four recovery groups demonstrated a superior ability in returning RMSSD and/or heart rate variability to baseline values.  4.3 Muscle Soreness (Visual Analog Scale) Stand to Sit  A two-way mixed model ANOVA was performed to assess the between groups and repeated measure differences through the stand to sit position. Muscle soreness was measured by assessing a participant’s self-reported score along a 10-cm Visual Analog Scale. Mean VAS scores for each group and each time point are listed in Table 3. A repeated measures analysis was performed to investigate the effect of time on an individual’s muscle soreness scores. There was no significant interaction effect (group x time), as observed using the corrected Greenhouse-Geisser adjustment [F(5.269,35.127) = 1.571, p = 0.191; Partial Eta-Squared = 0.191; Observed power = 0.496]. There was a significant main effect for time (test sessions), using the corrected Greenhouse-Geisser adjustment [F(1.756,35.127) = 21.436, p = 0.000; Partial Eta-Squared = 0.517; Observed power = 1.000]. Bonferroni pairwise comparisons were utilized to determine where the significant differences occurred for the main effect. There was a significant increase across all time points in comparison to baseline values. At 24 hr post-exercise, a 27.3% increase from baseline values occurred [24 hr mean difference = 2.73 cm, p=0.000]. At 48 hr post-exercise, a 26.7% increase from baseline values was observed [48 hr mean difference = 2.67 cm, p = 0.000]. At 72 hr post-exercise, a 13.9 % increase from baseline values was demonstrated [72 hr mean difference = 1.39, p = 0.002]. The distribution of means across all time points is demonstrated in Figure 2.        	  	  	   46	  Figure 2 Mean Stand to Sit VAS Scores (Mean ±  SD).   A between-groups analysis was performed to investigate the effects of the four groups (CWT, VIP, NormaTec, Placebo) on muscle soreness scores. No statistically significant differences between groups were observed at baseline [F(3,20) = 0.35, p = 0.991; Partial Eta-Squared = 0.005; Observed power = 0.55], 24 hr post-exercise [F(3,20) = 0.732, p = 0.545; Partial Eta-Squared = 0.099; Observed power = 0.178] and 48 hr post-exercise [F(3,20) = 0.930, p = 0.444; Partial Eta-Squared = 0.122; Observed power = 0.217]. A statistically significant difference between groups was observed at 72 hr post-exercise [F(3,20) = 5.606, p = 0.006; Partial Eta-Squared = 0.457; Observed power = 0.891]. Tukey’s HSD was used post-hoc to determine where the significant differences occurred at 72 hr post-exercise. The VIP was associated with significant elevation in VAS scores compared to CWT [Mean difference = 3.158 cm, p = 0.013], the placebo condition [Mean difference = 3.008 cm, p = 0.018] and NormaTec [Mean difference= 3.058 cm, p = 0.016] groups. The VIP remained elevated above baseline levels from 24-72 hr, while all other groups’ VAS scores reduced towards baseline levels at 72 hr. There were no significant differences between any other groups, or at any other time points. VIP group was not effective in minimizing muscle soreness exhibited during the stand to sit movement at 72 hr post-eccentric exercise, 0	  0.5	  1	  1.5	  2	  2.5	  3	  3.5	  4	  4.5	  5	  5.5	  6	  6.5	  7	  0	  hr	   24	  hr	   48	  hr	  	   72	  hr	  	  VAS	  Score	  (cm)	  Test	  Session	  (hr)	  CWT	  VIP	  Placebo	  NormaTec	  	  	  	   47	  compared to NormaTec, placebo and CWT groups. The distribution of means across each recovery strategy at 72 hr post-exercise is demonstrated in Figure 3.  Figure 3: 72 hr post-exercise Stand to Sit Visual Analog Scale Mean Scores (Mean ±  SD).  Sit to Stand  A two-way mixed model ANOVA was performed to determine the between groups differences and/or the interaction of group x time. Mean VAS scores for each group, at each time point are listed in Table 3. A between-groups analysis was performed to determine if there were significant differences occurring between each of the recovery strategies. There were no significant differences found between groups at baseline [F(3,20) = 0.261, p = 0.852; Partial Eta-Squared = 0.038; Observed power = 0.091], 24 hr post-exercise [F(3,20) = 0.174, p = 0.913; Partial Eta-Squared = 0.025; Observed power = 0.077], 48 hr post-exercise [F(3,20) = 1.279, p = 0.309; Partial Eta- Squared= 0.161; Observed power = 0.289], and 72 hr post-exercise [F(3,20) = 1.168, p = 0.347; Partial Eta-Squared = 0.149; Observed power = 0.266].  A repeated measures analysis was performed to determine the effects of group x time on muscle soreness from the sit to stand position. There was no statistically significant interaction effect between group x time, using an adjusted Greenhouse-Geisser’s Epsilon 0	   0.5	   1	   1.5	   2	   2.5	   3	   3.5	   4	   4.5	   5	   5.5	   6	   6.5	   7	  CWT	  VIP	  Placebo	  NormaTec	  VAS	  Score	  (cm)	  Recovery	  Strategy	  	  	  	   48	  value [F(5.809, 38.725) = 1.102, p = 0.378; Partial Eta-Squared = 0.142; Observed power = 0.374]. A significant main effect was observed for test sessions, using the adjusted Greenhouse-Geisser’s Epsilon value [F(1.936, 38.725) = 18.662, p = 0.000; Partial Eta-Squared = 0.483; Observed power = 1.000]. Bonferroni pairwise comparisons were performed to determine the differences between each test session’s mean. All time points were significantly increased from baseline values. 24 hr post-exercise demonstrated an increase of 23.5% from baseline values [24 hr mean difference = 2.35 cm, p = 0.000]. 48 hr post-exercise demonstrated an increase of 23.9% from baseline values [48 hr mean difference = 2.39 cm, p = 0.000]. 72 hr post-exercise exhibited an increase of 9.9% from baseline values [72 hr mean difference = 0.99cm, p = 0.015]. None of the four recovery strategies demonstrated a significant efficacy for reducing muscle soreness during the sit to stand movement at any time point.   Table 3: Mean Sitting and Standing Visual Analog Scale Scores (cm) (Mean)  Recovery Strategies    CWT VIP Placebo NormaTec Grand Mean Significance Stand to Sit       Baseline 0.28 0.30 0.22 0.23 0.26 0.991 24 hr 2.93 4.12 2.01 2.89 2.99 0.545 48 hr 2.19 4.08 2.09 3.35 2.93 0.444 72 hr 0.79 3.95 0.94 0.89 1.64 0.006 Sit to Stand       Baseline 0.28 0.14 0.22 0.13 0.19 0.852 24 hr 2.72 2.83 1.98 2.63 2.54 0.913 48 hr 2.04 3.46 1.31 3.50 2.58 0.309 72 hr 0.58 2.08 1.01 1.06 1.18 0.347 Passive Quadriceps Stretch  Measurements of muscle soreness were taken on both the left and right leg to determine if differences existed between the two limbs.  A two-way mixed model ANOVA was performed to determine the differences within groups, group x time interaction, and between groups. For both the left and right leg, descriptive statistics at each time point, and for each group are listed in Table 4.  	  	  	   49	  The repeated measures analysis for the left leg did not elicit a statistically significant interaction effect (group x time). Utilizing the adjusted Greenhouse-Geisser value the interaction effect was found to be not significant at F(3,20) = 1.159, p = 0.345. A measure of effect size was calculated (Partial Eta-Squared = 0.148), as well as the observed power (0.427). A significant main effect was observed for time at F(3,20) = 11.420, p = 0.000. Effect size (Partial Eta-Squared = 0.363) and observed power (0.993) were also calculated for the main effect. Bonferroni pairwise comparisons were utilized to determine where the significant main effects occurred. Significant increases were observed from baseline values to 24 hr post-exercise and 48 hr post-exercise. At 24 hr post-exercise, mean VAS score increased by 19.3% from baseline values [24 hr mean difference = 1.93cm, p = 0.001]. At 48 hr post-exercise, mean VAS scores increased by 22.5% [48 hr mean difference = 2.25 cm, p = 0.005]. There was no significant difference between baseline values and 72 hr post-exercise VAS scores [72 hr mean difference = 0.735, p = 0.301].  A between groups analysis was performed for the left leg. No significant differences were observed between groups at baseline [F(3,20) = 0.749, p = 0.536; Partial Eta-Squared = 0.101; Observed power = 0.181], 24 hr post-exercise [F(3,20) = 0.473, p = 0.705; Partial Eta-Squared = 0.066; Observed power = 0.128], and 48 hr post-exercise [F(3,20) = 0.803, p = 0.507; Partial Eta-Squared = 1.07;  Observed power = 0.192]. A statistically significant difference was calculated at 72 hr post-exercise [F(3,20) = 4.301, p = 0.017]. Effect size (Partial Eta-Squared= 0.392) and observed power (0.787) were also calculated. Tukey’s HSD post-hoc test was utilized to determine which groups demonstrated significant differences in muscle soreness compared to others. The only significant difference observed was between CWT and VIP, with VIP demonstrating a significant difference in VAS scores at 72 hr post-exercise compared to CWT [VIP mean difference = 2.87 cm, p = 0.016]. There were no other statistically significant differences observed through post-hoc testing.       	  	  	   50	  Table 4: Mean VAS Scores: Passive Quadriceps Stretch [cm] (Mean ±  S.D.)   CWT VIP Placebo NormaTec Left Right Left Right Left Right Left Right Baseline 0.33 (± 0.39) 0.25 (± 0.33) 0.74 (± 0.76) 0.84 (± 0.61) 1.18 (± 1.95) 1.42 (± 2.77) 1.25 (± 1.14) 0.75 (± 0.65) 24 hr 2.09 (± 2.09) 2.53 (± 1.96) 2.81 (± 1.70) 3.16 (± 2.15) 2.76 (± 2.89) 3.50 (± 2.69) 3.57 (± 1.69) 3.49 (± 1.56) 48 hr 2.38 (± 1.84) 2.46 (± 2.02) 4.32 (± 2.94) 3.68 (± 2.12) 2.41 (± 2.17) 2.48 (± 1.30) 3.42 (± 2.97) 3.70 (± 2.38) 72 hr 0.58 (± 0.56) 0.92 (± 0.98) 3.44 (± 2.21) 3.49 (± 2.38) 1.10 (± 1.72) 1.37 (± 1.52) 1.33 (± 0.83) 1.72 (± 0.39)   A mixed-model ANOVA was also performed for the mean VAS scores obtained from the right leg of participants. Mean passive quadriceps stretch VAS scores are listed in Table 4. There was not a significant interaction effect between group x time [F(9,60) = 1.141, p = 0.349). Partial Eta-squared was calculated (0.146) as a measure of effect size, while observed power was also calculated (0.509). There was a significant main effect (test session) observed [F(3,60) = 15.561, p = 0.000). Observed power (1.000) and effect size (Partial Eta-squared = 0.438) were also calculated. Bonferroni pairwise comparisons demonstrated two significant differences between test sessions. There was a significant increase in passive quadriceps stretch VAS scores by 23.6% from baseline to 24 hr post-exercise [24 hr mean difference = 2.36 cm, p = 0.000]. A significant increase in passive quadriceps stretch VAS scores was also demonstrated (22.7% increase) from baseline to 48 hr post-exercise [48 hr mean difference = 2.27 cm, p = 0.001]. There was no significant main effect observed between baseline values and 72 hr post-exercise [72 hr mean difference = 1.1 cm, p = 0.084].  A between groups analysis was performed, and a significant difference between groups was observed at only 72 hr post-exercise [F(3,20) = 3.360, p = 0.039; Partial Eta-Squared= 0.335; Observed power= 0.672]. No statistically significant differences were observed at baseline [F(3,20)= 0.639, p = 0.599], 24 hr post-exercise [F(3,20) = 0.273, p = 0.844] or 48 hr post-exercise [F(3,20) = 0.748, p = 0.536]. Tukey’s HSD post-hoc test was 	  	  	   51	  utilized to determine where the significant difference(s) between groups occurred at 72 hr post-exercise. The only significant difference revealed through post-hoc testing occurred between CWT and VIP. The VIP group demonstrated an increased mean VAS score during the passive quadriceps stretch (right leg) difference of 2.58 cm compared to the mean VAS score of the CWT group (p = 0.036). This was the only significant difference calculated between groups during the passive quadriceps stretch on the right leg. Both legs demonstrated significantly increased VAS muscle soreness scores for the VIP group compared to the CWT at 72 hr post-exercise. The group differences for both legs are demonstrated in Figure 4.  Figure 4: Passive Quadriceps Stretch VAS Scores at 72 hr post-exercise (Mean ±  S.D.)  Passive Hamstrings Stretch  A two-way mixed model ANOVA was utilized to compare the between groups and repeated measures means of recovery methods and test sessions during the passive hamstring stretch. Descriptive statistics for both right and left legs were calculated and are included in Table 5.   	  0	  1	  2	  3	  4	  5	  6	  Left	   Right	   Left	   Right	   Left	   Right	   Left	   Right	  CWT	   VIP	   Placebo	   NormaTec	  Visual	  Analog	  Scale	  Score	  (cm)	  Recovery	  Strategy	  (left	  and	  right	  leg	  measured)	  	  	  	   52	  Table 5: Right and Left Leg Passive Hamstring Stretch Mean Visual Analog Scale Scores (Mean ±  S.D.) Time CWT VIP Placebo NormaTec Left Right Left Right Left Right Left Right Baseline 0.71 (± 0.37) 0.78 (± 0.51) 1.10 (± 1.3) 1.47 (± 1.69) 1.76 (± 1.52) 1.50 (± 1.69) 2.63 (± 1.75) 2.20 (± 1.51) 24 hr 2.42 (± 2.00) 2.38 (± 2.02) 3.19 (± 2.36) 2.67 (± 1.96) 1.49 (± 0.53) 1.43 (± 0.54) 3.46 (± 2.12) 2.92 (± 1.53) 48 hr 2.59 (± 1.99) 2.13 (± 1.62) 3.0 (± 2.65) 3.04 (± 2.65) 1.80 (± 1.42) 1.72 (± 1.02) 3.78 (± 1.77) 3.35 (± 1.92) 72 hr 1.45 (± 1.23) 1.55 (± 1.53) 2.47 (± 1.90) 2.26 (± 1.76) 1.38 (± 1.15) 0.91 (± 0.41) 2.35 (± 0.39) 1.86 (± 0.61)   Left leg muscle soreness measurements were analyzed separately from right leg. A repeated measures analysis for the left leg was undertaken to assess the interaction between recovery strategy x test session. Using the adjusted Greenhouse-Geisser value, there was no significant interaction between left leg passive hamstring stretch VAS scores for group x test session [F(6.624, 44.159) = 1.214, p = 0.316]. There was a significant main effect for test session, utilizing the same adjusted Epsilon value [F(2.208, 44.159) = 6.663, p = 0.002]. Partial eta-squared as utilized as a measure of effect size, and was calculated to be 0.25. Observed power for the main effect was calculated to be 0.915. Bonferroni pairwise comparisons were implemented to determine at which time point(s) the significant main effect occurred. Compared to baseline values, the only statistically significant difference between test sessions occurred at 24 hr post-exercise [24 hr mean difference = 1.01 cm, p = 0.048). A between groups analysis demonstrated no significant differences at baseline [F(3,20 = 2.63, p = 0.102], 24 hr post-exercise [F(3,20) = 1.304, p = 0.301], 48 hr post-exercise [F(3,20) = 1.018, p = 0.405], or 72 hr post-exercise [F(3,20) = 1.201, p = 0.335] between any of the four recovery strategies.   Right leg muscle soreness measurements were analyzed separately of left leg values. There was no statistically significant interaction effect [F(9,60) = 0.979, p = 0.457]. A significant main effect (test session) was observed [F(3,60) = 6.372, p = 0.001]. Effect size 	  	  	   53	  (partial eta-squared = 0.242) and observed power (0.958) were calculated for the significant main effect. Bonferroni pairwise comparisons were utilized, and the significant difference from baseline values occurred at 48 hr post-exercise (48 hr mean difference = 1.24 cm, p = 0.041).   Between group analysis demonstrated no significant differences between recovery strategies at baseline [F(3,20) = 1.51, p = 0.242], 24 hr post-exercise [F(3,20) = 0.961, p = 0.431], 48 hr post-exercise [F(3,20) = 0.974, p = 0.424], or 72 hr post-exercise [F(3,20) = 1.305, p = 0.300]. None of the four recovery strategies demonstrated superior efficacy in blunting muscle soreness during the passive hamstring stretch movement, for either leg, at any time point.  Maximal Quadriceps Contraction  Descriptive statistics for both left and right leg VAS scores during the maximal quadriceps contraction movement were calculated and are presented in Table 6. A two-way mixed model ANOVA was performed to investigate the between group and repeated measures differences for both the left and right legs during the maximal quadriceps contraction. For the left leg analysis, repeated measures ANOVA was performed to determine if there was a group x time interaction effect or main effect (time). Using the adjusted Greenhouse-Geisser’s value, it was determined that there was no significant difference between group x time for maximal quadriceps contraction scores [F(6.317, 42.11) = 1.250, p = 0.300]. Furthermore, a main effect was observed using the adjusted Epsilon value [F(2.106, 42.11) = 10.901, p = 0.000]. Effect size (Partial Eta-Squared = 0.353) and observed power (0.989) were calculated for the main effect analysis.  Bonferroni pairwise comparisons were utilized to determine where the significant differences in test sessions occurred. Compared to baseline values there were significant differences at 24 hr post-exercise [Mean difference = 1.837 cm, p = 0.002], and 48 hr post-exercise [Mean difference =1.448 cm, p = 0.020]. A between groups analysis revealed no significant differences between recovery groups at baseline [F(3,20)= 1.145, p = 0.355], 24 hr post-exercise [F(3,20) = 0.579, p = 0.636], 48 hr post-exercise [F(3,20) = 1.636, p = 0.212], or 72 hr post-exercise [F(3,20) = 1.776, p = 0.184].   	  	  	   54	  Table 6: Left and Right Leg - Maximal Quadriceps Contraction Mean Visual Analog Scale Scores (Mean ±  S.D.)  CWT VIP Placebo NormaTec Left Right Left Right Left Right Left Right Baseline 0.29 (± 0.37) 0.36 (± 0.43) 0.27 (± 0.34) 0.34 (± 0.43) 0.98 (± 1.39) 0.88 (± 1.40) 0.69 (± 0.49) 0.70 (± 0.54) 24 hr 2.17 (± 1.82) 2.53 (± 2.29) 3.37 (± 2.28) 3.54 (± 2.6) 2.08 (± 2.76) 1.87 (± 2.41) 1.97 (± 1.28) 1.71 (± 1.10) 48 hr 1.18 (± 0.79) 1.03 (± 0.69) 3.29 (± 2.49) 3.71 (± 3.11) 1.08 (± 1.14) 1.29 (± 1.44) 2.47 (± 2.91) 2.61 (± 3.05) 72 hr 0.62 (± 0.68) 0.48 (± 0.52) 1.88 (± 1.74) 2.51 (± 2.07) 0.56 (± 0.69) 0.65 (± 0.74) 1.06 (± 1.02) 1.08 (± 0.97)   For the right leg analysis, a repeated measures ANOVA was utilized to determine group x time interaction effects and main (time) effects. Using the adjusted Greenhouse-Geisser value, no interaction effect between group x time was found [F(6.449,42.991) = 1.531, p = 0.187].  A significant main effect (test session) was observed [F(2.150, 42.991) = 9.409, p = 0.000]. Effect size (Partial eta-squared = 0.320) and observed power (0.977) was calculated for the significant main effect. Bonferroni pairwise comparisons were utilized to demonstrate the significant differences in test sessions occurred at 24 hr (mean difference = 1.84 cm, p = 0.006) and 48 hr (mean difference = 1.59 cm, p = 0.019) when compared to baseline values (baseline grand mean = 0.57 cm ± 0.79 S.D.).   A between groups analysis revealed no statistically significant differences at baseline [F(3,20) = 0.649, p = 0.593], 24 hr post-exercise [F(3,20) = 0.875, p = 0.470], or 48 hr post-exercise [F(3,20) = 1.721, p = 0.195]. There was a significant between groups difference found at 72 hr post-exercise [F(3,20) = 3.359, p = 0.039]. Partial-Eta Squared (0.335) was calculated as a measure of effect size for the differences between recovery strategies at 72 hr post-exercise, as was observed power (0.672). Tukey’s HSD post-hoc test was administered to determine between which recovery group(s) statistically significant differences occurred at 72 hr post-exercise. The only statistically significant difference at this time point occurred between CWT and VIP groups. The VIP group demonstrated a marked elevation in maximal 	  	  	   55	  quadriceps contraction VAS score (cm) [VIP mean difference = 2.025 cm, p = 0.045]. There appeared to be a trend approaching significance between Placebo and VIP groups at 72 hr as well [mean difference = 1.86 cm, p = 0.072], however this was not statistically significant. The differences across means at 72 hr for the right leg are demonstrated in Figure 5. There were no other statistically significant differences between any other recovery groups at 72 hr post-exercise. VIP was not as effective as CWT in attenuating muscle soreness during the maximal quadriceps contraction on the right leg. There was no significant difference observed between VIP and CWT or any other groups during the maximal quadriceps contraction on the left leg.   Figure 5: The 72 hr Max. Quad. Contraction Mean VAS Scores (Right Leg only) (Mean ±  S.D.)  Maximal Hamstrings Contraction  A two-way mixed model ANOVA was performed to analyze mean differences in VAS scores for both right and left leg during a maximal hamstring contraction. Descriptive statistics were calculated for each leg and each recovery strategy group, and are included in Table 7. Left and right legs were analyzed separately to determine if there were significant differences between either leg. For the left leg, a repeated measures ANOVA was performed to determine a group x time interaction effect and main effects. There was no significant interaction effect [F(9,60) = 1.193, p = 0.316]. There was a statistically significant main 0	  0.5	  1	  1.5	  2	  2.5	  3	  3.5	  4	  4.5	  5	  CWT	   VIP	   Placebo	   NormaTec	  VAS	  Score	  (cm)	  Recovery	  Strategy	  	  	  	   56	  effect for changes across test sessions [F(3,60) = 5.643, p = 0.002]. Effect size (Partial Eta-Squared= 0.220) and observed power (0.932) were calculated for the main effects variable (test sessions). Using Bonferroni pairwise comparisons, the statistically significant main effect occurred between baseline values and VAS scores at 24 hr post-exercise [24 hr mean difference = 1.048 cm, p = 0.013]. This demonstrates that at the 24 hr test session, there was a 10.48% increase from baseline values. Between groups analysis revealed no significant changes at baseline [F(3,20) = 0.527, p = 0.669], 24 hr [F(3,20) = 0.779, p = 0.520], 48 hr [F(3,20) = 2.435, p = 0.095], or 72 hr [F(3,20) = 1.342, p = 0.289] for the left leg. Tukey’s HSD demonstrated a trend towards significance between the Placebo and NormaTec groups at 48 hr post-exercise. NormaTec demonstrated an increase of 2.43 cm (24.3%) compared to the Placebo group at the same time point (p = 0.074), however this trend did not achieve statistical significance. During the maximal hamstring contraction on the left leg, muscle soreness peaked at 24 hr for CWT (2.96 ± 1.44 cm), VIP (3.32 ± 2.50 cm) and Placebo (1.7 ± 0.99 cm) groups. Muscle soreness peaked at 48 hr for the NormaTec group (3.46 ± 1.79 cm).  Table 7: Right and Left Leg - Maximal Hamstring Contraction Mean VAS Scores (Mean ±  S.D.)  CWT VIP Placebo NormaTec Left Right Left Right Left Right Left Right Baseline 1.68 (± 1.44) 2.24 (± 1.35) 1.31 (± 1.28) 1.99 (± 1.64) 1.43 (± 1.24) 2.12 (± 1.03) 2.28 (± 1.77) 2.15 (± 1.97) 24 hr 2.96 (± 2.05) 2.91 (± 1.97) 3.32 (± 2.50) 3.88 (± 2.34) 1.70 (± 0.99) 1.71 (± 1.09) 2.91 (± 1.96) 3.32 (± 2.00) 48 hr 2.28 (± 1.79) 2.20 (± 1.53) 2.81 (± 1.93) 2.67 (± 2.41) 1.03 (± 0.56) 0.99 (± 0.60) 3.46 (± 1.79) 3.66 (± 1.77) 72 hr 1.42 (± 1.45) 1.78 (± 0.66) 2.50 (± 2.19) 2.52 (± 2.49) 0.88 (± 0.93) 1.30 (± 0.57) 1.68 (± 0.67) 1.85  (± 0.74)    A mixed model ANOVA analysis was performed on the right leg. A repeated measures analysis revealed no significant interaction effect, although it was trending towards significance [F(9,60) = 1.985, p = 0.057; Partial-eta squared = 0.229; Observed power= 	  	  	   57	  0.798]. There was a significant main effect over the test sessions [F(3,60) = 5.192, p = 0.003; Partial Eta-Squared = 0.206; Observed power = 0.909]. Bonferroni pairwise comparisons revealed a significant difference from baseline to 24 hr post-exercise [24 hr mean difference = 0.829 cm, p = 0.018]. A between groups analysis demonstrated no significant differences between recovery strategies at baseline [F(3,20) = 0.027, p = 0.994], 24 hr post-exercise [F(3,20) = 1.404, p = 0.271], 48 hr post-exercise [F(3,20) = 2.523, p = 0.087], 72 hr post-exercise [F(3,20) = 0.609, p = 0.617]. Tukey’s HSD tests revealed a trend towards significance between Placebo and NormaTec groups at 48 hr post-exercise. The NormaTec group demonstrated a increase of 26.67% from the Placebo group [mean difference = 2.67 cm, p = 0.060], but ultimately it was not found to be statistically significant. There were no statistically significant differences between any recovery strategies at any time point. During the maximal hamstring contraction movement on the right leg, peak muscle soreness occurred at 24 hr for CWT (29.46% increase from baseline) and VIP (94.97% increase from baseline). The NormaTec group (70.23% increase from baseline) demonstrated peak muscle soreness during a maximal hamstring contraction at 48 hr post-exercise. The Placebo group demonstrated decreased VAS scores at 24 hr (19.34% decrease), 48 hr (53.30% decrease) and 72 hr (38.68% decrease) compared to baseline values in the right leg. None of the four recovery strategies demonstrated an ability to blunt maximal hamstring contraction muscle soreness at any time point, for either the left or right leg, compared to the other strategies.  Total Pain  A two-way mixed model ANOVA was performed. Descriptive statistics were calculated and mean total pain scores for each group are represented in Figure 5. A repeated measures analysis was performed to investigate the interaction of group x time. Using the adjusted Greenhouse-Geisser Epsilon value, it was determined that no statistically significant interaction effect (test session x recovery method) was present [F(6.107, 40.714) = 1.803, p = 0.122; Partial Eta-Squared = 0.213; Observed Power = 0.612]. A significant main effect was observed using adjusted Greenhouse-Geisser’s value [F(2.036, 40.714) = 20.598, p = 0.000; Partial Eta- Squared = 0.507; Observed power = 1.000]. Bonferroni pairwise comparisons of the main effect were performed to determine the differences that occurred between test sessions. There were significant differences from baseline at 24 hr post-exercise [Mean 	  	  	   58	  difference = 16.971 cm, p = 0.000] and 48 hr post-exercise [Mean difference = 16.037 cm, p = 0.001]. There was no significant difference in muscle soreness scores between baseline values and 72 hr post- exercise [Mean difference = 5.598 cm, p = 0.085].  Figure 6: Total Pain Visual Analog Scale Mean Scores (all time points) (Mean ±  SD).   A between groups analysis was performed. No significant between group differences were noted at baseline [F(3,20) = 0.878, p = 0.469; Partial Eta-Squared = 0.116; Observed power = 0.207], 24 hr post-exercise [F(3,20) = 0.724, p = 0.549; Partial Eta-squared = 0.98; Observed power = 0.176], and 48 hr post-exercise [F(3,20) = 2.101, p = 0.132; Partial Eta-squared = 0.240; Observed power = 0.456]. A significant between groups difference was observed at 72 hr post-exercise [F(3,20) = 4.043, p = 0.021; Partial Eta-squared = 0.377; Observed power = 0.759]. Tukey’s HSD was utilized post-hoc to determine where the significant difference(s) occurred at 72 hr post-exercise between the four recovery methods. The significant differences occurred between CWT and VIP [VIP Mean difference = 16.93 cm, p = 0.033], as well as between the placebo group and VIP [VIP Mean difference= 17.00 cm, p = 0.032]. There was no statistically significant difference between VIP and NormaTec 0	  hr	   24	  hr	   48	  hr	   72	  hr	  CWT	   7.18	   25.46	   20.42	   10.16	  VIP	   7.96	   32.88	   34.06	   27.09	  Placebo	   11.67	   20.53	   16.21	   10.09	  NormaTec	   13.03	   28.86	   33.29	   14.88	  0	  5	  10	  15	  20	  25	  30	  35	  40	  45	  50	  55	  Total	  Pain	  VAS	  Scores	  (/100)	  [cm]	  Test	  Session	  (hr)	  	  	  	   59	  [VIP Mean difference= 12.21 cm, p = 0.167]. There were no other statistically significant differences between groups for any of the recovery strategies (CWT, NormaTec, Placebo). Total pain peaked at 24 hr for CWT (25.46 cm / 100 total cm) and placebo groups (20.53 cm / 100 total cm). The VIP (34.06 cm / 100 total cm) group and NormaTec (33.29 cm / 100 total cm) group experienced peak cumulative muscle soreness scores at 48 hr post-exercise. Three recovery strategies were still exhibiting elevated cumulative muscle soreness at 72 hr post-exercise compared to baseline values: CWT (41.5% increase), VIP (240% increase), and NormaTec (14.2% increase). VIP does not appear to be as effective as CWT or placebo (passive recovery) in blunting cumulative muscle soreness, or in returning muscle soreness to baseline levels at 72 hr post-exercise. 4.4 Vertical Jump  A two-way mixed model ANOVA was administered to analyze the between group and within group changes for both peak and mean vertical jump (VJ). Descriptive statistics (mean and std. deviation) were calculated for each recovery group for measures of peak VJ [cm] at baseline (CWT = 46.79 ± 7.72, VIP = 49.99 ± 9.84, placebo = 45.72 ± 9.40, NormaTec = 48.07 ± 9.51), 24 hr post-exercise (CWT = 47.19 ± 9.15, VIP = 50.10 ± 10.48, placebo = 44.24 ± 12.35, NormaTec = 47.74 ± 8.56), 48 hr post-exercise (CWT = 48.05 ± 8.63, VIP= 49.95 ± 11.46, placebo = 45.09 ± 9.70, NormaTec = 45.78 ± 6.63), and 72 hr post-exercise (CWT = 48.47 ± 8.89, VIP = 50.17 ± 10.25, placebo = 45.09 ± 8.83, NormaTec = 48.07 ± 8.73).  A repeated measures analysis was performed. There was no significant interaction (group x time) effect [F(9,60) = 0.755, p = 0.658] or main effect [F(3,60) = 0.571, p = 0.636]. A between groups analysis did not demonstrate a significant difference at baseline [F(3,20) =  0.241, p = 0.866], 24 hr post-exercise [F(3,20) = 0.332, p = 0.802], 48 hr post-exercise [F(3,20) = 0.344, p = 0.794], or 72 hr post-exercise [F(3,20) = 0.317, p = 0.813].  CWT group did not demonstrate statistically significant differences in peak VJ scores; however the group did exhibit noticeable increases in peak VJ scores (cm) over time. Compared to baseline values CWT demonstrated a slight increase at 24 hr post-exercise (0.88%), 48 hr post-exercise (2.71%), and 72 hr post-exercise (3.61%). VIP group did not demonstrate a significant increase or decrease in peak VJ scores (cm) at any time point. 	  	  	   60	  Compared to baseline values VIP demonstrated maintenance of performance across time points. The VIP group exhibited slight increases in peak VJ at 24 hr post-exercise (0.22%), and 72 hr post-exercise (0.36%). VIP group demonstrated a slight decrease at 48 hr post-exercise (-0.08%). Compared to baseline values the placebo group demonstrated a decrease in peak VJ scores at 24 hr (-3.24%). During the remaining test sessions (48 and 72 hr) the placebo group exhibited a slight increase of 1.38%. Compared to baseline values the NormaTec group exhibited a minimal decrease at 24 hr post-exercise (-0.69%), and no change at 72 hr post-exercise. The NormaTec group demonstrated a noticeable decrease of (-4.76%) at 48 hr post-exercise. These changes for each recovery strategy are demonstrated in Figure 7. None of the four recovery strategies demonstrated statistically significant changes in peak vertical jump at any time points. Figure 7:  Peak Vertical Jump [cm] (Mean ±  SD).   Descriptive statistics (mean and std. deviation) were calculated for each recovery group for measures of mean VJ at baseline (CWT = 45.16 ± 8.32, VIP = 47.29 ± 10.6, placebo = 43.22 ± 9.01, NormaTec = 44.63 ± 9.36), 24 hr post-exercise (CWT = 45.02 ± 8.70, VIP = 47.91 ± 10.71, placebo = 41.98 ± 11.35, NormaTec = 45.02 ± 8.24), 48 hr post-exercise (CWT = 45.86 ± 7.97, VIP = 47.91 ± 10.91, placebo = 42.97 ± 10.33, NormaTec = 30	  32	  34	  36	  38	  40	  42	  44	  46	  48	  50	  52	  54	  56	  58	  60	  62	  0	  hr	   24	  hr	   48	  hr	   72	  hr	  Vertical	  Jump	  (cm)	  Test	  Session	  (hr)	  CWT	  VIP	  Placebo	  NormaTec	  	  	  	   61	  43.53 ± 8.25), and 72 hr post-exercise (CWT = 47.13 ± 8.11. VIP = 48.23 ± 10.03, placebo = 42.97 ± 7.20, NormaTec = 46.37 ± 9.09).  A repeated measures analysis was performed for mean VJ. It was determined that there was no significant interaction (group x time) effect [F(9,60) = 0.668, p = 0.734] or main effect (test session) [F(3,60) = 1.766, p = 0163]. A between groups analysis did not demonstrate significant difference at baseline [F(3,20) = 0.195, p = 0.899], 24 hr post-exercise [F(3,20) = 0.363, p = 0.780], 48 hr post-exercise [F(3,20) =  0.346, p = 0.792], or 72 hr post-exercise [F(3,20) = 0.410, p = 0.748].  CWT did not exhibit statistically significant differences across any time points compared to baseline values: 24 hr (-0.31%), 48 hr (1.55%), and 72 hr (4.36%). VIP did not demonstrate statistically significant changes when comparing baseline values to subsequent test sessions: 24 hr (1.31%), 48 hr (1.31%), and 72 hr (1.99%). The Placebo group did not demonstrate statistically significant changes in mean VJ scores when compared to baseline values: 24 hr (-2.87%), 48 hr (-0.58%), and 72 hr (-0.58%). The NormaTec group did not exhibit statistically significant changes when compared to baseline values at any time point: 24 hr (0.87%), 48 hr (-2.46%), and 72 hr (3.90%). These changes, while not necessarily statistically significant, are demonstrated in Figure 8. None of the four recovery strategies demonstrated significant changes in mean VJ at any time point.  Figure 8: Mean Vertical Jump Scores [cm] (Mean ±  SD).  	  30	  34	  38	  42	  46	  50	  54	  58	  62	  0	  hr	   24	  hr	   48	  hr	   72	  hr	  Vertical	  Jump	  (cm)	  Test	  Session	  (hr)	  CWT	  VIP	  Placebo	  NormaTec	  	  	  	   62	  4.5 10m and 30m Sprint  Peak (fastest) and mean values were recorded for 10m splits and 30m sprint times. 10m splits were taken during 30m sprints. Descriptive statistics (mean ± std. dev.) for mean 10m sprint times [sec] were calculated at baseline (CWT = 2.22 ± 0.19, VIP = 2.20 ± 0.12, placebo = 2.24 ± 0.27, NormaTec = 2.17 ± 0.18), 24 hr post-exercise (CWT = 2.27 ± 0.20, VIP = 2.19 ± 0.10, placebo = 2.42 ± 0.51, NormaTec = 2.16 ± 0.14), 48 hr post-exercise (CWT = 2.26 ± 0.13, VIP = 2.17 ± 0.08, placebo= 2.30 ± 0.24, NormaTec = 2.18 ± 0.18) and 72 hr post-exercise (CWT = 2.23 ± 0.12, VIP = 2.14 ± 0.06, placebo = 2.24 ± 0.23, NormaTec = 2.20 ± 0.21). A repeated measures analysis was performed utilizing the adjusted Greenhouse-Geisser’s value. There was no significant interaction (group x time) effect [F(4.651,29.456) = 1.574, p = 0.456] or main effect (test sessions) [F(1.55, 29.456) = 2.365, p = 0.390]. A between groups analysis revealed no significant differences between recovery strategies at baseline [F(3,19) = 0.148, p = 0.930], 24 hr post-exercise [F(3,19) =1.038, p = 0.398], 48 hr post-exercise [F(3,19) = 0.847, p = 0.485] or 72 hr post-exercise [F(3,19) = 0.415, p = 0.744].  CWT demonstrated no statistically significant percentage changes from baseline values at any time point: 24 hr (-2.25%). 48 hr (-1.80%), and 72 hr (-0.45%). The VIP group demonstrate consistent improvements in across time points (but these changes did not reach statistical significance) when compared to baseline values: 24 hr (0.45%), 48 hr (1.36%), and 72 hr (2.72%). The placebo group demonstrated slight changes in mean 10m sprint times compared to baseline values, however these differences were not statistically significant: 24 hr (-8.04%), 48 hr (-2.68%), and 72 hr (no change from baseline values). The NormaTec group’s percentage changes over the test sessions compared to baseline values were also not statistically significant: 24 hr (0.46%), 48 hr (0.46%), and 72 hr (-1.38%). These varying differences are demonstrated in Figure 9. There were no statistically significant differences between recovery groups or interaction effects demonstrated at any time points for mean 10m sprint scores.    	  	  	   63	  Figure 9: Mean 10m sprint times [sec] (Mean ±  SD).    Descriptive statistics (mean ± std. dev.) for peak 10m sprint [sec] were calculated at baseline (CWT = 2.16 ± 0.21, VIP = 2.12 ± 0.14, placebo = 2.17 ± 0.24, NormaTec = 2.10 ± 0.18), 24 hr post-exercise (CWT = 2.19 ± 0.21, VIP = 2.12 ± 0.9, placebo = 2.28 ± 0.34, NormaTec = 2.09 ± 0.11) 48 hr post-exercise (CWT = 2.20 ± 0.13, VIP = 2.11 ± 0.10, placebo = 2.22 ± 0.22, NormaTec = 2.13 ± 0.18) and 72 hr post-exercise (CWT = 2.17 ± 0.12, VIP= 2.08 ± 0.09, placebo = 2.18 ± 2.1, NormaTec = 2.12 ± 0.17). A repeated measures analysis was utilized, and with the Greenhouse-Geisser’s value, no significant interaction (group x time) effect [F(6.411, 40.606)= 1.080, p = 0.392] or main effect (test sessions) [F(2.137, 40.606)= 1.801, p = 0.176] was observed. A between groups analysis revealed no statistically significant differences between any of the recovery strategies in regards to peak 10m sprint splits at any time point [Baseline: F(3,19)= 0.159, p = 0.923; 24 hr: F(3,19)= 0.966, p = 0.429; 48 hr: F(3,19)= 0.654, p = 0.590; 72 hr: F(3,19) = 0.614, p = 0.614].     1.8	  1.9	  2	  2.1	  2.2	  2.3	  2.4	  2.5	  2.6	  2.7	  2.8	  2.9	  3	  0	  hr	   24	  hr	   48	  hr	   72	  hr	  10m	  sprint	  split	  times	  (sec)	  Test	  Session	  (hr)	  CWT	  VIP	  Placebo	  NormaTec	  	  	  	   64	  Figure 10: Peak 10m sprint split times [sec] (Mean ±  SD).      There were no statistically significant changes across any of the recovery groups. CWT group demonstrated slight decreases in peak 10m sprint performance (slower splits) compared to baseline values: 24 hr (-1.39%), 48 hr (-1.85%) and 72 hr (-0.46%). VIP exhibited either no difference or slight increases in performance (ie. faster sprints) at various time points (24 hr = no change; 48 hr = 0.47%; 72 hr = 1.89%), however these changes were not statistically significant. The placebo group demonstrated considerable performance decreases from baseline values (24 hr = -5.07%; 48 hr = -2.03%; 72 hr = -0.46%), again however; these differences were not statistically significant. The NormaTec group experienced a slight improvement in sprint performance at 24 hr (0.48%), however at 48 hr (-1.43%) and 72 hr (-0.95%) their sprint performance declined. These reported valued are reported percent changes relative to baseline values. Negative percentages illustrate increased sprint times (and therefore demonstrating performance decrements at a given time point), whereas positive percentages represent improved sprint times, and subsequent improved sprint performance. The changes in means over all time points, for each recovery strategy are exhibited in Figure 10.  Descriptive statistics for mean 30m sprint times [sec] (mean ± std. dev.) were calculated for each recovery strategy at baseline (CWT = 5.27 ± 0.48, VIP = 5.15 ± 0.23, 1.9	  2	  2.1	  2.2	  2.3	  2.4	  2.5	  2.6	  2.7	  0	  hr	   24	  hr	   48	  hr	   72	  hr	  10m	  sprint	  splits	  (sec)	  Test	  Session	  (hr)	  CWT	  VIP	  Placebo	  NormaTec	  	  	  	   65	  placebo = 5.28 ± 0.72, NormaTec = 5.23 ± 0.45), 24 hr post-exercise (CWT = 5.46 ± 0.44, VIP = 5.20 ± 0.25, placebo = 5.76 ± 1.47, NormaTec = 5.34 ± 0.48), 48 hr post-exercise (CWT = 5.40 ± 0.38, VIP = 5.15 ± 0.26, placebo = 5.43 ± 0.76, NormaTec = 5.41 ± 0.59) and 72 hr post-exercise (CWT = 5.37 ± 0.34, VIP = 5.14 ± 0.20, placebo = 5.36 ± 0.82, NormaTec = 5.42 ± 0.64). A repeated measures analysis utilizing Greenhouse-Geisser’s adjusted value did not reveal a significant interaction (group x time) effect [F(4.962, 31.428) = 1.280, p = 0.297]. A significant main effect for test sessions was revealed [F(1.654, 31.428) = 3.949, p = 0.036]. Partial Eta-Squared (0.168) was calculated as a measure of effect size, as was observed power (0.614). Bonferroni pairwise comparisons revealed a significant difference between baseline values and mean 30m sprint performance at 48 hr post-exercise [48 hr mean difference = 0.115 sec, p = 0.024]. There were no other statistically significant differences between test sessions compared to baseline mean 30m sprint performance. A between groups analysis reported no significant differences between recovery strategies 30m sprint performance at baseline [F(3,19) = 0.091, p = 0.964], 24 hr post-exercise [F(3,19) = 0.530, p = 0.667], 48 hr post-exercise [F(3,19) = 0.369, p = 0.776], or 72 hr post-exercise [F(3,19) = 0.325, p = 0.807]. CWT demonstrated decreases in sprint performance at all time points compared to baseline values (24 hr = -3.61%; 48 hr = -2.47%; 72 hr= -1.90%); however none of these performance decrements were statistically significant. VIP demonstrated little to no change in mean 30 m sprint times at all time points compared to baseline values (24 hr = -0.97%; 48 hr = no change; 72 hr = 0.19%). The placebo group demonstrated noticeable performance decreases at all time points (24 hr = -9.09%; 48 hr = -2.84%; 72 hr = -1.52%). Similarly, the NormaTec experienced noticeable performance decreases at all time points (24 hr = -2.10%; 48 hr = -3.44%; 72 hr = -3.63%). This distribution of means for all four recovery strategies is exhibited in Figure 11. None of these changes from baseline values were found to be statistically significant. None of the recovery strategies appear to be statistically superior in improving or maintaining mean 30m sprint scores.    	  	  	   66	  Figure 11: Mean 30m Sprint Times [sec] (Mean ±  SD).  Descriptive statistics (mean ± std. dev.) were calculated for peak 30m sprint times [sec] for each recovery strategy group at baseline (CWT = 5.21 ± 0.48, VIP = 5.07 ± 0.28, placebo = 5.17 ± 0.68, NormaTec = 5.11 ± 0.45), 24 hr post-exercise (CWT = 5.37 ± 0.46, VIP = 5.11 ± 0.26, Placebo = 5.43 ± 1.00, NormaTec = 5.21 ± 0.45), 48 hr post-exercise (CWT = 5.31 ± 0.38, VIP = 5.08 ± 0.26, placebo = 5.32 ± 0.72, NormaTec = 5.29 ± 0.60) and 72 hr post-exercise (CWT = 5.31 ± 0.33, VIP = 5.05 ± 0.24, placebo = 5.23 ± 0.69, NormaTec = 5.24 ± 0.58).  A repeated measures analysis demonstrated no significant interaction (group x time) effect [F(9,57) = 0.974, p = 0.471]. A significant main effect (test sessions) was observed [F(3,57) = 4.762, p = 0.005; Partial Eta-Squared = 0.200; Observed power = 0.880]. Bonferroni pairwise comparisons revealed a significant difference between baseline test sessions and 24 hr post-exercise test sessions [24 hr mean difference = 0.136 sec, p = 0.015]. A between groups analysis revealed no statistically significant differences between recovery groups at baseline [F(3,19) = 0.091, p = 0.964], 24 hr post-exercise [F(3,19) =0.354, p = 0.787], 48 hr post-exercise [F(3,19) = 0.305, p = 0.822] or 72 hr post-exercise [F(3,19) = 0.330, p = 0.804]. CWT demonstrated performance decreases at all time points (24 hr= -3.07%; 48 hr= -1.92%; 72 hr= -1.92%) compared to baseline values. VIP demonstrated negligible changes in 4.2	  4.6	  5	  5.4	  5.8	  6.2	  6.6	  7	  7.4	  0	  hr	   24	  hr	   48	  hr	   72	  hr	  30m	  sprint	  times	  (sec)	  Test	  Session	  (hr)	  CWT	  VIP	  Placebo	  NormaTec	  	  	  	   67	  peak 30m sprint times at 24 hr post-exercise (-0.79%), 48 hr post-exercise (-0.20%), and 72 hr post-exercise (0.39%) compared to baseline values. The placebo group experienced performance decrements at all time points (24 hr = -5.03%; 48 hr = -2.90%; 72 hr = -1.16%). The NormaTec group slight decreases in performance at all time points compared to baseline values (24 hr = -1.96%; 48 hr = -3.52%; 72 hr = -2.54%). The distributions of these means over time, while not significant, are demonstrated in Figure 12. None of these changes from baseline value, amongst any of the recovery interventions, was found to be statistically significant.  Figure 12: Peak 30m Sprint Times [sec] (Mean ±  SD).    4.6 Limb Circumference Limb circumference was measured at 3 locations along the leg: sub-gluteal, mid-thigh and above-the-knee. Each location, for both limbs, was analyzed by a two-way mixed model ANOVA [recovery group (4) x test sessions (4)]. Descriptive statistics (mean ± S.D.) for all 3 measurements sites (sub-gluteal, mid-thigh, above the knee) are included in Table 8.  Sub-gluteal measures on both the left and right leg were analyzed separately. For the left leg, a repeated measures analysis did not demonstrate a significant interaction (group x time) effect [F(9,60)= 0.338, p = 0.959] or main effect [F(3,60) = 2.268, p = 0.090]. A 4.4	  4.6	  4.8	  5	  5.2	  5.4	  5.6	  5.8	  6	  6.2	  6.4	  6.6	  0	  hr	   24	  hr	   48	  hr	   72	  hr	  30m	  sprint	  times	  (sec)	  Test	  Session	  (hr)	  CWT	  VIP	  Placebo	  NormaTec	  	  	  	   68	  between groups analysis revealed no significant differences at baseline [F(3,20) = 1.014, p = 0.407], 24 hr [F(3,20) = 1.008, p = 0.410], 48 hr [F(3,20) = 1.168, p = 0.347], or 72 hr [F(3,20) = 1.198, p = 0.336]. Sub-gluteal right leg measurements were analyzed utilizing a repeated measures analysis, no statistically significant interaction (group x time) effect [F(9,60)= 1.975, p=0.058] or main effect of time [F(3,60)= 2.301, p  = 0.086]. Between groups analysis demonstrated no significant differences between recovery strategies at baseline [F(3,20) = 0.513, p = 0.678], 24 hr [F(3,20) = 0.893, p = 0.462], 48 hr [F(3,20) = 1.304, p = 0.301], or 72 hr [F(3,20) = 0.968, p = 0.427]. Although there was no statistically significant interaction (group x time) effect), the statistics were trending towards significance (p = 0.058). This trend is demonstrated in Figure 13.  Figure 13: Sub-gluteal Limb Circumference Measurements - Right Leg Only [cm] (Mean ±  SD).          52	  53	  54	  55	  56	  57	  58	  59	  60	  61	  62	  63	  64	  65	  66	  67	  68	  0	  hr	   24	  hr	   48	  hr	   72	  hr	  Limb	  Circumference	  (cm)	  Test	  Session	  (hr)	  CWT	  VIP	  Placebo	  NormaTec	  	  	  	   69	  Table 8: Mean limb circumference measurements – three location sites [cm] (Mean ±  SD).  CWT VIP Placebo NormaTec Left Right Left Right Left Right Left Right Sub-Gluteal  Baseline 59.48 (± 4.83) 58.58 (± 5.27) 58.48 (± 4.73) 59.08 (± 5.86) 56.37 (± 2.47) 57.50 (± 2.36) 60.85 (± 5.70) 60.98 (± 5.61) 24 hr 59.60 (± 4.25) 59.62 (± 5.07) 58.82 (± 4.31) 59.35 (± 5.09) 57.10 (± 2.73) 57.40 (± 2.74) 61.20 (± 5.00) 61.72 (± 5.34) 48 hr 59.77 (± 5.03) 59.40 (± 5.03) 58.73 (± 4.25) 58.75 (± 4.99) 56.43 (± 2.91) 56.50 (± 2.48) 60.88 (± 4.69) 61.72 (± 5.34) 72 hr 59.25 (± 4.78) 59.83 (± 4.84) 58.53 (± 4.79) 59.10 (± 5.86) 56.15 (± 2.37) 56.70 (± 2.27) 60.75 (± 4.72) 61.27 (± 5.24) Mid-thigh  Baseline 55.22 (± 3.98) 55.95 (± 4.48) 53.70 (± 4.84) 53.95 (± 5.13) 52.18 (± 2.54) 52.63 (± 2.25) 56.48 (± 4.82) 56.72 (± 4.90) 24 hr 56.15 (± 3.92) 55.95 (± 4.48) 54.35 (± 3.97) 54.00 (± 5.36) 53.58 (± 3.79) 54.32 (± 3.62) 55.97 (± 5.52) 56.98 (± 4.93) 48 hr 55.88 (± 4.16) 55.70 (± 4.89) 54.53 (± 4.29) 53.47 (± 5.22) 53.73 (± 3.53) 53.15 (± 3.26) 56.40 (± 5.40) 56.63 (± 4.99) 72 hr 55.90 (± 3.84) 50.07 (± 4.62) 54.03 (± 4.85) 54.12 (± 4.95) 53.08 (± 3.28) 53.47 (± 3.26) 56.10 (± 5.22) 56.88 (± 5.25) Above-the-knee  Baseline 38.88 (± 2.25) 39.37 (± 2.88) 39.40 (± 2.97) 39.72 (± 2.97) 37.43 (± 1.55) 37.12 (± 1.72) 40.52 (± 3.65) 40.88 (± 4.01) 24 hr 39.63 (± 2.63) 39.72 (± 2.69) 39.62 (± 2.95) 39.55 (± 2.77) 37.75 (± 1.65) 37.35 (± 1.63) 40.55 (± 3.71) 40.73 (± 4.04) 48 hr 39.48 (± 2.60) 39.43 (± 2.81) 39.85 (± 3.34) 39.50 (± 2.61) 37.33 (± 1.34) 37.17 (± 1.19) 40.45 (± 3.71) 40.87 (± 4.00) 72 hr 38.77 (± 2.15) 39.07 (± 2.63) 38.93 (± 2.51) 39.20 (± 2.65) 37.73 (± 1.30) 37.12 (± 1.17) 40.40 (± 3.71) 40.68 (± 4.12) 	  	  	   70	    Mid-thigh girth was assessed for both the right and left leg. For the left leg, a repeated measures analysis revealed no statistically significant interaction (group x time) effect [F(9,60) = 1.718, p = 0.146]. A significant effect for the main effect of time was observed [F(3,60) = 5.134, p = 0.012]. Partial Eta-Squared (0.204) was calculated as a measure of effect size, while observed power (0.779) was also calculated. Bonferroni pairwise comparisons revealed a significant difference between mean mid-thigh measurements at baseline and 48 hr post-exercise of 0.733 cm [24 hr mean difference = 0.733 cm, p = 0.018]. Between groups analysis revealed no significant differences between recovery strategies at baseline [F(3,20) = 1.204, p = 0.334], 24 hr [F(3,20) = 0.493, p = 0.691], 48 hr [F(3,20) = 0.464, p = 0.711], or 72 hr [F(3,20) = 0.675, p = 0.578].  Right leg mid-thigh girth measurements included the same measurements and analysis exhibited for the left leg. It was determined that there was no statistically significant interaction (group x time) effect [F(9,60) = 0.927, p = 0.508]. A significant main effect for time was observed [F(3,60) = 3.430, p = 0.023; Partial-Eta Squared= 0.146; Observed power= 0.744]. Bonferroni pairwise comparisons did not reveal any significant mean differences compared to baseline values at 24 hr [24 mean difference = 0.650 cm, p = 0.138], 48 hr [48 hr mean difference = 0.075 cm, p = 1.000], or 72 hr [72 hr mean difference = 0.471 cm, p = 0.437]. A significant difference did occur between 24 hr and 48 mid-thigh right leg measures of 0.575cm increase at 48 hr [p = 0.044]. Between groups analysis did not demonstrate statistically significant differences between recovery strategies at baseline [F(3,20)= 0.895, p = 0.461], 24 hr [F(3,20) = 0.549, p = 0.655], 48 hr [F(3,20) = 0.799, p = 0.509], or 72 hr [F(3,20) = 0.738, p = 0.542].  Above-the-knee girth was assessed for both the right and left leg. Left leg above the knee girth was analyzed with a repeated measures ANOVA. It was determined that there was no significant interaction (group x time) effect [F(9,60) = 1.616, p = 0.131]. There was a significant main effect for time [F(3,60) = 3.254, p = 0.028]. Partial Eta-Squared, as a measure of effect size, was calculated to be 0.140, and observed power (0.719) was also calculated. Utilizing Bonferroni pairwise comparisons, there did not appear to be significant mean differences compared to baseline values at 24 hr [mean difference = 0.329 cm, p = 0.166], 48 hr [mean difference = 0.221 cm, p = 1.00] or 72 hr [mean difference = 0.100 cm, p 	  	  	   71	  = 1.000] . Between groups analysis demonstrated no significant differences between recovery strategies at baseline [F(3,20) = 1.327, p = 0.294], 24 hr [F(3,20) = 1.032, p = 0.400], 48 hr [F(3,20) = 1.319, p = 0.296] or 72 hr [F(3,20) = 1.115, p = 0.366].  Above-the-knee right leg measurements were assessed utilizing a repeated measures analysis demonstrated no significant interaction (group x time) effect [F(9,60) = 0.492, p = 0.874] or main effect (time) [F(3,60) = 1.847, p = 0.148]. Between groups analysis demonstrated no significant differences between recovery strategies at baseline [F(3,20) = 1.649, p = 0.210], 24 hr [F(3,20) = 1.439, p = 0.261], 48 hr [F(3,20) = 1.757, p = 0.188] or 72 hr [F(3,20) = 1.589, p = 0.223]. None of the four recovery strategies demonstrated a significant efficacy in minimizing swelling or changes in limb circumference that occur following strenuous eccentric exercise.  4.7 Likert Recovery Questionnaire   A one-way between groups ANOVA was performed to determine differences in Likert scores between recovery strategies. Descriptive statistics (mean ± std. dev.) were calculated for each recovery group’s total score from the Likert recovery questionnaire (50 possible points): CWT= 35.33 ± 4.03, VIP= 35.25 ± 5.60, Placebo= 32.17 ± 6.37, NormaTec= 33.50 ± 4.89).  Figure 14: Mean Likert Scale Recovery Questionnaire (Mean ±  SD).  30	  32	  34	  36	  38	  40	  42	  CWT	   VIP	   Placebo	   NormaTec	  Likert	  Scale	  Recovery	  Score	  (/50)	  Recovery	  Strategy	  	  	  	   72	   The between groups analysis revealed no significant difference between recovery strategies in relation to Likert recovery scores [F(3,20)= 0.495, p = 0.690]. The mean differences are observed in Figure 14. There does not appear to be a statistically significant difference amongst any of the four recovery strategies in regards to an individual’s perception of recovery immediately following the application of a recovery strategy.   Pearson correlations were utilized to determine if there was a significant correlation between an individual’s perception of recovery (Likert Recovery Score) and their physical performance (Mean VJ 24 hr post-exercise). The means (std. dev.) were compared between Likert Scores (34.06  ± 5.12) and Mean VJ at 24 hr post-exercise (44.98  ± 9.42). Pearson correlation was found to not be statistically significant between Mean VJ at 24 hr post-exercise and Likert score (r = 0.285, p = 0.176). Pearson correlations were also utilized to determine if there was a significant correlation between an individual’s perception of recovery (Likert Recovery Score) and their total pain at 24 hr post-exercise. The means (std. dev.) were compared between Likert Scores (34.06  ± 5.12) and Total Pain (VAS) scores at 24 hr post-exercise (26.93  ± 14.80). Pearson correlation was found to not be statistically significant between total pain at 24 hr post-exercise and Likert score (r = 0.030, p = 0.888). There does not appear to be a correlation between an individual’s perception of recovery, as expressed on the Likert recovery questionnaire, and physical performance (mean VJ 24 hr post-exercise) or muscle soreness (total pain 24 hr post-exercise). This would indicate that their perception of recovery did not influence their physical performance during the subsequent training session.   Based on the criteria determined previously, CWT (mean= 35.33; 70.60%) and VIP (mean= 35.25; 70.50%) groups were categorized as moderately recovered following their scores on the Likert Recovery Questionnaire. Furthermore, NormaTec (mean= 33.5; 67.00%) and placebo (mean= 32.17; 64.34%) groups were categorized as somewhat recovered based on their Likert Recovery Questionnaire scores. The placebo group demonstrated the lowest perception of recovery based upon their scoring, with a mean percentage of 64.34%.       	  	  	   73	  Chapter 5: Discussion   The purpose of this study was to determine the efficacy of a variety of recovery strategies in maintaining physical performance, as well as mitigating the physiological effects of EIMD. While statistically speaking there was no clear recovery strategy that facilitated recovery and maintained performance from the present study, there were some noteworthy trends that occurred. While there is still considerable contradiction in the literature, the present findings provide some insight into the uncertainties of the field.  5.1 Heart Rate Variability  There were no statistically significant differences between CWT, VIP, Placebo or NormaTec groups in regards to RMSSD measurements at baseline, 24 hr, 48 hr or 72 hr post-exercise. RMSSD is the most commonly utilized measurement to analyze HRV, as it is  utilized to determine vagal (parasympathetic) tone (Thayer et al., 2000; Plews et al., 2013). The leading theory regarding the efficacy of recovery strategies post-exercise focuses on the potential increase in venous return, which subsequently activates cardiac baroreceptors, which in turn facilitates parasympathetic reactivation (Schaal et al., 2013). With venous return maximized, an increase in central blood volume occurs, which is the driving factor behind cardiopulmonary baroreceptor reactivation (Vail et al., 2008a; Wilcock et al., 2006; Schaal et al., 2013). It has been reported previously (Stanley et al., 2012) that cardiac parasympathetic dominance is indicative of an individual’s ability to maintain exercise intensity. As a result, cardiac parasympathetic dominance is thought to be an effective measure to determine if an athlete is fully recovered (Stanley et al., 2012). Therefore, recovery strategies that are efficacious in reactivating the parasympathetic nervous system would be crucially important to include in an athlete’s recovery program (Schaal et al., 2013). The present findings however, were unable to determine any significant changes in RMSSD values over the test sessions. The results of this investigation demonstrated changes typical of individuals following a strenuous exercise session. The participants exhibited parasympathetic withdrawal (decreased RMSSD values) from baseline values at 24, 48 and 72 hr. RMSSD reached maximum decreases at 24 hr for VIP (-12.45%), Placebo (-26.68%), and NormaTec (-41.22%) groups. Interestingly, CWT group demonstrated maximum RMSSD decrease at 72 hr (-23.39%). Overall, while not statistically significant, the VIP 	  	  	   74	  group demonstrated the smallest reductions in parasympathetic activity of (-12.45%), while the remaining groups demonstrated a range of RMSSD reductions from (-23) to (-41)%.The increased sympathetic activity and subsequent parasympathetic withdrawal observed during the follow-up test sessions is the body’s attempt at modulating heart rate during exercise (Aubert et al., 2003). While these findings do not suggest one recovery methodology’s superiority compared to other recovery applications, there are interesting trends that can be observed. The placebo group was the only group that was able to return to baseline values by 72 hr post-exercise, suggesting that CWT, NormaTec and VIP are unsuccessful in blunting the sympathetic response to exercise immediately following the eccentric exercise protocol.   Previous literature suggests that CWT and CWI was able to increase parasympathetic reactivation when compared to passive recovery (Stanley et al., 2012). However, it is difficult to determine whether it is the presence of hydrostatic pressure during immersion or the cold stimulation that participants are exposed to during their recovery treatment (Cochrane, 2004; Schaal et al., 2013). Bastos et al. (2012) suggest that CWI to the mid-sternal level influences the baroreceptors and subsequently influences HRV. The present findings are inconsistent with previous literature (Stanley et al., 2012; Bastos et al., 2012) that indicates cold stimulation hydrotherapies (CWT and CWI) are effective in stimulating parasympathetic reactivation and facilitating an athlete’s autonomic nervous system (ANS) return to basal levels. CWT was the only recovery strategy investigated in this study that reached maximum decrease in RMSSD values at 72 hr post-exercise (-23.39%). While the results were not statistically significant, it was hypothesized and expected that CWT would have a noticeable impact on parasympathetic reactivation, which was not demonstrated. Schaal et al. (2013) reported similar findings; as CWT did not demonstrate noticeable differences, compared to passive recovery, in relation to returning HRV measurements to baseline values. Regardless of whether it is the cold-water stimulation during CWT or the presence of hydrostatic pressure, it would not appear that CWT was beneficial for these athletes in returning their HRV to normal resting values. However, it has been postulated in the literature that in highly trained athletes, inability to reactivate the parasympathetic nervous system may not be indicative of subsequent exercise performance (Schaal et al., 2013).  	  	  	   75	  The VIP recovery methodology demonstrated the smallest reduction in RMSSD values with a maximum decrease of (-12.45)% occurring at 24 hr post-exercise. This decrease in parasympathetic activity, while not significant, when compared to the other recovery strategies could provide insight into the physical performance measures investigated in this study. Furthermore, VIP demonstrates alternate mechanisms that may be responsible for blunting the parasympathetic withdrawal that is evident during and following strenuous exercise. The VIP utilizes unique mechanisms that could influence the venous return and subsequent increase in central blood volume and cardiac pre-load (Wilcock et al., 2006; Krip et al., 1999). The alternation of negative pressure and positive pressure is reported to have a pumping effect similar to the intended mechanisms observed with the NormaTec and CWT. The alternation of low-level pressures is thought to mimic massage therapy in the alternations in skin blood flow and changes in venous return. It is also important to note that while all attempts were made to control extraneous variables that may influence HRV during the test sessions (i.e. noise and light stimuli, posture changes) a large influence on subsequent HRV during test sessions 3, 4, and 5 may have been continued exercise. Due to the fact that participants were highly trained individuals, mostly consisting of varsity-level collegiate athletes, we were unable to restrict them from continuing training during the study. One of the most common limitations of research regarding EIMD and recovery strategies is due to the fact that elite athletes rarely want to participate in studies that will influence their training programs or that could impact their physical performance (Barnett, 2006; Bahnert et al., 2013). As a result, in order to recruit the appropriate population to make the results generalizable to highly trained or elite athletes, participants continued their regular training throughout the test sessions. Sands et al. (2014a) attempted to mitigate the influence of a study on an individual’s training program. Although participants were able to maintain their regular training, no specific DOMS inducing protocol was implemented (Sands et al., 2014a), and as a result, regular training may not have induced sufficient intensity or DOMS to influence the dependent variables. Previous literature has primarily utilized untrained individuals due to the ease of recruitment, as well as inducing EIMD and DOMS (Connolly et al., 2003; McHugh et al., 1999), however these results may be vastly different than the response highly trained athletes would exhibit. Heart rate variability, and RMSSD specifically, are highly sensitive measurements. Exercise, 	  	  	   76	  and even the anticipation of upcoming exercise, causes an increase in sympathetic activity and concurrent withdrawal of parasympathetic activity (Aubert et al., 2003; Stanley et al., 2013). This fluctuation of parasympathetic and sympathetic increases between test sessions due to additional training could impact the reliability of the HRV measurements observed in the present study.  5.2 Muscle Soreness  The present findings demonstrate that there were no significant differences between CWT, VIP, placebo or NormaTec groups for muscle soreness measurements during any movement at baseline, 24 hr or 48 hr post-exercise. VIP was the only recovery strategy to demonstrate significantly elevated muscle soreness values at 72 hr post-exercise during several movements, and compared to varying groups. VIP demonstrated significantly elevated VAS scores compared to all groups only during the stand to sit movement: CWT (mean difference = 3.16 cm), placebo (mean difference = 3.01 cm), and NormaTec (mean difference = 3.06 cm). The VIP group also experienced significantly elevated VAS scores during the passive quadriceps stretch for both left leg and right leg and maximal quadriceps contractions (right leg only) when compared to the CWT group. VIP also had increased cumulative VAS scores compared to CWT (mean difference = 16.93 cm) and placebo groups (mean difference = 17.00 cm).  Overall, CWT exhibited reduced VAS scores on 2.5 of the 6 movements compared to VIP. This indicates that the VIP recovery strategy was unable to attenuate the response to muscle soreness and return to baseline by 72 hr compared to CWT, NormaTec and placebo groups. Both CWT and VIP intend to facilitate a similar mechanistic response through the alternation of pressure or temperatures to elicit vaso-dilatation and vaso-constriction (Esch et al., 2007; Vaile et al., 2008b; Wilcock et al., 2006). A key differentiation is the inclusion of temperature changes in the CWT group compared to the VIP group. The alternation of HWI and CWI is intended to prompt a vaso-pumping mechanism (Wilcock et al., 2006) that mimics the skeletal muscle pump (Ingram et al., 2009; Crampton et al., 2013), in order to facilitate venous return. However, Higgins and Kaminski (1998) demonstrated that the exposure to CWT for 4 min HWI: 1 min CWI (total time 31 min) was not sufficient compared to prolonged HWI (31 min) in altering intramuscular temperature. While the 4:1 protocol differs significantly from the protocol used in the present 	  	  	   77	  investigation, it has been suggested in other literature (Wilcock et al., 2006) that CWT, due to the brief exposure to cold temperature (typically 1 min) is not sufficient exposure to provide a considerable effect on recovery in athletes. Conversely, it has been hypothesized by several studies that the administering of CWI results in reduced perception of fatigue, and muscle soreness, owing to the effect that results following exposure to cold temperatures (French et al., 2008; Vaile et al., 2008b; Vaile et al., 2008a). CWI (only CWI or during CWT) is believed to reduce nerve conduction velocity (French et al., 2008; Wilcock et al., 2006; Ascensao et al., 2011), stimulate the ANS via parasympathetic reactivation (Schaal et al., 2013; Stanley et al., 2012; Bastos et al., 2012), and decrease perception of effort (due to buoyancy) (Wilcock et al., 2006). This would indicate that CWT, although logical, might not be sufficient to elicit the desired vaso-pumping mechanism during such brief exposures to HWI: CWI immersion. However, the differences observed between CWT and VIP could be due to the analgesic influence that CWT experiences, unlike the VIP group. VIP elicits the skeletal muscle pump through active recovery and vaso-pumping via pressure alternation, while NormaTec also elicits a pumping mechanism (Sands et al., 2014a, Talbot et al., 2012). Neither the NormaTec nor VIP was effective in significantly reducing muscle soreness.  Both CWT and VIP have similar mechanistic approaches, as they each aim to facilitate venous return in order to restrict oedema pooling in the limbs, and subsequently increase central blood volume (Schaal et al., 2012; De Pauw et al., 2014). However, a key differentiator between the two methodologies is that CWT includes the presence of CWI, which results in the analgesic effects on individuals after immersion (Montgomery et al., 2008; Vaile et al., 2008b; Bieuzen et al., 2013; Wilcock et al., 2006). The considerable differences between VIP and CWT may be largely due to the cold temperature stimulation provided by the CWI and the direct water contact with the body.  There were no significant between group differences during any movements targeting the hamstrings, and this is likely due to the eccentric movement of the drop jump, largely elicited through the eccentric contraction of the quadriceps and gluteus muscle groups. This is demonstrated further by the VIP displaying significantly elevated muscle soreness during the stand to sit movement at 72 hr compared to the other recovery strategies, as this movement most closely mimics the plyometric exercise protocol. It could be hypothesized that the VIP group experienced greater muscle soreness for a variety of reasons. The 	  	  	   78	  significant increases in muscle soreness scores for the VIP group are in contrast to previously unpublished reports (Warburton, 2008-2015) in which athletes demonstrated improved performance, perceptions of recovery, and reductions in muscle soreness.  One explanation could be that as the VIP group experienced indirect pressure application, it did not administer the direct physical compression that the NormaTec (intermittent pneumatic compression) or CWT group (hydrostatic pressure) provides. It has been reported that studies involving direct application of compression via compression garments provides mechanical support that can physically reduce the available space for oedema to pool, therefore improving the circulatory ability and subsequently reducing the perception of soreness (Jakeman et al., 2010; Hill et al., 2013), and it is possible that similar effects are exhibited by other mechanisms of direct compression. The direct compressive forces applied by CWT and NormaTec may result in increased haemodilution (Wilcock et al., 2006) compared to indirect pressure application observed with VIP. The CWT group also experienced underwater jets, unlike the VIP, which has been reported to activate proprioceptors and stimulate the neuromuscular system (Cochrane, 2004). These alternative explanations however, do not account for the differences in the placebo group, as they did not experience any active pressure application (wore the NormaTec sleeves but they were not inflated). The placebo group may possibly have demonstrated a placebo effect, as they thought they were receiving the NormaTec treatment (Cochrane et al., 2013). This placebo effect could be responsible for reducing their perception of muscle soreness and/or overall fatigue, especially considering that while reliable and validated (Mattacola et al., 1997), perception of muscle soreness remains a subjective measure (Leeder et al., 2011).  Although Leeder et al. (2011) focused on the placebo effect and CWI, it is plausible that the subjective nature of assessing muscle soreness could be influenced by any application of a placebo condition. Interestingly, there was a trend approaching significance between the placebo condition and the NormaTec condition for both the left (p = 0.074) and right legs (p = 0.060), during the maximal hamstring contraction movement. This suggests that the NormaTec may not be effective in blunting the progression of muscle soreness compared to the placebo condition, likely due to a combination of factors. Firstly, the NormaTec only compresses to approximately the sub-gluteal fold, however, this would not fully target the hamstrings, as the biceps femoris originates at the ischial tuberosity. The inability of the NormaTec to fully cover the length of 	  	  	   79	  the hamstrings could explain some elevated VAS scores for the hamstring movements. Secondly, it is possible that the placebo effect was in effect during this movement, as there was (while not statistically significant) attenuation of VAS scores compared to the NormaTec. The participants assigned to the placebo condition believed they were receiving the NormaTec, and it is possible that this ultimately resulted in the participants reporting lower muscle soreness scores as a result. This is purely speculative, but seems likely when observing the trends in both legs between the NormaTec and placebo conditions during the maximal hamstring contraction group. The NormaTec group demonstrated a 2.43 cm mean difference compared to the placebo group for the left leg, and a 2.67 cm mean difference for the right leg. This is especially interesting, as the NormaTec is one of the few recovery strategies that is currently able to demonstrate a true placebo condition, which could provide insight into the presence of the placebo effect in recovery research.  Individual or group VAS differences across recovery strategies could be due to the novel task that the individuals experienced while filling out the VAS (Mattacola et al., 1997). This learning effect could explain the relatively comparable placebo scores compared to CWT, VIP and NormaTec groups. Furthermore, a consequence of utilizing highly trained individuals, almost entirely varsity athletes, is that the potential for the repeated bout effect is present. The repeated bout effect from eccentric muscle contractions has been reported to last up to 6 months (Connolly et al., 2002; Barnett, 2006; Nosaka et al., 2001; McHugh, 2003). The athletes utilized in the study had a significant history of resistance training, which could dictate their response to the eccentric exercise protocol, even though they may have never undergone the specific eccentric protocol. It is likely, that the highly trained athletes observed in this investigation have undergone an eccentric training protocol utilizing similar muscle groups such as the depth jumps administered in this investigation (McHugh, 2003).  Eston et al. (1996) found that a prior bout of eccentric isokinetic training, two weeks prior to a subsequent exercise bout, offered a protective effect in regards to CK levels, and muscle soreness during downhill running. The minimal discrepancies in VAS scores throughout various movements between each of the recovery strategies could be due to the protective effect provided by the repeated bout effect, even if the activities were performed within weeks, or even months of the testing sessions (McHugh, 2003). Previous literature (Chleboun et al., 1995) utilized an extensive washout period for resistance training prior to the 	  	  	   80	  commencement of test sessions, however this study ultimately used untrained individuals. It is extremely difficult to implement and ensure that the target population avoids resistance training (specifically eccentric training) for upwards of 6 months in order to participate in testing of this nature. It is possible that the potential for the repeated bout effect could have ultimately reduced the amount of EIMD implemented by the plyometric drop jump protocol. While studies that have previously used a similar plyometric protocol (Jakeman et al., 2010; Miyama & Nosaka, 2004; Fond & Sarabon, 2015) demonstrated considerable increases in muscle soreness and muscle damage markers following the exercise, the mean VAS scores in the present study were not substantially elevated. Most scores peaked around 2.5-3.5 cm, on a scale of 10cm. This further suggests the presence of a repeated bout effect, which could have ultimately provided a protective effect on the targeted muscles, and therefore mitigated the magnitude of EIMD experienced. Future research should aim to maximize EIMD and minimize the potential for the repeated bout effect through a washout period.  The utilization of highly trained, healthy volunteers could further explain the potential discrepancies observed between recovery strategies and their efficacy following eccentric exercise. Negative and/or positive pressure (as observed with the VIP and NormaTec) has been predominantly utilized to treat deep vein thrombosis, venous insufficiency, lymphedema, and other circulatory issues (Chen et al., 2001; de Haro et al., 2010; Talbot et al., 2012). Due to the effectiveness of these devices in improving venous return, reducing arterial issues such as claudication (Chen et al., 2001), and decreasing limb girth (Chen et al., 2001; Talbot et al., 2012), it has be hypothesized that various compression or pressure applications could have similar benefits on athletes following strenuous exercise. However, the majority of research regarding negative or positive pressure, as well as IPC treatment, has focused on individuals with considerable vascular and circulatory issues. Cochrane et al. (2013) suggested that apparently healthy individuals might not respond as effectively to IPC treatment as individuals following a post-surgical treatment. It is possible that the EIMD was not extensive enough to elicit similar physiological responses, and subsequently did not respond to the IPC or VIP treatment.   	  	  	   81	  5.3 Vertical Jump  The present findings indicate that there were no significant differences in peak or mean VJ across any of the recovery strategies. However, CWT demonstrated an increase at 72 hr post-exercise of 4.36% from baseline values. While not statistically significant, it would appear that a gradual increase was exhibited for both peak and mean VJ. During mean VJ testing, the CWT group demonstrated a marked increase at 48 and 72 hr post-exercise. Cochrane et al. (2013) reported that as little as a 5% change in VJ is considered clinically relevant. While the CWT group did not achieve this 5% by 72 hr, their increase of 4.36% from baseline values was trending towards this relevance. These findings diverge from previous literature (Byrne & Eston, 2002) that has demonstrated concentric-only vertical jump (squat jump, no countermovement) experienced noticeable reductions in lower body power, likely due to the absence of stretch-shortening cycle activation. This would indicate that without the potentiation of muscles via the stretch-shortening cycle, observed during static vertical jump, an individual should not be able to achieve peak VJ performance (Byrne & Eston, 2002; McHugh et al., 1999). This is owing to the damage from the eccentric exercise protocol, caused to the force-generating capacity of the muscle fibres (Byrne & Eston, 2002; McHugh et al., 1999). However, Cochrane et al. (2013) demonstrated no change in VJ performance following extensive eccentric muscle contractions, and the application of the NormaTec IPC or a placebo condition. The authors (Cochrane et al., 2013) propose that this is due to the VJ being a multi-joint movement, which could have allowed the athletes to compensate with complementary muscles to maximize their performance. Furthermore, it is possible that the training status of the participants could influence their performance, in that they were still able to find a way to perform at or near their peak ability, regardless of muscle soreness or reduced force capacity (King & Duffield, 2009).  Similarly to Cochrane et al. (2013), the present findings support no beneficial effect of either NormaTec or the placebo condition in peak VJ performance. The findings revealed the placebo group to exhibit a noticeable decline in peak VJ performance at 24 hr (-3.24%) compared to baseline values. Interestingly, the marked (although not statistically significant) decline in peak VJ occurred in concert with the peak total pain experienced by the placebo group. Similarly, the NormaTec group experienced peak total pain at 48 hr post-exercise, 	  	  	   82	  while also demonstrating a considerable decline in peak VJ performance (-4.76%) compared to baseline values. As mentioned previously, a change in VJ performance of 5% has been reported to be clinically meaningful (Cochrane et al., 2013). It appears that the NormaTec peak VJ performance at 48 hr is approaching this clinically meaningful threshold for performance decrements. These decrements in performance for both the placebo and NormaTec recovery groups could likely be due to the fact that both of these groups did not experience any pressure or compression (or perceived compression for the placebo) of the gluteus muscle group, as the NormaTec sleeves (worn by both groups) only fit the participants to approximately the sub-gluteal fold. The two prime movers of the VJ movement are the quadriceps and the gluteus maximus (Pandy & Zajac, 1991), so it is feasible that the lack of exposure to pressure or compression of one of the main prime movers for the VJ movement could result in noticeable performance decrements. In comparison, both CWT and VIP groups were exposed to full lower body exposure to hydrostatic pressure (CWT) or intermittent negative and positive pressure (VIP). The VIP group demonstrated a maintenance of performance at all time points for peak and mean VJ. Similarly to the mean VJ performance, CWT exhibited gradual increase in performance over time with noticeable increases in peak VJ at 48 hr (2.71%) and 72 hr (3.61%). Rowsell et al. (2009) demonstrated that CWI and TWI showed no significant difference following sternum-level immersion with regards to performance during a countermovement VJ. These findings suggest that the presence of hydrostatic pressure may be a key element in maintaining vertical jump performance. While there are no published studies regarding the VIP, it is feasible to suggest that the pressure being applied to the entire lower body, such as during CWT, would have comparable results. While these trends are not statistically significant, it may reflect a potential limitation of the NormaTec device as a useful recovery strategy for athletes that commonly perform explosive jumping movements (football, volleyball, basketball, etc). The NormaTec group demonstrated a considerable rebound in mean VJ performance at 72 hr (3.90%), which is especially impressive considering the marked performance decrements observed for the same measure at 48 hr (-2.46%). As mentioned previously, the NormaTec’s performance decrements all occurred at 48 hr, which coincides with the group’s maximal total pain scores (VAS). It is possible that the increase in mean VJ performance at 72 hr occurred following the time-course of muscle damage, with DOMS 	  	  	   83	  typically peaking at 48 hr for most individuals. As a result, while NormaTec demonstrated a noticeable improvement in mean VJ at 72 hr, it does not appear that the recovery strategy was effective in facilitating recovery or even maintaining performance during the initial inflammation phase (24-48 hr) compared to VIP and CWT groups. Due to the lack of published research regarding the NormaTec device and exercise performance (Sands et al., 2014a; Sands et al., 2014b; Cochrane et al., 2013; Hanson et al., 2013), only one study has investigated (Cochrane et al., 2013) the impact of post-eccentric exercise NormaTec application and vertical jump performance. Cochrane et al. (2013) demonstrated no significant differences between NormaTec or placebo conditions (NormaTec sleeves worn with no inflation) during average or peak VJ between groups or throughout repeated measures. This coincides with the results observed in the present study, as the placebo and NormaTec conditions demonstrated no significant difference between each other. Both groups however, did appear to exhibit a noticeable decline in VJ performance relative to CWT and VIP groups. While not statistically significant, these performance decrements suggest that passive recovery and the NormaTec device may not elicit the complementary effect to an athlete’s anaerobic power recovery relative to the VIP and CWT methodologies. This could, however, owe to the recovery protocol utilized. Due to the limited research available on the NormaTec device, investigations have focused strictly on a manufacturer’s default protocol (Hanson et al., 2013; Cochrane et al., 2013), and without further investigation of this device, it cannot be determined whether this protocol, or an alternative pressure/treatment length is more appropriate. 5.4 10m and 30m Sprint  The present findings do not illustrate statistically significant differences between either in 10m and/or 30m sprint times for any of the four recovery strategies. However, the 10m split times recorded during the 30m sprint provided insight regarding explosive lower body power in a horizontal plane. Both the 10m and 30m sprint provides a more complete picture than VJ results alone. VJ and 10m performances represent singular instances of explosive lower body power (1-2 sec), whereas 30m sprints provide information regarding anaerobic power (<10 sec) and repeated sprint ability (<60 sec rest) (Galvin et al., 2013). While the 10m split times demonstrate comparable energy system utilization to that of VJ, 	  	  	   84	  similar results were not translated to the 10m splits for CWT. Mean 10m split times for CWT demonstrated peak performance decrements (-2.25%) at 24 hr post-exercise, unlike VJ in the same group which gradually increased over test sessions, reaching a 4.36% increase at 72 hours compared to baseline VJ measures. It has been reported that a key contributor to sprinting and VJ is the stretch shortening cycle (Harrison et al., 2004). Due to the use of a static vertical jump with no countermovement in the present study, there is little activation of the stretch shortening cycle. Subsequently, it has been reported that shorter sprints (ie. 10m) predominantly rely on knee extensor activation as opposed to the stretch shortening cycle (Harris et al., 2008). As a result, it does not appear that the differences observed between CWT’s explosive lower body power, as expressed via VJ compared to 10m sprints, can be due to the utilization of muscular mechanisms. Furthermore, CWT group’s 10m sprint times were comparable to the decline in performance observed in previous literature (Twist & Eston, 2005) following 10 sets of 10 repetitions for maximal vertical jumps, and without the application of a recovery strategy. Twist & Eston (2005) demonstrated 3% decline in cycle sprint times at 30 min, 24 and 48 hr post-eccentric plyometric exercise. However, several studies have reported no difference in sprint performances of CWI, CWT or control conditions (Rowsell et al., 2009; French et al., 2008). While the present findings do not demonstrate a statistically significant difference between CWT and the placebo group, decrements of 2% and 8% respectively may be noteworthy for the athletes. The decline in CWT sprint performance is further demonstrated in the present study during mean 30m sprint times, with declines at 24 hr (-3.61%), 48 hr (-2.47%) and 72 hr (-1.90%). Comparably, the placebo group demonstrated the largest (not statistically significant) decrements in mean 10m and 30m sprint performance. The largest decrements in both mean 10m and 30m sprint performance for the placebo group occurred at 24 hr post-exercise with decreases of (-8.04%) and (-9.09%), respectively.  The NormaTec group demonstrated minimal changes in mean 10m split times, and a slight decrease in performance at 72 hr post-exercise (-1.38%). However, during the mean 30m sprint performance, performance decrements were much more noticeable with decreases at 24, 48 and 72 hr post-exercise (-2.10%, -3.44% and -3.63%, respectively). While not statistically significant, these percentage decreases in sprint performance are noteworthy, and may be considered meaningful for athletes looking to maintain or even improve performance 	  	  	   85	  through recovery mechanisms. Furthermore, while these results did not achieve statistical significance (p > 0.05), the differences between reduced performance decrements observed from the CWT group compared to the placebo group are consistent with previous findings (King & Duffield, 2009) regarding repeated 20m sprint performance. NormaTec percentage decrements from baseline speed scores during 30m sprint performance are consistent with previous literature investigating cycling sprint declines following EIMD and no recovery intervention (Twist & Eston, 2005). The placebo group, however, exceeds the expected 3% decline at 24 hr post-exercise (Twist & Eston, 2005), with sizeable increases of 8-9% for both mean 10m and 30m sprint times. NormaTec and placebo groups’ power and repeated sprint ability results are similar to results observed during VJ in the present study, in that neither appear to be effective in blunting the effects of EIMD on subsequent physical performance measures. The placebo group demonstrated peak sprint performance decrements at 24 hr, which as mentioned previously coincides with peak total muscle soreness/pain, as well as VJ performance decrements.  This was observed for both mean 30m sprint (-9.09%) and peak 30m sprint (-5.03%). Similarly, the NormaTec group demonstrated marked performance decrements at 48 hr for peak 30m sprint (-3.52%), and mean 30m sprint            (-3.44%), which also coincides with peak total muscle soreness/pain. Interestingly, for mean 10m sprint times, the NormaTec group demonstrated maintained performance (0.46% increase in performance at 24-48 hr), but then a performance decrement (-1.38%) at 72 hr. While this decrement occurs after peak muscle soreness, it further substantiates that the NormaTec does not appear to be effective in facilitating recovery in order to maintain physical performance.  Overall, the present findings lack of statistical significance available for both VJ, 10m and 30m sprint times is consistent with previous literature suggesting no differences observed with compression garments and performance, during countermovement VJ and 20m sprints (Higgins et al., 2009). Due to the lack of available research regarding the NormaTec device and sprint performance, compression garments offer the nearest comparison in mechanism application.   Conversely, VIP demonstrated similar group results during both VJ and 10m split times, with a gradual increase in sprint performance from baseline values, particularly at 72 hr (2.72%), and minimal to no change during mean 30m, mean VJ and peak VJ. The findings 	  	  	   86	  regarding VIP coincide with previous research on EIMD and anti-inflammatory drugs (Semark et al., 1999), in which individuals undergoing 7x10 repetitions of maximal vertical jumps demonstrated no significant changes in 30m sprint times compared to a control. While this study does not reflect the application of a recovery modality, it is relevant, as the individuals (Semark et al., 1999) also demonstrated considerable DOMS prior to the sprint testing, as was observed with the VIP group in the present study. As mentioned previously, VIP demonstrated statistically significant increased VAS scores compared largely to CWT during several movements (stand to sit, maximal quadriceps contraction [right leg], passive quadriceps stretch [both legs], total pain), as well as placebo (stand to sit, total pain) and NormaTec (stand to sit) groups. However, VIP was the only group to demonstrate (although not statistically significant) gradual increases in mean 10m sprint performance (faster sprint times), and no change in mean 30m sprint performance (performance maintenance). While VIP was unable to blunt or reduce the perception of muscle soreness for participants, this did not appear to impact physical performance, as exhibited for VJ, 10m and 30m sprint performances. This was not expected, particularly considering that the significant increases in muscle soreness occurred during movements involving the gluteus muscle group and quadriceps, which are muscles primarily involving in sprinting (knee extension and hip extension) (Semark et al., 1999). This could be a result of compensation from other muscles to enable performance (Cochrane et al., 2013), or an athlete’s ability to perform maximally despite increased muscle soreness (King & Duffield, 2009). Interestingly, as mentioned earlier, previous unpublished reports (Warburton, 2008-2015) demonstrated a reduction in muscle soreness and maintenance (and even enhancement) in performance. Our current findings contrast previous trials from our laboratory with respect to muscle soreness likely reflecting differences in testing and training protocols and participant population. However, the maintenance of performance in the face of high intensity training was consistent across trial.   Overall, it appears that the VIP, while not statistically significant, was the only group to demonstrate performance maintenance for both peak and mean measures of 10m and 30m sprint performance. The changes demonstrated in this trial would have significant implications for elite athletic performance. This is especially important when considering the target population for this type of research is elite athletes. A performance decrement of 	  	  	   87	  anywhere from 2-9% would be noticeable in any elite athletic competition, for example the World Championships or the Olympics. For mean 10m sprints, the VIP group demonstrated peak performance improvement of 2.72% (0.06 sec faster than baseline) at 72 hr. All other groups demonstrated performance decrements: placebo (-8.04%; 0.18 sec slower than baseline @ 24 hr), CWT (-2.25%; 0.05 sec slower than baseline @ 24 hr) and NormaTec     (-1.38%; 0.03 sec slower than baseline @ 72 hr). The meaningful differences are further demonstrated for mean 30m, where all the recovery groups demonstrated marked performance decrements, except the VIP group. The peak performance decrements for each group illustrate considerable reductions in sprint time that could be meaningful for elite athletes considering how to structure their training programs: placebo group (-9.09%; 0.48 sec slower than baseline @ 24 hr), CWT (-3.61%; 0.19 sec slower than baseline @ 24 hr), and NormaTec (-3.63%; 0.19 sec slower than baseline @ 72 hr). Conversely, the VIP did not demonstrate considerable performance decline and subsequently slower sprint times for mean 30m sprints, with peak decline (-0.97%; 0.05 sec slower than baseline) occurring at 24 hr. At 48 and 72 hr test sessions, the VIP was gradually trending towards maintained sprint performance, with little or no change from baseline values at 24-72 hr post-exercise. The noticeable performance decline observed during mean 30m sprint for the placebo, CWT and NormaTec group (0.19-0.48 sec) could be noteworthy for athletes, particularly athletes that value lower body explosive power and anaerobic capacity for maintained performance. Athletes demonstrating little to no change on 30m sprint, as observed with the VIP group, would be considered a meaningful performance maintenance, especially considering the marked decline in sprint performance observed by the other groups. Changes in performance, particularly resulting in performance declines, could be the difference between an athlete winning a medal, or finishing off the podium. All attempts should be made to maintain physical performance as best as possible, which is something that the VIP group was able to demonstrate for sprint performance compared to CWT, placebo and NormaTec. Previous literature (Hamlin, 2007) investigated repeated sprint performance (10x40m sprints, 30 seconds rest between each sprint) for CWT and active recovery (light jog). These findings suggest no significant difference between active recovery and CWT in regards to sprint performance, as neither group was effective in maintaining sprint performance compared to baseline values (Hamlin, 2007). These results provide further insight into the 	  	  	   88	  underlying mechanisms that could be impacting the performance of CWT, and VIP, as represented in the present study. Due to the negligible differences between active recovery, and CWT (hydrostatic pressure) on subsequent repeated sprint ability (40m), it could be hypothesized that while separately there is no added benefit, the combination of pressure and active recovery may be beneficial. This could explain the trends towards improvement in mean 10m sprint performance and maintenance of performance during 30m sprint performance for VIP, relative to CWT and placebo in particular.   Due to the noticeable (but not statistically significant) decrements in performance during both mean 10m and 30m sprint performance at 24 hr post-exercise for the placebo group (8%, 9% respectively), it appears as though all of the recovery methods in the present study have more impact than passive recovery in maintaining sprint performance. Versey et al. (2011) reported that the minimal meaningful change in performance during repeated 15 sec cycling sprints to be 0.9% for total work and 1.1% for peak power. While a different modality for speed/power was utilized in the present study, this assertion indicates that minimal significant performance change tend to be quite low when dealing with highly trained athletes. Previous literature has suggested there to be no noticeable difference between CWT and passive recovery (control) in maintaining performance or preventing performance decrements (Ingram et al., 2009; Rowsell et al., 2009; French et al., 2008). The present study, to the best of our knowledge, is the first study to investigate the NormaTec recovery device and sprint performance. One previous study utilized Wingate testing (Hanson et al., 2013), which is a useful measure of power output, however, the outcome variable investigated was blood lactate, which was not monitored during the present study. As a result, there is no available research regarding the NormaTec recovery device and sprint performance. Similar limitations in the research are present for VIP as a recovery strategy. Subsequently, compression garments (CG) appear to provide the nearest comparison modality, as some aspects of each are captured amongst these two modalities, respectively. In a meta-analysis of literature regarding compression garments, Hill et al. (2013) reported that 66% of the population analyzed demonstrated recovery of power (countermovement jump, 5m sprint) following CG usage. King & Duffield (2009) reported no significant differences between active recovery, CWI or CWT during a 20m sprint. However, it has also been reported that active recovery, CWI and massage therapy were effective in minimizing 	  	  	   89	  reductions in power output during repeated cycling sprints (5-15 sec) (Lane & Wenger, 2004). Overall, the previous literature surrounding the various mechanisms and methodologies utilized in the present study are conflicting and contradicting.  While there were no statistically significant differences observed between recovery groups at any time point, it is feasible to suggest that decrements in performance of 2-9% during the 10m and 30m sprints would be meaningful to highly trained and/or elite athletes. In particular, it appears that the largest performance decrements were observed in the placebo group at 24 hr post-exercise, indicating that CWT, NormaTec and VIP may have an impact on the recovery of lower body power and speed compared to passive recovery. Furthermore, the VIP group was the only group to demonstrate maintained sprint performance, with no considerable performance decrements at any time point. While not statistically significant, this performance maintenance may be meaningful for athletes looking to maintain lower body explosive power and anaerobic power. 5.5 Limb Circumference  The present findings demonstrated no significant differences between the four recovery strategies applied (CWT, placebo, VIP, NormaTec) in changes of limb circumference, for either leg, at any of the three sites measured: sub-gluteal, mid-thigh, or above the knee. Sub-gluteal measurements on the right leg demonstrated a trend towards a significant interaction effect (p = 0.058), however this was not statistically significant. The trend appears to occur as a result of the interaction between CWT and VIP. VIP demonstrated a 0.46% increase from baseline at 24 hr, whereas CWT demonstrated a 1.78% increase from baseline at 24 hr. The remaining measurement locations (mid-thigh, above the knee) for both limbs demonstrated no statistically significant differences across any time points (baseline, 24, 48 72 hr). Following EIMD, increased limb circumference is expected at the site of muscle damage due to the pooling of oedema during the inflammatory process (Eston, Byrne and Twist, 2003). The findings of the present study are supported by previous literature demonstrating no differences between passive recovery and CWI (Halson et al., 2014; Howatson et al., 2009), CWT (French et al., 2008), or compression garments (Montgomery et al., 2008) in limb circumference and/or limb girth measurements. Conversely, 	  	  	   90	  Montgomery et al. (2008) reported that CWI demonstrated a slight trend of superior efficacy relative to compression garments and passive recovery in reduction of thigh girth following team sports games, however the results for thigh girth and calf girth across recovery methodologies were ultimately miniscule. Furthermore, Vaile et al., (2008b) demonstrated CWI and CWT were superior to passive recovery in minimizing post-exercise oedema, however HWI demonstrated no difference compared to passive recovery. One study investigating IPC (Chleboun et al., 1995), demonstrated significant decreases in arm circumference following strenuous elbow flexion in the IPC group at certain time points, however, this decrease appeared to be acute, with circumference increased before compression at subsequent test sessions.  The primary mechanism thought to be initiating the reduction in oedema pooling at the site of muscle damage, is the compression of the vasculature. When compression, either direct (hydrostatic, IPC) or indirect (VIP) is applied, there is an increase in the pressure gradient between interstitial compartments and vasculature (Vaile et al., 2008b). The compression, which ultimately results in vasoconstriction, reduces the available space for fluids to accumulate in the interstitial space following muscle damage (Leeder et al., 2011), and the fluid shifts to the area of lower pressure, in this case the intravascular space (Vaile et al., 2008b, Wilcock et al., 2006). The ability of a recovery application to minimize the pooling of oedema in the interstitial space could subsequently result in reduced muscular damage and therefore reduce the impact on subsequent physical performances (Zelikovski et al., 1993). The present findings were unable to demonstrate significant differences amongst CWT, VIP, NormaTec or placebo groups for changes in limb circumference at any of the three measurement locations, over the four test sessions. This lack of significance indicates that it is unclear which of the types of compression (variable pressure, hydrostatic pressure, IPC) can ultimately reduce the permeability of the vessels (Leeder et al., 2011), resulting in excessive oedema pooling in the interstitial space. There was a trend approaching a significant interaction effect between CWT and VIP for the right leg sub-gluteal measurements at 24 hr post-exercise, however this trend was ultimately not statistically significant (p = 0.058). The lack of changes with the experimental groups compared to the placebo condition is surprising, as the placebo condition is the only condition that did not apply any method of compression to the lower body. As it has been reported that the 	  	  	   91	  reduction and removal of fluid from the interstitial space can potentially result in reduced muscular disruption following EIMD (Zelikovski et al., 1993), the lack of statistical significance does not provide conclusive support for any of the recovery methodologies examined in blunting the influx of oedema in the interstitial space following eccentric exercise.  Previous studies regarding recovery strategies and reduction in limb circumference have been conflicting (Vaile et al., 2008b, Chleboun et al., 1995, Zelikovski et al., 1993; Howatson et al., 2009; Montgomery et al., 2008; French et al., 2008).  Vaile et al. (2008b) reported significant improvements and beneficial effects on thigh girth were observed from CWI and CWT groups, compared to HWI and passive recovery. While compression clearly plays a role in reduction of pooling in the interstitial space as mentioned previously, the lack of change resulting from HWI would indicate that compression is not the sole factor influencing fluid shifts in the limbs (Vaile et al., 2008b). CWI is thought to provide significant compression via hydrostatic pressure, as well as vasoconstriction due to the changes in temperature (Bastos et al., 2012). This change in the pressure gradient within the vasculature appears to be enhanced with the combination of temperature and pressure, rather than with pressure alone (Vaile et al., 2008b). The primary theory initiating support for the use of CWT in athletes is that the alternation in CWI:HWI creates a vaso-pumping mechanism (Cochrane, 2004; Pournot et al., 2011;Wilcock et al., 2006), as described previously. However, it has been reported that CWT may not cause sufficient exposure to changes in intramuscular temperature (Vaile et al., 2008b; Higgins & Kaminski, 1998) to cause the anticipated circulatory changes (vasodilatation, vasoconstriction). As a result, it is possible that the CWT exposure in the present study may not be sufficient exposure to CWI to elicit sufficient vasoconstriction, and subsequent fluid shifts that are needed to minimize changes in limb circumference following EIMD. In particular, due to the increased immersion (compression) level observed for the CWT group (head and neck out only) compared to the VIP (umbiculus) and NormaTec (sub-gluteal), greater fluid shifts and subsequently larger increases in central blood volume, and stroke volume were expected (Wilcock et al., 2006). Wilcock et al. (2006) reported that changes in stroke volume during head and neck out only immersion increased by 28-95%. Such noticeable increases in stroke volume would be the result of large influxes in central blood volume stemming from 	  	  	   92	  compression being applied to the vasculature (Wilcock et al., 2006). As a result, CWT, which experienced the largest surface area exposure to compression, should ultimately demonstrate the largest fluid shifts and reduction in limb circumference. However, the present findings do not support this. Consequently, it is possible that the exposure length may not have been a sufficient combination of compression or temperature to create the vaso-pumping mechanism desired to remove the excess fluids from the damaged muscle (French et al., 2008; Talbot et al., 2012; Pournot et al., 2011).  This insufficiency could also explain the trend towards a significant interaction effect between VIP and CWT at 24 hr post-exercise as observed during right leg sub-gluteal measurements. As mentioned previously, the 1 min alternating exposure to CWI:HWI may not have induced sufficient vasoconstriction, in concert with the hydrostatic pressure applied to the immersed portions of the body. Conversely, there was a trend approaching significance (p = 0.058) for VIP and CWT at 24 hr post-exercise at the sub-gluteal measurement location on the right leg, and VIP is the only recovery application with extended exposure to pressure (5 min cycles). VIP demonstrated a (0.46%) increase in sub-gluteal limb circumference, whereas CWT demonstrated (1.78%) increase at the same measurement location. In comparison, the NormaTec group exhibited mean increases in sub-gluteal limb girth at 24 hr post-exercise of (1.21%), with intermittent pneumatic compression being applied at a location for one min at a time throughout the cycle.  The placebo group demonstrated little to no change in sub-gluteal right leg limb measurements at 24 hr, with a reduction of (-0.17%). There is potential that the measurement locations were not all encompassing of the swelling and fluid changes in the lower body during the recovery period following the eccentric exercise protocol. The eccentric exercise protocol resulted in significant and noticeable soreness predominantly in the gluteus muscle group, as observed with peak VAS scores occurring during the stand to sit movement (eccentric movement of the gluteus muscles). However, the limb circumference measurement locations were targeted largely at fluid shifts in the thigh (quadriceps and hamstrings specifically).  It is possible that the sub-gluteal measurement was not sufficient in capturing the oedema or fluid shifts that may have presented during follow up test sessions. The measurements utilized in this study were commonly used in the studies investigating limb circumference/girth (Vaile et al., 2008b; French et al., 2008; Howatson et al., 2009;). However, some studies utilized only one 	  	  	   93	  (Howatson et al., 20009; Chleboun et al., 1995), or two (French et al., 2008; Montgomery et al., 2008) total measurement locations. This severely limits the scope of fluid shifts that the measurements are able to capture. However, it is possible that although the present study included measurements at three location sites, that there were aspects of the fluid shifts that may not have been observed as a result of the location selection. Previous studies utilizing this eccentric plyometric exercise protocol did not investigate limb circumference (Jakeman et al., 2010; Howatson et al., 2009; Twist & Eston, 2005). Future research may want to consider the broader spectrum of limb circumference changes when utilizing a predominantly gluteus dominant eccentric exercise protocol.  5.6 Likert Recovery Questionnaire  The recovery questionnaire utilized in the present study was a very simple model of 10 questions. The findings revealed no statistically significant differences between any of the recovery methodologies. Furthermore, there was no correlation between an individual’s perception of recovery, as indicated on the Likert Recovery Questionnaire, and their perception of muscle soreness (total pain at 24 hr post-exercise) or their physical performance (mean vertical jump at 24 hr post-exercise). Although not statistically significant, as expected, the VIP (70.50%) and CWT (70.60%) demonstrated the highest levels of perception of recovery. Compared to passive recovery (64. 34%), it appears that  while not statistically significant, both VIP and CWT do have some effect on an individual’s perception of recovery. Due to the fact that the findings were not statistically significant, the present study contradicts previous literature that demonstrated a noticeable (p < 0.05) increase in perception of recovery following CWT and contrast water showers, compared to passive recovery  (Juliff et al., 2014). Due to the nature of the placebo condition, it is possible that participants in the passive recovery/placebo group overestimated their perception of recovery due to the fact they believed that they received an experimental condition (Ascensao et al., 2011). This would indicate that a placebo effect was in fact present (Ascensao et al., 2011). Relative to other recovery strategies, hydrotherapy (CWI, CWT) has been proposed to improve the perception of recovery due to the analgesic effects provided by CWI (Leeder et al., 2011; Ascensao et al., 2011; Vaile et al., 2008a; Vaile et al., 2008b; French et al., 2008). This effect has been proposed to last for as little as 1-3 hr 	  	  	   94	  (Ascensao et al., 2011), and upwards of 96 hr post-exercise (Leeder et al., 2011). Furthermore, hydrotherapy also provides buoyancy, which can eliminate the gravitational stress on the body, which ultimately could provide a greater overall perception of recovery (Wilcock et al., 2006). The present findings were unable to demonstrate CWT increased perception of recovery relative to the other recovery methodologies, despite the potential for analgesic effects from cold temperature and buoyancy in the water. Furthermore, previous literature (Montgomery et al., 2008) indicates that the changes in blood flow observed with CWI is similar to changes observed during an active muscle contraction. Anecdotally, participants reported feeling refreshed following the VIP and CWT recovery mechanisms, and, as observed, both groups did demonstrate the highest scores on the Likert Recovery Questionnaire. However, neither CWT nor VIP, were able to demonstrate statistically significantly improved perception of recovery relative to NormaTec and placebo groups. As a result, the present findings were unable to support previous literature stating that active recovery or CWI/hydrotherapy was effective in minimizing an individuals’ perception of fatigue relative to other recovery methodologies.  5.7 Training Status  As was mentioned previously, research regarding elite athletes is difficult to undertake, as many athletes are hesitant to interrupt or halt their training to participate in a study (Barnett, 2006; Bahnert et al., 2013). As a result, in order to achieve the desired sample size utilizing the desired target population, the athletes recruited were not restricted from partaking in their regularly schedule training and/or team practice. It is possible that continued training during this period could have impacted their performance during the physical testing sessions and/or their physiological measures. In addition to the stress of physical training, the population in which the participants were drawn from, university students (undergraduate/graduate), are very susceptible to a variety of stressors.  Mental and emotional stress has been reported to result in decreased parasympathetic activity (Dishman et al., 2000; McCraty et al., 1995), which could ultimately impact the HRV results, and even the physical performance (10m/30m sprint, VJ) tests during this study. As participants were recruited and tested over a three-month period during the semester, it is also possible that 	  	  	   95	  other stressors, particularly school, could influence their resting HRV. It may be advisable to investigate this population during a less stressful time period, such as during the summer months. In order to work with varsity athletes from the University of British Columbia, participation in the study did not require participants’ avoidance of extraneous training. Previous literature has largely used recreationally active/trained athletes or untrained participants (French et al., 2008; Chleboun et al., 1995; Cochrane et al., 2013; Connolly et al., 2003; Eston & Peters, 2010; Glasgow et al., 2014; Sellwood et al., 2007) to avoid this issue. One study utilizing U.S. National level athletes training at the U.S Olympic Training Center (Sands et al., 2014a) allowed athletes to undergo regular training so as to avoid disrupting their scheduled programs. However, this study (Sands et al, 2014a) did not induce EIMD through an exercise protocol, such as the one applied in the present study, rather, participants rated their muscle soreness based solely on their regularly scheduled training, This can be problematic as well because it is difficult to standardize the fatiguing intervention, as strength programs are individualized and tailored to a particular athlete. Conversely, utilizing recreationally trained or untrained subjects reduces the ability to generalize the findings and conclusions to the desired population.  In order to generalize the results to highly trained and/or elite athletes, concessions in the present study had to be made. The athletes were unable to halt or avoid their regular scheduled training, so they undertook both their training, and the fatiguing exercise protocol in the present study. Consequently, this could have influenced their results and/or performance during testing. Future research regarding varsity athletes should ideally occur during out of school sessions (i.e. summer months) in order to avoid the mental and emotional stress that school can have on the autonomic nervous system (Dishman et al., 2000; McCraty et al., 1995). Furthermore, depending on the sport or selected athletes, summer may provide the best opportunity to test the athletes without sport training potentially influencing results. This may be difficult, as with highly trained or elite athletes programs are planned months and/or years in advance, with carefully constructed off-loading periods designed for adequate rest. Further research into this area may require considerable co-ordination between researchers, athletes, coaches, and organizational staff.   	  	  	   96	  5.8 Protocols  A large factor influencing the consistency of the results produced from the field of recovery research, including the present study, is the large variance in protocols utilized to determine the efficacy of the recovery strategies being investigated (Bahnert et al., 2013). Several studies acknowledge the limitations surrounding the available recovery protocols, and the need for a defined standard (Bieuzen et al., 2013; Bahnert et al., 2013; Versey et al., 2013; Leeder et al., 2011; Cochrane, 2004). An overwhelmingly large amount of the literature currently available regarding recovery strategies is difficult to compare and/or contrast, as they tend to use unique or varying recovery protocols (Versey et al., 2013; Pournot et al., 2011). Recovery protocols involving hydrotherapy have been investigated ranging from intermittent CWI (alternated with segments of no immersion) (Glasgow et al., 2014; Sellwood et al., 2007), CWT of equal time ratios however for different lengths of time (Vaile et al., 2008a; Vaile et al., 2008b; French et al., 2008 ), CWT with CWI and hot water showers (Hamlin, 2007), CWT with unequal CWI:HWI ratios (Cochrane, 2004), and immersions of varying depths (full body/head and neck out, xiphoid process immersion, hip-level) (Hamlin, 2007; Vaile et al., 2008a; 2008b; 2007; 2011; Stanley et al., 2012; Higgins et al., 2013; Higgins et al., 2002; French et al., 2008). This inconsistency has lead to the contradiction of results, and ultimately the inconclusiveness. Future research should focus on refining protocols, in order to provide substantial support for one protocol over another.  Furthermore, with so few studies published regarding the NormaTec MVP recovery device as a recovery strategy, the only protocol utilized, including in the present study, was a 20-min manufacturer’s default protocol (Cochrane et al., 2013; Hanson et al., 2013; Sands et al., 2014a; Sands et al., 2014b). With so little known about the efficacy of the device, it is difficult to determine whether this is an appropriate protocol to utilize, or if changes need to be made to truly determine the device’s efficacy. Future research is required to fully understand the device’s intensity settings and recovery protocols to conclude which setting is most effective (if any). Similarly, the VIP system, due to its novelty, utilized a protocol that has not been published. Further refinement of all the protocols investigated in the present study may be required to enhance and substantiate the beneficial claims surrounding each methodology.  	  	  	   97	  In an attempt to refine the protocols regarding CWT, Vaile et al. (2007; 2008a; 2008b) focused on using the same protocol throughout their research on CWT. Furthermore, these temperature selections were supported in a study investigating whether there was a dose-response during CWT (Versey et al., 2011). As a result of these studies, the CWT protocol was determined for the present study. It is possible that the protocol selected was insufficient in maximizing the benefits proposed for CWT. The results of the present study reinforce that further research is required to identify an optimal protocol that could elicit the benefits reportedly provided by each of these recovery strategies. Additional research should be undertaken regarding each of the available protocols to add depth to the available literature, and ultimately provide some consistency to the recovery field.  It is also important to note that the while the test protocols selected have been previously utilized by several studies (French et al., 2008; Cochrane et al., 2013; Eston & Peters, 1999; Rowsell et al., 2009), the present study did not investigate aerobic capacity. Aerobic capacity, specifically in cyclists and swimmers, has been studied in detail in regards to recovery strategies effectiveness (Halson et al., 2014;Vaile et al., 2011; Vaile et al., 2008a; Vaile et al., 2008b; Montgomery et al., 2009; Stanley et al., 2012). It is possible that the changes in blood flow may be more enhanced during aerobic capacity test measures, as endurance trained athletes have demonstrated increased blood volume relative to untrained individuals (Krip et al., 1997). Consequently, while the present study focused largely on power measures for physical performance, inclusion of an aerobic capacity outcome measure (ie. Time trial, VO2max) could provide further insight into the magnitude of blood volume changes, or the ability of recovery strategies to attenuate performance decrements. Future research should consider including a measure of aerobic endurance to capture this information.  5.9 Conclusion  Overall, CWT and VIP groups both demonstrated maintained and in some cases improved physical performance during VJ and 30m sprint compared to Placebo and NormaTec conditions. Each recovery strategy was able to demonstrate some capacity for facilitating recovery and/or maintaining performance, although not all of these trends were 	  	  	   98	  found to be statistically significant. While these results were not statistically significant, the percent changes from baseline observed amongst the groups for measures of physical performance are likely meaningful for elite athletes aiming to maintain physical performance following strenuous training sessions. Although not statistically significant, CWT demonstrated noticeable increases in mean (4.36%) and peak VJ (3.71%) performance compared to other groups, particularly NormaTec and placebo groups. The VIP group appeared to have an impact on performance maintenance for both VJ, 10m and 30m sprints. The VIP demonstrated performance maintenance for peak and mean vertical jump, peak and mean 30m sprints, while also demonstrating performance enhancements in peak (1.89%) and mean (2.72%) 10m sprint performance. The placebo group was the only group to demonstrate a complete return to baseline values for parasympathetic activity (RMSSD) measures. The NormaTec exhibited an ability to recovery above baseline values by 72 hr post-exercise for mean VJ (3.90%), despite having considerable performance decrements at 48 hr. Perceptions of muscle soreness were significantly increased in the VIP group relative to NormaTec (Stand to sit), placebo (Stand to sit, total pain) and particularly CWT (Stand to sit, passive quadriceps stretch: right and left legs, maximal quadriceps contraction: right leg only, total pain).  Perception of recovery was not significantly different between groups, however, VIP and CWT demonstrated maximal scores (70.50%, 70.60%, respectively).  It appears that both hydrostatic pressure and differential pressure applied by CWT and VIP, respectively, could be effective in facilitating performance improvements and/or maintenance, when compared to NormaTec and placebo conditions. CWT demonstrated an improved ability to reduce muscle soreness compared to the VIP, which was one of the few outcome measures on which the two groups differed. It is likely that the differences observed were due to the mechanical support provided by direct physical compression application implemented by CWT compared to the indirect pressure application observed with VIP. Overall, it appears the CWT and VIP, while not statistically significant, could demonstrate clinically meaningful trends that could be useful to athletes looking to facilitate recovery and maintaining physical performance. This study adds to the limited available literature regarding the novel recovery strategies (such as the VIP and NormaTec), which will provide depth to the scarce amount of literature. Furthermore, this study contributes to the understanding of the commonly utilized 	  	  	   99	  recovery protocols and their effectiveness, which should be further researched to add consistency to the current literature. Future research should focus on refining the recovery protocols to develop and/or determining optimal application of CWT, VIP and NormaTec methodologies as a post-exercise recovery tool. Future research should also aim to focus further on elite athletes to allow for generalizability to this population that is under-represented in the available literature.   5.10 Limitations   There are a few limitations worth noting that could impact the statistical significance of the present findings. Due to the specific requirements of our inclusion criteria (highly trained athletes, two years resistance training experience), the sample size in the present study was noticeably small and limited. In order to ensure the desired target population of highly trained athletes, there was a small pool of participants that we could recruit from, and ultimately this could have reduced the observed findings. Statistical significance and observed power were likely impacted by the limited sample size. Future studies should aim at recruiting larger sample sizes in order to increase the statistical power of the findings. Furthermore, in order to ensure adequate training status for the participants utilized, participants were not restricted from previously scheduled team training during the testing period. While not ideal, participants were not able to participate if they could not continue with their regularly scheduled training. This is a common occurrence with research involving elite athletes, as athletes are typically hesitant to participate in studies that will disrupt or impact their training schedule (Bahnert et al., 2013; Barnett, 2006). 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L., Fink, G., Spitzer, S. a, & Shapiro, Y. (1993). The effects of the modified intermittent sequential pneumatic device (MISPD) on exercise performance following an exhaustive exercise bout. British Journal of Sports Medicine, 27(4), 255–9. Retrieved from http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1332015&tool=pmcentrez&rendertype=abstract. 	  	  	   110	  Appendices  Appendix A: Recruitment Notice     T H E  U N I V E R S I T Y  O F  B R I T I S H  C O L U M B I A     Version 3/January 8th, 2015     RECRUITMENT NOTICE  Researchers at the University of British Columbia are interested in examining the effects of recovery strategies following high intensity training in athletes.  We are looking for highly trained able bodied athletes (male or female):  1. Between the ages of 18 and 35 years old, 2. Who participate in regular moderate to vigorous training 4 or more days of the week, 3. Who have at least two years experience in resistance training (weight training), 4. Who are free of severe orthopaedic injuries to the back and knees, 5. Who are free of known heart and lung symptoms/disease.  All subjects will be asked to participate in 5 consecutive days of testing.  One day of testing will consist of a fatiguing exercise protocol.   Your total time commitment will be 3.5 hr.  Principal Investigator: Dr. Darren Warburton If you are interested and would like further information, please feel free to contact Lauren Buschmann at the University of British Columbia.     School of Kinesiology Faculty of Education   Rm. 128, Unit II Osborne Centre 6108 Thunderbird Blvd.  Vancouver, B.C., Canada V6T 1Z3 Tel: 604.822.3131  Fax: 604.822.2684 Tel: (604) 822-1337 Fax: (604) 822-9451 www.hkin.educ.ubc.ca    	  	  	   111	  Appendix B: Consent Form    	  	  	   112	   	  	  	   113	  	  	  	   114	  	  	  	   115	  	  	  	   116	  	  	  	   117	        	  	  	   118	  Appendix C: The Physical Activity Readiness Questionnaire (PAR-Q+).    	  	  	   119	  	  	  	   120	  	  	  	   121	       	  	  	   122	  Appendix D: Training and Health History Questionnaire      Participant)#):)_________________________)Version)2/November)7th,)2014) 1)Training and Health History Questionnaire   How often do you participate in moderate to vigorous physical activity (RPE 8-10) per week? ________________________________________________________________________________  Do you regularly (consistently; 2-3 times a week) participate in resistance training (weights)?                             Yes / No  Do you regularly participate in organized sports or athletic events?        Yes / No    If Yes, what sport/event? ________________________________________________________________________________   Are you currently training for a specific event and/or sport? Yes / No  Have you done any of the following types of training:   Type of Training Yes No Frequency (Days & Hours per week) Long Slow Distance (LSD) Training    Interval training    Mileage    Percentage of VO2Max    Resistance Training    Circuit Training     Do you currently utilize any recovery strategies following training?   Yes / No  If yes, what types of strategies have you used/tried?   Do you have any severe orthopaedic injuries (specifically back, ankles, knees) that would be further exacerbated by a maximal squat assessment?            Yes / No  If yes, please explain and describe the injuries.   ________________________________________________________________________________ 	  	  	   123	      	  	  	   124	  Appendix E: Likert Recovery Questionnaire      Novel&Recovery&Strategies&for&Elite&Athletic&Performance/Version&1/November&28,&2014& 1&Recovery(Questionnaire((1.&I&have&used&recovery&applications&in&my&training&preparation&in&the&past.&&&Never( ( (Rarely( (((Occasionally(((((((((((((Frequently(((((((((((((Very(Frequently((2.&I&believe&recovery&applications&are&important&in&facilitating&recovery&following&exercise.&&Strongly(Disagree(((((((((((((((((Disagree(((((((((((((Undecided(((((((((((((((((((((Agree((((((((((((((((((((((Strongly(Agree(&3.&I&feel&I&have&recovered&following&the&recovery&application.&&Strongly(Disagree(((((((((((((((((Disagree(((((((((((((Undecided(((((((((((((((((((((Agree((((((((((((((((((((((Strongly(Agree((4.&I&feel&physically&recovered&for&my&next&training&session.&&Strongly(Disagree(((((((((((((((((Disagree(((((((((((((Undecided(((((((((((((((((((((Agree((((((((((((((((((((((Strongly(Agree((5.&I&could&perform&at&my&absolute&best&if&I&had&to&compete&tomorrow.&&Strongly(Disagree(((((((((((((((((Disagree(((((((((((((Undecided(((((((((((((((((((((Agree((((((((((((((((((((((Strongly(Agree(&6.&I&did&not&feel&refreshed&following&the&recovery&modality.&&&Strongly(Disagree(((((((((((((((((Disagree(((((((((((((Undecided(((((((((((((((((((((Agree((((((((((((((((((((((Strongly(Agree(&7.&If&I&had&a&competition&tomorrow,&I&would&not&be&able&to&perform&to&the&best&of&my&ability.&&&Strongly(Disagree(((((((((((((((((Disagree(((((((((((((Undecided(((((((((((((((((((((Agree((((((((((((((((((((((Strongly(Agree(&8.&I&do&not&feel&physically&recovered&for&my&next&training&session.&&&Strongly(Disagree(((((((((((((((((Disagree(((((((((((((Undecided(((((((((((((((((((((Agree((((((((((((((((((((((Strongly(Agree((9.&I&feel&that&the&recovery&application&will&allow&me&to&perform&better.&&Strongly(Disagree(((((((((((((((((Disagree(((((((((((((Undecided(((((((((((((((((((((Agree((((((((((((((((((((((Strongly(Agree((10.&I&believe&that&the&recovery&application&is&an&important&part&of&physical&preparation&for&athletes.&&Strongly(Disagree(((((((((((((((((Disagree(((((((((((((Undecided(((((((((((((((((((((Agree((((((((((((((((((((((Strongly(Agree(&&&&&&	  	  	   125	  Appendix F: Randomization of Recovery Applications        Recovery Application (Number Code) # Of Participants CWT (1) 6 VIP (2) 6 Placebo (3) 6 NormaTec (4) 6                  	  	  	   126	  Appendix G: Grip Strength Categorizations           	  	  	   127	  Appendix I: Visual Analog Scale 	  	  	   128	   Participant:*___________________________* * *Testing*Session:*___________________**Sit$to$Stand:$*** * No* * * * * * * * Pain*as*bad*** Pain* * * * * * * * as*it*could*** * * * * * * * * possibly*be*****Stand$to$Sit:$$$** * No* * * * * * * * Pain*as*bad*** Pain* * * * * * * * as*it*could*** * * * * * * * * possibly*be******Passive$Quadriceps$Stretch$(Left):$$$$** * No* * * * * * * * Pain*as*bad*** Pain* * * * * * * * as*it*could*** * * * * * * * * possibly*be*$$$$$$$$$	  	  	   129	       	  

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