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The effect of recovery strategies on high-intensity exercise performance and lactate clearance Peeters, Mon Jef 2008

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THE EFFECT OF RECOVERY STRATEGIES ON HIGH-INTENSITY EXERCISEPERFORMANCE AND LACTATE CLEARANCEbyMON JEF PEETERSB.H.K., The University of British Columbia, 2004A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FORTHE DEGREE OFMASTER OF SCIENCEinThe Faculty of Graduate Studies(Human Kinetics)THE UNIVERSITY OF BRITISH COLUMBIA(Vancouver)March 2008© Mon JefPeeters, 2008AbstractPURPOSE: To compare the effects of recovery intensity on performance of a bicycle sprint taskand blood L& clearance. METHODS: On three separate days twelve trained male subjects (27.4± 3.9 yrs) performed three supramaximal exercise (SE) bouts at 120% of maximum aerobicpower (MAP) for 60% of the time to exhaustion (TTE). Bouts were separated by 5 mm ofpassive recovery (PR), active recovery (AR) or combined active recovery (CAR). The third boutwas followed by a 14 mm recovery. Recovery intensities were: PR (rest), AR at 50% of theworkload difference between the individual anaerobic threshold (TAT) and the individualventilatory threshold (IVT) below the IVT(IVT_50%AT), or CAR at the TAT workload for 5 mmand at the IVT_50%AT workload for 9 mm. Five 10 s sprints were performed 2 mm post-recovery.Blood lactate (L&) concentration, power parameters (Peak Power (PP), Mean Power (MP),Fatigue Index (Fl), and Total Work (TW)), Heart Rate (HR), and Oxygen Uptake (V02)werecompared using repeated-measures ANOVA. Pairwise comparisons and dependent T-tests wereperformed to analyze differences. RESULTS: Mean La values for AR and CAR were lowerthan PR (9.7 ± 3.5, 9.5 + 3.5, 11.7 + 3.6, respectively, pO.O5). La was significantly lower withCAR versus PR at the3Id, 6th 9thand14thmm of recovery (pO.OS). AR versus PR La waslower at the 6,9thand14thmm of recovery (pO.O5). Mean MP was greater in the AR groupcompared to the PR group (800.1 ± 114.5 vs 782.2 ± 111.7 W, pO.O5). TW during AR wasgreater than PR (p0.05) but not CAR(p>O.O5,40003.3 ± 5110.2, 39108.3 ± 4852.9, 39335.8 ±5022.6 J, respectively). CONCLUSIONS: AR and CAR both demonstrated improved L&clearance when compared to PR, but differences in L& clearance did not determine performanceon the sprint task. AR resulted in more TW than PR and greater maintenance of power over thesprints.11Table of ContentsAbstract.iiTable of ContentsiiiList of TablesvList of FiguresviCHAPTER I: INTRODUCTION11.1 Introduction 11.2 Rationale 21.3 Purpose 21.4 Significance of the Study 31.5 Hypotheses 31.6 Definitions 41.7 Delimitations 71.8 Limitations 8CHAPTER II: LITERATURE REVIEW 92.1 Introduction 92.2 The New View on Lactate 102.3 Lactate and its Relation to Fatigue During High-Intensity Exercise 102.3.1 Inorganic Phosphate as a Cause of Fatigue 112.3.2 Other Mechanisms of Fatigue 122.4 Active Recovery and Lactate Clearance 132.4.1 Exercise Intensity, Mode, and Duration 152.4.2 Combined Active Recovery and Lactate 192.5 Lactate and Performance 212.6 Active Recovery and Performance 222.6.1 No Performance Benefit with Active Recovery 232.6.2 Performance Benefit with Active Recovery 252.6.3 Performance and Active Recovery Duration 282.7 Summary 28CHAPTER III: METHODS 303.1 Subjects 303.2 Experimental Design 303.3 Facilities and Instrumentation 313.3.1 Wingate and Sprint Tests 313.3.2 Ventilatory and Gas Exchange Variables 323.3.3 Blood Lactate 323.3.4 Heart Rate 333.4 Testing Procedures 333.4.1 Day 1: Anthropometric Measures, 7O2max, and WAnT 333.4.2 Day 2: Time to Exhaustion Test 343.4.3 Day 3: Familiarization Tasks 353.5 Data Analysis38CHAPTER IV: RESULTS394.1 Subject Characteristics 391114.2 BloodLactate.394.3 Sprint Task Performance 444.3.1 Peak Power 454.3.2 Mean Power 474.3.3 Fatigue Index 504.3.4 Total Work 524.4 Heart Rate 534.4.1 Exercise and Recovery Heart Rate 544.4.2 Sprint Task Heart Rate 564.5 Volume of Oxygen Consumed 58CHAPTER V: DISCUSSION 615.1 Subject Characteristics 615.2 Blood Lactate 615.2.1 Combined Active Recovery and Lactate Clearance 635.3 Sprint Task Performance 645.3.1 Peak Power 645.3.2 Mean Power 665.3.3 Fatigue Index 715.3.4 Total Work 735.4 Heart Rate and Volume of Oxygen Consumed 745.4.1 Exercise and Recovery Heart Rate 745.4.2 Sprint Task Heart Rate 755.4.3 Volume of Oxygen Consumed 765.5 Practical Significance 77CHAPTER VI: CONCLUSION 796.1 Conclusions 796.2 Recommendations for Future Research 796.2.1 Performance Criteria 806.2.2 Active versus Passive Recovery and Duration Dependency 806.2.3 Mechanisms 806.3.3 Suggested Modifications and Additions 80References 82APPENDIX I 93APPENDIX II 94APPENDIX III 95APPENDIX IV 96APPENDIX V 97APPENDIX VI 98APPENDIX VII 99APPENDIX VIII 100APPENDIX IX 101APPENDIXX 10’LivList of TablesTable 1. Subject Characteristics40Table 2. Subject Workload and Recovery Characteristics 41Table 3. Mean Blood Lactate Values42Table 4. Mean Blood Lactate Differences for Sample Time42Table 5. Group Means for Peak Power, Mean Power, Fatigue Index and TotalWork 45Table 6. Mean Peak Power Outputs45Table 7. Sprint Number Means for Peak Power, Mean Power, and Fatigue Index46Table 8. Mean Mean Power Outputs 48Table 9. Mean Fatigue Indexes50Table 10. Mean Exercise and Recovery Heart Rate Values54Table 11. Mean Exercise and Recovery Heart Rate Differences for Sample Time56Table 12. Mean Maximum Sprint Task Heart Rate56Table 13. Mean Sprint Task Heart Rate Differences for Sample Time57Table 14. Mean Volume of Oxygen Consumed Values 59Table 15. Mean Volume of Oxygen Consumed Differences for Sample Time60Table 16. Daily and Overall Maximum and Minimum Blood Lactate Values93Table 17. Daily and Overall Maximum and Minimum Peak Powers94Table 18. Daily and Overall Maximum and Minimum Mean Powers 95Table 19. Daily and Overall Maximum and Minimum Fatigue Indexes 96Table 20. Individual Total Work Outputs and Maxima and Minima 97Table 21. Daily and Overall Maximum and Minimum Exercise and Recovery Heart Rate Values98Table 22. Daily and Overall Maximum and Minimum Sprint Task Heart Rate Values 99Table 23. Daily and Overall Maximum and Minimum Volume of Oxygen Consumed Values 100Table 24. Sprint Task Fatigue Scores 101vList of FiguresFigure 1. Example of Determination of Individual Anaerobic Threshold in Subject 11 6Figure 2. Example of Determination of Individual Ventilatory Threshold in Subject 2 7Figure 3. Schematic Representation of the Testing Day Protocol 37Figure 4. Mean Blood Lactate Values 43Figure 5. Mean Peak Power Outputs 46Figure 6. Mean Mean Power Outputs 49Figure 7. Mean Fatigue Indexes 51Figure 8. Total Work 53Figure 9. Mean Exercise and Recovery Heart Rate Values 55Figure 10. Mean Sprint Task Heart Rate 58Figure 11. Mean Volume of Oxygen Consumed Values 60viCHAPTER I: INTRODUCTION1.1 IntroductionHistoricallylactatea(L&) and its accumulation during high-intensity exercise has beenidentified as a causative factor in fatigue development (Hill & Kupalov, 1929; Karisson, BondePetersen, Henriksson, & Knuttgen, 1975; Klausen, Knuttgen, & Forster, 1972; Stamford,Weitman, Moffatt, & Sady, 1981; Yates, Gladden, & Cresanta, 1983). More recently, the role ofL& as a causative agent in fatigue development has been questioned, but results remaininconclusive (Fitts, 2003; Gladden, 2004). It appears that the relationship of La accumulation tofatigue is part of a complex interactive process. Nonetheless, the association between L&accumulation and the onset of fatigue during high-intensity exercise remains irrefutable. Though,it must be stressed that the chronological associations of the two events does not necessarilyindicate causation. It has been suggested that an increased rate of L& clearance may lead to fasterrecovery and/or postpone fatigue during repetitive exercise (Gisolfi, Robinson, & Turrell, 1966;Lindinger, McKelvie, & Heigenhauser, 1995). This has large implications for performanceathletics, where the ability to recover quickly for subsequent high-intensity exercise bouts iscrucial to success. This is especially true for sports where athletes may compete more than oncein a day (e.g. track, cycling, swimming, ref. Dodd, Powers, Callender, & Brooks, 1984) orperform repetitive high-intensity bouts within one competition (e.g. hockey, football, soccer,basketball). The unequivocal findings that active recovery (AR, i.e. low-intensity aerobicexercise performed after high-intensity exercise) increases the rate of L& clearance (Ahmaidi etal., 1996; Belcastro & Bonen, 1975; Davies, Knibbs, & Musgrove, 1970; Dupont, Moalla,Guinhouya, Abmaidi, & Berthoin, 2004; Gupta, Goswami, Sadhukhan, & Mathur, 1996;Hermansen & Stensvold, 1972; Jervell, 1928; Newman, Dill, Edwards, & Webster, 1937;Rämmal & Strom, 1949; Siebers & McMurray, 1981; Stamford et al., 1981; Taoutaou et al.,1996; Weltman, Stamford, & Fulco, 1979), has lead to the belief that AR is beneficial tosubsequent exercise performance. However, studies investigating the effect of active versuspassive recovery (PR, i.e. no activity) on subsequent performance have been inconclusive, withsome investigations showing benefits (Ahmaidi et al., 1996; Signorile, Ingalls, & Tremblay,1993; Spierer, Goldsmith, Baran, Hryniewicz, & Katz, 2004; Thiriet et al.,1993) and others not(Dupont et al., 2004; Franchini, Yuri Takito, Yuzo Nakamura, Ayumi Matsushigue, & PedutiDaUMolin Kiss, 2003; Siebers & McMurray, 1981; Weltman & Regan, 1983). Furthermore, theaThe term La will be used rather than lactic acid throughout this paper since at a physiological muscularpH range (6.2O-7.OO) lactic acid is more than 99% dissociated to La and a proton due to its pKa value (pH=3 .87,ref. Gladden, 2004; Robergs, Ghiasvand, & Parker, 2004)1optimal method(s) by which to perform AR remains uncertain since previous research has used awide array of protocols. It has been suggested that recovery (and exercise) intensities should beexpressed relative to individual thresholds rather than maximum oxygen consumption(VO2max,ref. Baldari, Videira, Madeira, Sergio, & Guidetti, 2004; McLellan & Skinner, 1982), since themetabolic outcome is dependent on thresholds. There is some evidence to support the use ofacombined active recovery (CAR) of varying intensity to improve the clearance rate of La incomparison to AR at one intensity (Gmada et al., 2005). However, further research is neededtocongeal this assertion. Additionally, there is currently no research available as to whether or notthe increased rate of La clearance with a CAR translates to improved performance or what theeffects of CAR are on performance independent of the effect on L& clearance.1.2 RationaleIn 1981, Stamford et al. suggested that there may not be one optimal exercise intensity atwhich to clear LaZ Rather than use a continuous submaximal constant load for AR (as hadpreviously been used in most research protocols), they suggested using a progressivelydecreasing load starting above the anaerobic threshold (AT) and finishing below the AT. Theauthor is aware of two studies that have used this suggestion and employed a CAR. Dodd et al.(1984) compared CAR (i.e. moderate-to-high-intensity followed by low-intensity exercise) toboth passive and two traditional continuous constant load recoveries at moderate-to-high- andlow-intensity, respectively. Their results showed that the CAR and low-intensity AR had thefastest L& clearance rates, but that there were no statistically significant differences betweenthose two recovery modalities. Recently Gmada et al. (2005) showed that CAR resulted in afaster L& clearance rate when compared with constant load moderate-to-high-intensity, low-intensity active, and passive recovery (the effect was more pronounced in trained subjectscompared to untrained). Together, these investigations demonstrate that CAR is at least equal toor better than AR with respect to blood La clearance rate. However, neither of these studiesexamined the effect of the recovery periods on subsequent performance.1.3 PurposeThe purpose of this investigation was two-fold: to examine the effects of two activerecoveries, relative to individual thresholds (i.e. CAR and AR), and PR in trained male cyclistson the subsequent performance of five 10 s bicycle sprints after a work bout of threesupramaximal exercise (SE) intervals. Secondly, to examine the effects of the three recoveries onblood L& clearance rate.21.4 Significance of the StudyThe results of investigations examining the effects of different recovery methods onperformance have implications for the design and implementation of training programs andcompetition strategies. Specifically, this investigation provides insight into the use of differentrecovery intensities and their effects on subsequent performance of high-intensity exercise aswell as blood La clearance. The results help to clarify what the effects of various recoverystrategies are on performance and whether or not the use of active recoveries provide a benefit tohigh-intensity athletic performance and training.1.5 HypothesesThe following hypotheses were suggested:a. Blood Lactate Alternate Hypothesis (Hi): A CAR blood L&> A AR blood L&> A PRblood L&The change in blood La in the CAR trial will be greater than the change in the AR trialwhich will in turn be greater than in the change PR trial. This hypothesis has beensuggested because it has been previously shown that CAR is more effective than (Gmadaet al., 2005) or as effective as (Dodd et a!., 1984) AR at one sole intensity with respect toL& clearance. It has been theorized that the faster L& clearance rate with CAR is a resultof the increased blood flow from the higher exercise intensity (Gmada et al., 2005).Previously it had been suggested that a CAR may be more effective at removing L&since the decreasing exercise intensity would be commensurate with the decreasing L&concentration (Stamford et al., 1981). The pairing of exercise intensity and L&concentration is predicted to be beneficial because the rate La clearance is proportionalto its concentration (Jorfeldt, 1970). Furthermore, it is hypothesized that AR will clearL& faster than PR, since there is an abundance of literature that already supports thishypothesis (Baldari, Videira, Madeira, Sergio, & Guidetti, 2005; Franchini et a!., 2003;McAinch et aL, 2004; Spierer et al., 2004).b.Peak Power (PP) Output H1: CAR = AR = PRppNo differences in PP output on the sprint task are hypothesized between recovery trials.This hypothesis has been suggested because it has previously been shown that ARmodalities did not affect the development of PP in subsequent high-intensity exercisetasks with similar recovery durations (Ainsworth et a!., 1993; Spierer et a!., 2004;Weltman, Stamford, Moffatt, & Katch, 1977). Peak power (sometimes called anaerobicpower) is mainly dependent on the phosphocreatine (PCr) system and free ATP, and3therefore is not expected to change significantly with the recovery durations in thisinvestigation, since the prolonged 14 mm recovery should provide ample time forreplenishment of PCr levels..Mean Power (MP) Output H1: CARMP> ARMP> PRThe MP output on the sprint task will be statistically significantly greater in the CAR trialthan the MP in the AR trial, which will be greater than the MP output in the PR trial. It ishypothesized that AR will result in a greater MP output than PR recovery since it hasbeen previously shown that AR can improve subsequent performance with respect to MPoutput (Spierer et a!., 2004; Thiriet et aL, 1993). Combined active recovery ishypothesized to result in the greatest MP output since it has been shown that CAR canclear L& faster than the other two recovery modes being tested (Gmada et al., 2005).High L& and proton transport, as would occur during AR, has been suggested to preventfatigue because of the beneficial effects of L& anions in providing oxidizable substrateand gluconeogenic precursors (Thomas et al., 2005). The greater clearance of La istherefore not predicted to prevent fatigue by eliminating L&, an agent in fatigue, butrather by utilizing L& as fuel source to prevent fatigue. In the case of this investigation, itis being suggested that the fastest rates of L& transport (i.e. clearance) will occur in theCAR trial and thus in this trial subjects will have the greatest resistance to fatigue. Thatis, their anaerobic capacity (or MP output) will be maintained.d.Fatigue Index (Fl) H1:PRFI> ARFI> CARFIFatigue index will be greater in the PR trial than Fl in the AR trial, which will be greaterthan FT in the CAR trial. Fatigue index is the percent power decrease over the course of asprint and therefore will have the opposite results of MP.e.Total Work (TW) H1: CARTW> ARTW> PRTWTotal work on the sprint task will be statistically significantly greater in the CAR trialthan TW in the AR trial, which will be greater than TW in the PR trial. This hypothesis issuggested because TW is the product of MP and time over the five sprints, and thusfollows the above hypothesis of MP output.1.6 Definitions• Maximum Oxygen Consumption (VO2m) — a measure of cardiorespiratory fitness. VO2maxis highest amount of 02 the body is able to consume and the product of maximal cardiacoutput (L.min’) and arterial-venous difference (mL O2L’, ref. ACSM, 2006).4• Active Recovery (AR) — moderate- to low-intensity exercise performed after high-intensityexercise to promote a faster return to pre-exercise conditions.• Combined Active Recovery (CAR) — moderate- to high-intensity exercise followed bymoderate- to low-intensity exercise performed after high-intensity exercise to promote afaster return to pre-exercise conditions.• Passive Recovery (PR) — resting post high-intensity exercise to promote a faster return topre-exercise conditions.• Individual Anaerobic Threshold (IAT) — a specific form of anaerobic threshold defined asthe highest sustainable workload without an accumulation of La (i.e. maximal L& steadystate, ref. Baldari & Guidetti, 2000; Stegmann, Kindermann, & Schnabel, 1981). IAT isoperationally defined as the workload corresponding to the second L& increase of at least0.5 mmolL’ from the previous value (Baldari & Guidetti, 2000, see Figure 1 for visualrepresentation).• Individual Ventilatory Threshold (IVT) — a specific form of ventilatory threshold alsoknown as the point of optimum ventilatory efficiency (Hollmann, 2001). IVT is the lowestvalue of the ventilatory equivalent (VEIVO2), when VE/V02 is plotted as a function of V02(Baldari & Guidetti, 2001, see Figure 2 for visual representation).5Figure 1. Example of Determination of Individual Anaerobic Threshold in Subject 115. -______________X4.34•3.4•3.2E3E4-,‘I-,0-2 12.011.6•1.70- I I I90 120 150 180 210 240 270 300Workload (W)TAT is the workload corresponding to the second L& increase of at least 0.5 mmol•L1from the previousvalue and is represented by thex6Figure 2. Example of Determination of Individual Ventilatory Threshold in Subject 22520•16.5hiT2 17016.0•16.<15.6167117.650 I I I I I1 1.5 2 2.5 3V02 (LJmin)WT corresponds to the lowest VE/V02 and is represented by the1.7 DelimitationsThis study will be delimited by:a. A sample of university-aged (18-35) subjects from University of British Columbiastudents and others from the Vancouver area.b. Setting the criteria for trained subjects as participating in competitive cycling with aheavy anaerobic component, PP and MP outputs greater than or equal to 11 and 9 W•kg’on the Wingate Anaerobic Test (WAnT), respectively, and having a VO2m greater than55 mLkg’•min’.c. A respiratory gas-sampling rate set at 20 sintervals.d. The measurement of performance on the sprint task as a measure of anaerobic capacity.e. The methodology used to determine IVT, IAT, and VO2m.71.8 LimitationsThis study will be limited by:a. The data collection capabilities of the SensorMedics Vmax 29 seriesmetabolic cart andthe interlaced Data Acquisition System.b. The individual’s metabolic responses to the testing protocols.c. The individual’s effort during testing procedures (e.g. the individual’s ability to performmaximally during the exercise tasks).d. The ability to determine TAT and IVT from the data collected.8CHAPTER II: LITERATURE REVIEW2.1 IntroductionIn performance athletics the ability to maintain power output and ward off fatigueisessential to success. In activities that are intermittent in nature or between competitions that areshortly spaced apart (e.g. tournament setting) the capacity for an athlete to recover quickly is adetermining factor in their performance. While the mechanism(s) of fatigue to date remainundetermined, the historical view has identified the accumulation of L& as the causative factor(Hill & Kupalov, 1929). Over time this paradigm has shifted to L& being an agent in thedevelopment of fatigue through its influence as an anion on the acid-base status of the muscleand blood (Lindinger et al., 1995; Stewart, 1981). The knowledge that the use of AR results in anincreased clearance rate of blood L& and the anecdotal reports of the advantageous use of AR inathletic training regimens has led to a belief that AR is beneficial to repeated performance(Gisolfi et al., 1966). Despite the common belief that AR is beneficial to subsequentperformance, the research evidence is inconclusive with some research showing a benefit(Ahmaidi et al., 1996; Bogdanis et al., 1996b; Connolly et aL, 2003; Corder et al., 2000;Signorile et al., 1993; Spierer et al., 2004; Thiriet et al., 1993) and some showing no benefit(Bond, Adams, Teamey, Gresham, & Ruff, 1991; Franchini et al., 2003; McAinch et al., 2004;Siebers & McMurray, 1981; Watson & Hanley, 1986; Weltman et al., 1979; Weltman & Regan,1983). Furthermore, within the research that supports the use of AR to improve performance, therelationship of L& clearance to performance is inconsistent (Bogdanis et al., 1 996b; Connolly,Brennan, & Lauzon, 2003; Spierer et al., 2004; Thiriet et al., 1993). Interestingly, this lack ofcorrelation between L& clearance and improved performance may be explained by more recentevidence that is shifting the cause of fatigue away from La accumulation and the associatedincrease in acidity to an accumulation of inorganic phosphate (Westerblad, Allen, & Lannergren,2002). Nonetheless, the mechanism(s) for the development of fatigue still remain unresolved andare most likely a result of a complex interaction of events related to the availability andaccumulation of metabolites. Therefore the role of L& as an agent in the development ofmuscular fatigue remains valid as the onset of fatigue coincides with its accumulation. From apractical perspective, regardless of the role of L& in fatigue, the use of AR as a means to preventdecrements in performance in successive exercise remains a compelling research areaparticularly since AR may be beneficial for certain types of physical activity.92.2 The New View on LactateHistorically, the accumulation of L& in the blood associated with high-intensity exercisehas been viewed negatively and La has been labeled as a metabolic waste product that resultedfrom glycolysis in hypoxic conditions (Gladden, 2004). The initial concept of a relationshipbetween L& accumulation and hypoxia stemmed from research in the early part of the lastcentury (Fletcher & Hopkins, 1907; Hill, Long, & Lupton, 1924). Gladden (2004) has identifiedthe time frame from the 1930s to the 1970s as the dead-end waste product era of L&. During thistime La was believed to be a dead-end metabolite of glycolysis in hypoxic conditions(Wasserman, 1984). This paradigm has shifted greatly over the past few decades, as it has beenrepeatedly shown that the production of L& is not necessarily a result of 02 lack (e.g.Richardson, Noyszewski, Leigh, & Wagner, 1998). Currently, the perspective on L& metabolismis very different in light of the advent of the La shuttle hypothesis (Brooks, 1985) and the widelyheld acceptance of the extracellular L&shuttleb.Lactate is now recognized as a metabolicintermediate rather than an end, and a movable source of energy substrate that can be passedabout the body for metabolism.2.3 Lactate and its Relation to Fatigue During High-Intensity ExerciseDuring high-intensity exercise, anaerobic metabolic processes are heavily utilized tomeet the energy demand. As the glycolytic production of ATP increases, the mitochondria’ sability to aerobically oxidize pyruvate is exceeded (Spriet, Howlett, & Heigenhauser, 2000). Thisleads to an increased concentration of pyruvate and NADH, which are then converted to L& andNAD by the near-equilibrium enzymatic reaction of L& dehydrogenase (LDH, ref. Spriet et al.,2000). It is the processes that govern the production of pyruvate and NADH that predominantlycontrol the production of L& (Spriet et al., 2000). Blood La concentration is ultimately the resultof the balance between production and clearance processes. With sufficiently high-intensities ofexercise the balance between the production and clearance of L& is shifted to disequilibrium andLa begins to accumulate.The knowledge that L& accumulates in exercised muscle has a long history dating backto the work of Berzelius in 1807, who noted that hunted stags had elevated acid concentrations intheir muscles (as cited in Needham, 1971). More recently other researchers noted thebBrooks has also argued for an intracellular L& shuttle (Brooks, 1998) in addition to the original cell-to-cell(or extracellular) L& shuttle, and has provided support for its existence(Brooks, Dubouchaud, Brown, Sicurello, &Butz, 1999). However, other researchers have failed to fmdsupporting evidence to some of the central tenets of thehypothesis (Rasmussen, van Hall, & Rasmussen, 2002; Sahlin, Fernstrom, Svensson, &Tonkonogi, 2002; Yoshidaet al., 2007). Consequently, the cell-to-cell L& shuttle hypothesis is more or lessunanimously accepted while thestate of the intracellular L& shuttle remains to be determined with future research10accumulation of L& in working muscles and noted the effects of AR on its clearance (Jervell,1928; Newman et a!., 1937). In the early twentieth century, Hill and Kupalov (1929) proposedthat lactic acid accumulation was the cause of muscular fatigue. This formed the initialframework for the conception that La accumulation was the cause of fatigue. This conceptionwas maintained for years to come (Karisson & Saltin, 1970), and is still very prevalent amongstmost laypersons.Currently, more researchers attribute the associated development of fatigue that ariseswith L& accumulation to the associated decrease in pH (i.e. increase hydrogen ion concentration([Hj)) rather than to the increase in L& anion itself (Fitts, 2003). Remember that the formationof lactic acid at a physiological pH results in its immediate dissociation into the L& anion and aproton. Some researchers have misinterpreted the direct donation of this proton from lactic acidas the cause of the decrease in pH. This may be a result of attempting to simplify theexplanation. However, the relationship of body fluid acid-base status is more complex than this.The re-introduction of the concepts of earlier researchers such as Henderson and van Slyke byPeter Stewart (Stewart, 1981) has helped to clarify this understanding (Lindinger, 2003). In thisview acid-base status is determined by the independent effects of carbon dioxide(Pcü2),theconcentration of weak acid buffers ([Atot], in plasma mainly the amino acids in plasma proteins),and the strong ion difference ([SID], i.e. the sum of the strong cations minus the sum of thestrong anions, ref. Kowalchuk, Heigenhauser, Lindinger, Sutton, & Jones, 1988; Stewart, 1981).Lactate being a strong anion decreases pH by causing a decrease in the [SID]. The accumulationof L& in the blood that occurs with high-intensity exercise has been shown to increase theplasma [Hj,PCQ2,and osmolarity (Kowaichuk et al., 1988; Lindinger et al., 1995). Theincreased [Hj is believed to cause fatigue by: (1) inhibiting the glycolytic enzymephosphofructokinase, (2) reduction of myosin crossbridge activation via competitive inhibitionof Ca2 binding to troponin C, and (3) inhibiting sarcoplasmic reticulum (SR) ATPase reducingCa2 re-uptake and subsequently Ca2release (Fitts, 2003).2.3.1 Inorganic Phosphate as a Cause of FatigueRecently the role of increased [Hj in the development of fatigue has come into questionas the initial studies that attributed H accumulation to fatigue were not performedatphysiological temperatures, and recent investigations at physiological temperatures do notsupport the role of H in fatigue development (Gladden, 2004; Westerbiad et a!., 2002). Twolandmark studies that have been integral in this shift are that of Bangsbo et a!. (1996) andNielsen et al. (2001). Bangsbo et al. (1996) showed that muscle acidity in humans during intense11exercise did not reduce glycogenolysis/glycolysis. While Nielsen et a!. (2001) demonstrated thatthe reduced muscular force that normally developed with increased extracellular potassiumconcentration ([Kje) could be reduced with induced acidosis and was accompanied by theregeneration of action potential development. In place, the cause of fatigue is attributed to theaccumulation of inorganic phosphate (Pt) within the muscle. It is hypothesized that P1 causesmuscular fatigue by: (1) reducing maximum crossbridge force, or (2) altering SR Ca2handlingvia direct action on SR Ca2 release channels, inhibition of Ca2uptake, or formation of Ca2-P1precipitate (for review see Westerbiad et al., 2002). However, Gladden (2004) notes that the timecourse of fatigue development and the accumulation of P1 within the muscle do not coincide,since the majority of PCr is broken down in the initial seconds of high-intensity exercise.Similarly, Fills (2003) states that it may be premature to dismiss the role of H accumulation infatigue development since studies have not completely elucidated the effects of a combined lowpH, elevated P1 and reduced Ca2release. Recent research by Fitts and colleagues has providedsupport for the latter statement since they found that a combined reduction in myoplasmic Ca2and increased concentration of P1 act synergistically to reduce muscular force (Debold,Romatowski, & Fills, 2005). It yet remains to determine the role of changes in acidity.2.3.2 Other Mechanisms of FatigueIt should be noted that there are previous reports that have linked the L& anion itself tofatigue. In 1995, Hogan et al., using dog preparations showed that L& infusion at a constantarterial pH (7.40) reduced muscle tension development by 15%. However, more recently theeffects of the L& anion on muscle contractility have been shown to be minimal (Posterino,Dutka, & Lamb, 2001). Still, other researchers subscribe to the theory of muscular fatigueinduced via the accumulation of extracellular IC (Lindinger et a!., 1995; Renaud, 2002), whereL& may have an indirect effect on fatigue development. Lindinger (1995) states that in order forproper muscle function to continue L& must be removed, and intracellular IC concentration([K]) must be maintained, as L& clearance is essential for the recovery of [Hj and restorationof [Kj is necessary for both the recovery of [Hj and sarcolemmal and transverse tubulemembrane potentials. In this model La influences acid-base status, which in turn regulates themembrane excitability. Similarly, Renaud (2002) proposes a model of fatigue in which [Kie 5increased by the activation of ATP-sensitive IC channels (KATP channel) to prevent a decrease incellular ATP levels or prevent accumulation of metabolic end-products. Lactate, as well as ADPand H have been identified as potential modulators of the KATP channeland thus modulators offatigue in this model (Renaud, 2002).12To date, the exact mechanisms of muscular fatigue during high-intensity exercise remainundetermined and are most likely the result of a multitude of interacting factors. Fitts (2003)states that fatigue recovery from high-intensity exercise has both a rapid and slow componentlikely caused by separated mechanisms. The rapid component being reversible is related to P1and changes in the excitation-contraction coupling and Ca2 regulation, while the slowercomponent involves several sites and steps in the contraction process that are at least partiallymediated by H and P1 (Fitts, 2003). While the role of L& in the development of fatigue hasshifted from causative factor to a potential mediator, the fact that fatigued muscles displayincreased La concentrations attests to the fact that L& accumulation has some role in thedevelopment of fatigue.2.4 Active Recovery and Lactate ClearanceNumerous studies have provided unequivocal evidence that AR expedites blood L&clearance compared to passive recovery (Belcastro & Bonen, 1975; Davies et al., 1970;Hermansen & Stensvold, 1972; Jervell, 1928; Newman et a!., 1937; Rämmal & Strom, 1949;Siebers & McMurray, 1981; Stamford et a!., 1981; Weltman et a!., 1979). Beginning with Jervell(1928) it was noted that blood L& concentration declined more rapidly during exercisingrecovery. This was the first scientific paper on what would later become known as AR. Later,Margaria et a!. (1933) discovered that L& clearance rate is proportional to its concentration.Newman et a!. (1937) concluded that L& clearance rate increases in approximate proportion tometabolic rate up to a critical intensity, which varies among individuals and is higher in thosethat are trained. Subsequent studies confirmed these initial findings (Belcastro & Bonen, 1975;Davies et a!., 1970; Hermansen & Stensvo!d, 1972; Rämmal & StrOm, 1949; Siebers &McMurray, 1981; Stamford et al., 1981; Weitman et al., 1979), and the literature is conclusivethat AR increases the rate of L& clearance from the blood. At the same time AR has been shownto have the reverse effect on muscle La concentration in the exercised muscle groups (McAinchet al., 2004; Peters-Futre, Noakes, Raine, & Terblanche, 1987). These researchers found that ARincreased muscle L& concentration, and attributed the increase to increased local metabolicactivity that resulted in L& production. However, these findings are not unanimous as otherinvestigators have found AR to decrease muscle L& concentration (Bangsbo, Graham, Johansen,& Saltin, 1994; Spencer, Bishop, Dawson, Goodman, & Duffield, 2006).While it is agreed that AR clears blood L&, the fate of the cleared L& has been lessobvious. There are two main biochemical processes that have been identified as the route for L&elimination: (1) gluconeogenesis and glyconeogenesis, and (2) oxidation in the tricarboxylic13cycle to CO2 and H20 with energy production (Rontoyaimis, 1988). Gladden (2003) takes thedivision further and differentiates between glyconeogenesis in muscle and uptake by the liverand/or kidneys with subsequent formation of glucose and/or liver glycogen. Previously it wasbelieved that L& was predominantly removed via glyconeogenesis in the liver (Rowell et al.,1966). However, evidence shows that post-exercise the majority of L& (55-75%, ref. Brooks &Gaesser, 1980) is not resynthesized to glycogen, but rather is oxidized in the muscles (Bangsboet al., 1994; Hermansen & Stensvold, 1972; Peters-Futre et al., 1987; Rontoyannis, 1988).Human studies estimating the post-exercise conversion of L& to glycogen have shown variedresults: approximately 70% (Hermansen & Vaage, 1977), approximately 50% (Astrand,Huitman, Juhlin-Dannfelt, & Reynolds, 1986), and between 13-27% (Bangsbo, Gollnick,Graham, & Saltin, 1991). More recently it has been shown that in humans post-exercise L&makes minor contributions to glycogen synthesis (Bangsbo, Madsen, Kiens, & Richter, 1997).Furthermore, it has been shown that L& is specifically oxidized in the oxidative muscle fibres(type I), whereas it is predominantly produced in the glycolytic fibres (i.e. type II, ref. Donovan& Pagliassotti, 2000; Gladden, 2000). Taken in consideration with the ‘lactate shuttle’hypothesis introduced in 1984 by Brooks which states: “the shuttling of lactate through theinterstitium and vasculature provides a significant carbon source for oxidation andgluconeogenesis during rest and exercise” (Brooks, 1985) it is apparent that the L& produced byglycolytic muscle fibres is subsequently oxidized by oxidative fibres. When AR is performedafter high-intensity exercise the accumulated L& is cleared via oxidation in type I fibres that areactive during low-intensity exercise. Therefore, the major clearance pathway of L& post-exercise, especially with AR, appears to be oxidation (Gladden, 2003). It is now known that L&traverses the plasma membrane via stereo-specific, pH-dependant transmembrane proteins calledmonocarboxylate transporters (MCT5, ref. Bonen, 2001). In human skeletal muscle thetransporter is present in two isoforms (MCT1 and MCT4, ref. Bonen, 2001), with MCT1 beingimportant to L& clearance (Thomas et al., 2005).It is proposed that AR maintains blood flow post-exercise thereby allowing the transportand circulation of L& to sites where it can subsequently be oxidized, primarily by skeletalmuscle and additionally in smaller quantities by other tissues (i.e. heart, liver, kidneys). Inaddition to blood flow and membrane transport, L& release is dependent on exercise intensityand duration, training status, and age (Graham, Sinclair, & Chapler, 1976; Juel, 1997).142.4.1 Exercise Intensity, Mode, and DurationIn order for AR to successfully clear L&, the intensity must be such that the production ofL& does not exceed its clearance rate. If L& production surpasses L& clearance (i.e. utilization)then it will accumulate in the muscle and blood. The general agreement regarding the optimalintensity with which to perform AR is that the intensity should be moderate (approx. 30-45%VO2max,ref. Boileau, Misner, Dykstra, & Spitzer, 1983; Davies et al., 1970). Neverthelessintensities ranging from approximately 16-70% ofVO2max have been reported in the literature(Corder, Potteiger, Nau, Figoni, & Hershberger, 2000; Hermansen & Stensvold, 1972).Using a bicycle ergometer Davies et al. (1970) investigated the effects of four differentrecovery intensities on blood L& clearance in a group of four subjects. Following 6 mm ofexercise at 80% VO2max subjects performed 40 mm of recovery exercise at approximately 15, 30,45 or 60% VO2m. The results showed that the optimal L& clearance rate occurred between 30-45% VOmax. In contrast, using treadmill exercise consisting of three 60 s maximal effortsseparated by approximately 4 mm of rest with the final work bout being followed by 30 mm ofAR at one of four intensities (approx. 30, 60, 70 or 80% VO2m) Hermansen and Stensvold(1972) found that L& cleared fastest at approximately 63% (range 5570%) VO2max. Inaccordance with Davies et al. (1970), Belcastro and Bonen (1975) reported that optimal exerciseintensity for La clearance on a bicycle ergometer was predicted at 32% VO2m and additionallythose subjects were able to self-select adequate intensities to clear L&. Later, using treadmillexercise Bonen and Belcastro (1976) reported that self-selected running intensity, correspondingto approximately 61.4% (range 45.2-70.6%) VO2m, resulted in statistically significantly fasterL& clearance rates compared to self-selected intermittent exercise and resting recovery. Theynoted that though these findings are similar to that of Hermansen and Stensvold (1972), theirstudy did not allow the assertion of whether this intensity was optimal for L& clearance, sincethe two AR were self-selected (Bonen & Belcastro, 1976). In an attempt to differentiate betweenrecoveries below and above AT, Stamford et al. (1981) demonstrated that the apparent rate ofclearance could be manipulated by selecting different baseline asymptotes. Graphingsemilogarithmic plots of La disappearance using a resting baseline L& value of 0.9 mmol•L’showed statistically significantly faster clearance with AR at 40% VO2m compared to AR at70% VO2max and PR. Conversely, using the same data with experimentally determined baselinevalues of L& (1.3 mmolL’ and 3.5 mmolU’, respectively) yielded no differences indisappearance between active recoveries. Therefore, both AR intensities were able to return L&15levels to their respective baselines faster than PR, but AR at 40% cleared L& faster overall. Itmay be that the 70% recovery may not have been above threshold as evidenced by the lowbaseline La value of 3.5 mmolL1.This may explain the lack of difference between recoveryintensities, as L& would not have been accumulating in significant quantity if the workload wasin fact below AT.In order to investigate whether the inconsistencies surrounding clearance rate andrecovery intensity found above were related to exercise mode (i.e. bicycle vs. treadmill) Boileauet al. (1983) compared bicycle and treadmill recovery exercise at various intensities. They foundno statistically significant differences between optimal L& clearance rate intensities acrossmodalities (35.9% and 32.5% V02m for cycling and running, respectively). It should be notedthat this experiment was comprised of a small sample of three females. In addition as suggestedfrom another study with a larger sample size of seven males blood L& cleared fastest at moderateintensities (i.e. 28.2-43.1% VO2max, ref. Boileau et al., 1983). This study was conducted usingonly bicycle ergometry.It appears that the optimal recovery intensity to remove blood L& is moderate. This ismore definite for bicycle ergometer work, but it may be the case that the optimal intensity ishigher for treadmill recovery. It has been shown that for a given02 consumption there is agreater rate of lactate production for bicycle exercise compared to running on a treadmill (PetersFutre et al., 1987). From a theoretical perspective this may be a consequence of the greateramount of musculature involved in running versus cycling, which may provide more potentialfor the oxidation of L&. However, the difference in recovery modes within individuals has notbeen extensively investigated, as the one study that has addressed this issue used a small sample(Boileau et al., 1983).The inconsistencies of the aforementioned studies (Belcastro & Bonen, 1975; Bonen &Belcastro, 1976; Davies et al., 1970; Hermansen & Stensvold, 1972) with respect to the optimalintensity for clearance may also be a result of the quantification of exercise intensity. It is knownthat two subjects with similar maximal aerobic power (MAP) may display different thresholdsfor the accumulation of L& (Dodd et al., 1984). Since previous research has typically quantifiedrecovery loads as a percentage of V02m it follows that within and between studies subjectsexercise capacities relative to L& thresholds may have varied. Logically this can be avoided bybasing recovery intensities on L& thresholds. McLellan and Skinner (1982) investigated theintersubject variability of L& clearance rates when expressed relative to VO2max or aerobicthreshold (AerT). Aerobic threshold was defined by the authors as the first “break” in the plot of16VE versus V02 and the initial continuous rise in La. They found that in 15 males (VO2mof 51.5mL.kg1.min’) AerT values varied between 45-62% (X = 52.9%)VO2m and that recoveryintensity expressed relative to AerT explained 13% more variance thanVO2max (77% and 64%,respectively). Therefore it is slightly more advantageous to quantify recovery intensity by AerTthan solely by VO2max. Moreover, peak L& clearance rate was predicted to be 10% below AerT(i.e. 43% VO2max), which is in agreement with values previously reported (Davies et al., 1970).Subsequent research typically has selected AR intensities from the aforementionedstudies (e.g. Thiriet et al., 1993). As a result, the current belief is that AR at intensities between30-45% VO2max is optimal for La clearance. This perception has been reinforced by research thathas shown that L& clears fastest at moderate workloads (Dodd et al., 1984; Gmada et al., 2005;McAinch et al., 2004; Spierer et al., 2004). However, there are still investigations that have usedhigher intensity recoveries for both cycling (50% VO2max, ref. Monedero & Donne, 2000) andrunning (approx. 60% VO2m, ref. Bonen & Belcastro, 1976) and reported substantial L&clearance.More recently Baldari et al. (2004; 2005) have quantified recovery intensity in relation toboth the IVT and TAT. They compared the effects of four 30 mm recovery intensities on bloodL& clearance after 6 mm of treadmill running at 75% of the difference between TAT and VO2max(approx. 90% VO2m) in both soccer players and triathletes (Baldari et al., 2004; Baldari et al.,2005, respectively). The recovery intensities were: IVT, IVT+50%AT, TVT_50%AT and PR, where Ais the difference between TAT and TVT. In soccer players it was found that the two lowestintensity recoveries (IVT_50%AT and IVT) were the most efficient for L& clearance andstatistically faster than IVT+50%AT and PR (Baldari et al., 2004). Tn the triathietes IVT_50%ATremoved L& statistically faster than the other three intensities (Baldari et aL, 2005). The authorsnote that all recovery intensities used were within the range (3 0-70% VO2m) previouslyreported for optimal L& clearance.Other investigations have used combined recoveries (CR, i.e. more than one recoverymethod within one recovery period). Taoutaou et al. (1996) compared PR (20 mm seated rest onbicycle ergometer followed by 40 mm seated rest) to partially AR (20 mm bicycling at 40%VO2max followed by40 mm seated rest) and found that the partially AR cleared L& 1.5- and 3-fold faster in untrained and trained individuals, respectively. Donne and Monedero (2000)investigated blood L& clearance and subsequent exercise performance after four different 15 mmrecovery interventions. The recovery interventions were: PR, AR at 50% VO2max, massage17recovery, and CR consisting of AR at 50% VO2max for 3.75 mm then massage for 7.5 mmfollowed by AR for the remainder. Their performance indicator was the difference in completiontime for a 5 km bicycle time trial simulation performed before the recovery intervention andafter on each of the testing days. Their results showed that AR and CR were superior to PRrecovery with respect to L& clearance, that the fastest clearance rate occurred with AR, and thatthe clearance rate was fastest during the AR exercise periods of the CR. The increase in 5 kmcompletion time was significantly less in the CR intervention compared to all other recoveries.The authors speculate that the greater performance maintenance in the CR trial was due to thecombination of greater L& clearance in the active periods and increased intramuscular glycogenrestoration during the passive massage periods.Post-exercise blood L& levels peak after a small lag in time of approximately 1-7 mm(Bret et al., 2003; Dodd et al., 1984; Gmada et al., 2005; Taoutaou et al., 1996; Thiriet et al.,1993), since L& must be transported out of the cell via MCTs to the circulatory system. The timeto reach peak blood L& appears to be dependent on metabolic rate, since it peaks faster withhigher intensity recovery intensities, and sooner with AR versus PR (Gmada et al., 2005;Stamford et al., 1981; Taoutaou et al., 1996). Afterwards blood L& levels will begin to decreaseprovided that the energy demand is below the threshold at which blood L& accumulates.Depending on the peak blood L& levels and recovery intensity, values may remain elevated forup to 1.5 hours before reaching resting levels (Bret et al., 2003; Choi, Cole, Goodpaster, Fink, &Costill, 1994; Taoutaou et al., 1996).Studies have utilized a wide variety of recovery durations ranging from 4-90 mm toinvestigate La clearance (Corder et al., 2000; Taoutaou et al., 1996). When comparing clearancerates between AR and PR statistically significant differences are usually not evident untilapproximately 10 mm (Gmada et al., 2005; Monedero & Donne, 2000). Interestingly, the twoinvestigation previously discussed by Baldari et al. (2004; 2005) both demonstrated that allactive recoveries examined did not show further decreases in blood L& after the twentiethminute of recovery. The investigations examined two different subject pools: soccer players andtriathietes (VO2m of 62.3 and 69.7 mL.kg’•min’, ref. Baldari et al., 2004; Baldari et al., 2005,respectively). The recovery intensities were: IVT, IVT+50%iXT, IVT_50%AT and PR, and rangedbetween the previously described intensities of 3 0-70% VO2max that have been suggested to beoptimal for L& clearance (range 39-60% VO2max).182.4.2 Combined Active Recovery and LactateDodd et al. (1984) and more recently Gmada et al. (2005) have investigated the effects ofa two stage CAR on La clearance. The precedence for their research came from the work ofStamford et al. (1981) who compared the effects of three different 40 mm recoveries on L&clearance: PR, and AR at 40% and 70% VO2max (AR4O% and AR7O%, respectively). They foundthat L& clearance was greater in the AR4O% from 3 0-40 mm compared to PR and AR7O%.Additionally it was shown that L& levels peaked faster with AR7O%. Since LaT uptake isproportional to its concentration (Jorfeldt, 1970; Margaria et al., 1933) it was theorized that asL& concentration decreases, uptake decreases in proportion, resulting in a decrease in clearancerate since La is still being produced during active recovery, albeit at lower levels. Thus it washypothesized that optimal L& clearance may occur with an exercise intensity that matches itsconcentration (Stamford et al., 1981). That is, as L& concentration progressively decreases theexercise intensity should decrease to limit L& production and therefore enhance clearance.The first group to test the latter hypothesis was Dodd et al. (1984). They combinedmoderate- to high-intensity and moderate- to low-intensity work within one recovery period inan attempt to optimize L& clearance. A sample of seven trained males (VO2max of 48.7 mL•kg‘.min’) performed 50 s of supramaximal bicycle work at 150% VO2m followed immediately byone of four 40 mm recoveries: PR, AR at 35% VO2m (AR35%), AR at 65% VO2max (AR65%),or 7 mm at 65% followed by 33 mm at 35% VO2max (CAR). Differences in clearance rate at the6thmm and from mm 20 to 40 of recovery were examined, and results demonstrated that fromminute 20 to 40 La clearance was statistically significantly faster in the AR3 5% and the CARtrial. No statistically significant differences were observed between AR3 5% and CAR duringthis time frame and the authors therefore concluded “that these data do not support thehypothesis that following maximal work, a combination of submaximal exercise intensities ismore beneficial in lowering blood L& concentrations than a single intensity” (Dodd et al., 1984).Conversely, in retrospect their results could be interpreted such that CAR was able to clear La tothe same extent as AR35% since there were no statistical differences between the twoconditions. The question can then be proposed that if the two recovery strategies differ inintensity but still clear La to the same extent, do they differ in any other respects. For example,do they result in differences in performance independent of their respective effects on L&.Gmada et al. (2005) re-investigated this hypothesis with several modifications to thework of Dodd and colleagues. A larger sample of fourteen subjects (7 trained and 7untrained,VO2of 56.5 and 42.0n’.L.kg’.min’, respectively) performed three supramaximal intermittent19exercise bouts at 120% MAP for 60% of the time to exhaustion (TTE) separated by 5 mmintervals with the third bout being followed by 20 mm of recovery. The recovery bouts wereasfollows: PR, AR at 20% less than the first ventilatory threshold (VT1), AR at 20% less than thesecond ventilatory threshold (VT2), and CAR consisting of 7 mm at VT2 followed by 13 mmatVT1. Their findings demonstrated that peak blood L& occurred faster in CAR andVT2conditions for both trained and untrained subjects(4t11and7thmm, respectively). This was inaccordance with previous work (Dodd et a!., 1984; Stamford et al., 1981) and confirmed thatblood L& peaks sooner post-exercise with higher-intensity recovery. In contrast to Dodd et al.(1984) it was determined that L& disappeared statistically significantly faster in both groups withCAR, the effect being more pronounced in the trained group (Gmada et a!., 2005).The discrepancy between results with respect to the efficacy of CAR of the two studiescould be due the differences in subject’s fitness level or the protocols used. Dodd et a!. (1984)used only one group of seven trained subjects with an averageVO2m of 48.7 mL.kg’.min’.Whereas Gmada et al. (2005) used two groups of seven subjects, one trained and one untrainedwith VO2max of 56.5 and 42.0 mL.kg1•min’, respectively. Furthermore, Gmada et a!. (2005)quantified the recovery intensities specific to ventilatory thresholds, while Dodd et al. (1984)only used VO2max. Since two subjects with a similar VO2m can exhibit different anaerobicthresholds, the possibility exist that the recoveries chosen in the study by Gmada et a!. may havebeen less likely to surpass an individual’s anaerobic threshold and therefore result in less L&production during the recovery period (2005). Furthermore, Gmada et a!. used a repetitiveexercise task to induce increased blood La, which resulted in higher blood L& concentrations.Since the rate of L& uptake is proportion to its concentration (Jorfeldt, 1970; Margaria et al.,1933) it may be that the higher blood La levels had some effect on clearance rate. However,with respect to the actually blood L& concentrations this does not appear to be the case, althoughit may be that the effect was not evident in blood L& concentrations. Additionally, the 5 mmrecoveries between the repetitive exercise bouts in the study by Gmada et al. (2005) matched thelonger duration recovery period, with respect to recovery intensity, and may have influenced theresults.In summary it has been shown that the use of AR facilitates L& clearance compared toPR. It may be that the optimal AR intensity to clear blood L& is dependent on recovery mode orthe active muscle mass. Moderate intensity AR is recommended to clear blood La fastest whenperforming bicycle exercise. However, the optimal intensity with which to clear L& remains20undetermined and may be dependent on individual thresholds or occur with the use of more thanone recovery intensity.2.5 Lactate and PerformanceAs shown above AR is an appropriate means to remove L& following high-intensityexercise in which there is an accumulation of L&. However, the real interest surrounding AR forcoaches, athletic trainers, strength and conditioning coaches, and athletes is whether or not ARimproves performance. The evidence for the use of AR as a means of improving performancefollowing previous exercise is less obvious.Lactate is the one of the most researched metabolites. From an early time it was believedto be the direct cause of fatigue (Hill & Kupalov, 1929). The concept that AR from exercisebouts may be beneficial to subsequent performances like many training and competitiontechniques in the sport sciences has some of its origin in anecdotal observations. Gisolfi,Robinson and Turrell highlight this in their 1966 paper in which they conclude that their workprovides a physiological basis for the practice of AR post-competition; which they note athleteshad already learned from experience. The authors formulate this conclusion after finding thatmoderate aerobic exercise (approx. 38-53%VO2max)for 30-35 minutes following exhaustivetreadmill running reduced the “oxygen debt” and cleared L& faster than a resting recovery in thefour subjects they examined (Gisolfi et al., 1966). No attempt was made to examine performancein this investigation and their conclusion was likely established based on current beliefs of thattime pertaining to L& and fatigue.Later, more empirical evidence would imply that high “lactic acid” concentration may bethe reason for exhaustion in high-intensity exercise (Karlsson & Saltin, 1970). To test thehypothesis that high blood La concentration may limit maximal exercise performance Klausenet al. (1972) had subjects perform maximal bicycle work that was either preceded by rest orhigh-intensity arm ergometry. Therefore, high blood L& concentration was induced and its effecton a previously non-exercised muscle group was examined. While their results were notstatistically significant they did observe an average 10% reduction in TTE in the condition inwhich leg work was preceded by arm work. The authors concluded that increased L&concentration in the working muscles inhibited further La production, but that the hypothesisthat L& is a limiting factor in exercise was not confirmed since only a trend to reducedendurance time was observed. In a similar experiment in which arm exercise preceded legexercise (series A-L) and vice versa (series L-A, i.e. leg exercise preceding arm exercise) on aseparated occasion, it was observed that TTE occurred earlier in bothconditions with respect to21TTE without preceding exercise (Karlsson et al., 1975). The authors concluded that because L&was elevated prior to the second exercise bout in both conditions and therefore reached peakvalues sooner, these peak La values (20-30 mmolkg’ wet muscle) or related factors serve aslimiting factors to muscular performance.However, the latter two studies (Karlsson et a!., 1975; Klausen et a!., 1972) had smallsample sizes (n = 4 and 3, respectively) limiting the conclusiveness of their results. It is alsoworthwhile to note that the two investigations did not use SE bouts. Nonetheless, theinvestigations are foundational to the belief that increased blood L& concentration can limitperformance, or perhaps more appropriately stated, is related to performance decrements.Furthermore, it is this foundational belief that allows the conclusion that AR may be beneficial toperformance since AR can clear blood L& faster than a resting recovery.2.6 Active Recovery and PerformanceThe first empirical evidence that AR was beneficial to subsequent high-intensityperformance came from Weitman et a!. (1977). After performing an initial all-out SE task(bicycling for 1 mm at 5.5 kg resistance) subjects underwent one of eight recovery interventionsfollowed by the same supramaximal criterion exercise task. Recovery interventions consisted ofAR at 1 kg resistance or PR for either 10 or 20 mm breathing either room air or 100%02.Allcombinations of the aforementioned variables were examined. Their findings showed that L&clearance and subsequent performance were statistically significantly improved with active and20 mm recovery compared to the other interventions. However, they also concluded that otherfactors beside L& clearance are critical to subsequent performance since these variables were notcorrelated.In the time to come research findings would be divided on the effects of AR onsubsequent performance. While all studies showed that AR could decrease L& concentrationbetter than PR, many showed no additional benefits to subsequent exercise performance (Bond,Adams, Tearney, Gresham, & Ruff, 1991; Franchini et a!., 2003; McAinch et al., 2004; Siebers& McMurray, 1981; Watson & Hanley, 1986; Weltman et al., 1979; Weltman & Regan, 1983),while others would show benefits (Ahmaidi et al., 1996; Bogdanis et al., 1996b; Connolly et al.,2003; Corder et a!., 2000; Signorile et al., 1993; Spierer et al., 2004; Thiriet et al., 1993).Typically studies aimed at investigating subsequent performance have used recoverydurations of 10-20 mm. This is likely due to the fact that this time frame coincides withrequirements and restraints put on sporting events. Previously it has been suggested that20-40mm of AR should be used to prevent a decrease in power output (Ainsworth et al., 1993).22Interestingly, with respect to performance, recent evidence suggests that shorter durations of ARmay be beneficial to performance (i.e. approx. 6 mm) rather than longer durations (i.e. 15 mm orlonger, ref. Ahmaidi et al., 1996; Bogdanis et a!., 1996b; Spierer et al., 2004).2.6.1 No Performance Benefit with Active RecoveryA substantial body of research exists that shows that AR does not significantly improveperformance. Weltman et al. (1979) studied the effects of four recoveries (PR, AR<AT, AR>AT,and AR>AT + 100%02) on La clearance and subsequent performance for an endurance taskconsisting of 5 mm of cycling in nine males. Subjects cycled for 5 mm at MAP, recovered for 20mm at one of the respective recovery intensities, and then performed a second 5 mm cycle atMAP. They reported that while AR>AT + 100%02 cleared La significantly faster than PR, andAR>AT there were no significant differences in performance among recovery conditions.Performance was determined by work done over the 5 mm and assessed by pedal revolutionscompleted. Siebers and McMurray (1981) investigated blood L& clearance and subsequentperformance of a 200 yd swim 15 mm after a 2 mm swim at 90%VO2m on a swimmingergometer in six females. The 15 mm recoveries consisted of either walking at a moderate pace(2.5-3 mph) for 10 mm followed by 5 mm of PR or swimming continuous front crawl lengths ata moderate pace for 10 mm followed by 5 mm of PR. Despite reporting that swimming recoverycleared 22% more La than walking, there were no statistically significant differences for 200 ydswim time. Subjects took slightly longer than 2 mm to complete the 200 yd swims for the swimand walk recoveries (125.9 ± 5.9 s and 127.2 ± 5.8 s, respectively).In an attempt to amalgamate the literature, Weltman and Regan (1983) investigated theeffects of 20 mm of active and passive recovery on subsequent maximal constant load (i.e. nowork drop-off allowed) exercise performance. At this point in time research supporting thecontention that elevated blood L& concentration has a detrimental effect on subsequentperformance had used a constant load protocol (Karlsson et al., 1975; Klausen et al., 1972) andresearch not in support had used maximal effort work (i.e. allowing a work drop-off, ref.Weltman et al., 1979). In contrast to the previous work utilizing constant load tasks, they foundno statistical differences in work output between the recovery conditions.An applied investigation had eight hockey players perform two simulated hockey tasksseparated by one of three 15 mm recovery modes: skating, bench-stepping, or PR (Watson &Hanley, 1986). The hockey task was comprised of six 45 s sprints each separated by 90 s PR,with the distance skated determining each player’s performance. Results demonstrated that onlybench-stepping reduced L& values with statistical significance compared to rest, but thatneither23of the AR altered performance with statistical significance. However, the practical nature of thisinvestigation resulted in difficulty standardizing recovery duration and intensity, since the ARcondition had substantial passive periods to take measurements and the PR condition hadsubstantial active periods to prepare for the subsequent exercise task. The authors note that theskating recovery may have resulted in slowed La clearance because of the ability of the playersto glide, limiting the amount of muscular work they performed. The effect of this onperformance cannot be determined.Bond et al. (1991) investigated the effects active and passive recovery on subsequentisokinetic muscle function. They used a 60 s bicycle ergometer task at 150%VO2max to elevateblood L& levels followed by either 20 mm of AR at 30% VO2max or PR. Subjects then performed60 repeated isokinetic knee extensions at an angular velocity of 1500.s4.Results again confirmedthe superiority of AR to PR with respect to La clearance but no differences in peak torque, totalwork or fatigue index were noted between recovery conditions or control values. Anotherapplied investigation used two simulated hockey tasks consisting of seven 40 s ‘shifts’ separatedby 90 s rest with 15 mm of AR or PR between skating tasks (Lau, Berg, Latin, & Noble, 2001).The AR, which consisted of self-selected resistance “low-intensity” cycling, did not clear L&faster than the PR or effect subsequent performance in a beneficial way with respect to statisticalsignificance. However, the authors did note a trend towards a greater distance skated in thesecond bout of simulated hockey shifts with AR. Additionally, the authors note that theirfindings may have been limited by the fact that the recovery intensity was self-selected and thatthe skating bouts only induced moderate L& concentrations. Furthermore, similar to Watson &Hanley’s (1986) investigation the recoveries were not strictly passive or active due to constraintsof the experimental design.Recently two investigations have examined the effects of active versus passive recoveryon La clearance and subsequent anaerobic and aerobic performance, respectively (Franchini eta!., 2003; McAinch et a!., 2004). In one of the investigations a group of seventeen subjects firstparticipated in a 5 mm judo combat followed by 15 mm of AR (running at 70% of the anaerobicthreshold velocity) or PR (Franchini et al., 2003). They then completed an intermittent anaerobictask comprised of four upper body WAnT each separated by 3 mm PR. Performance on theWAnT was not altered by recovery mode. The authors note that this finding is in accordancetheir observations that AR seems to be beneficial to performance when the recovery period is 6mm or less, and that with recoveries of 15 mm or longer AR does notappear to be beneficial.This is further supported by the work of McAinch et a!. (2004). They investigatedthe effects of24AR (40% VO2max) and PR on muscle biopsies and plasma L& clearance, as well as performanceof intense aerobic exercise. Seven male subjects performed two 20 mm bicycle trials separatedby 15 mm of recovery. No differences in work performed or muscle glycogen and Laconcentrations were observed, but plasma L& concentration was significantly lower in the ARprotocol.2.6.2 Performance Benefit with Active RecoveryDespite the wealth of literature that has shown that AR does not appear to be beneficial toperformance there is a similar amount of literature to the contrary. In addition to the initialresearch that exhibited that AR may be advantageous to recovery and/or maintenance ofperformance (Karisson et al., 1975; Klausen et al., 1972; Weitman et a!., 1977) others haveproduced supporting literature. Pendergast et al. (1983) confirmed the earlier results of Karissonet al. (1975) that preceding high-intensity exercise considerably reduces the potential for furthersupramaximal performances. They found that endurance for both aerobic and anaerobic workwas reduced in the presence of high blood L&. Other investigators have documented a similarrelationship of increased blood L& concentration and reduced muscular endurance (Yates et al.,1983). These investigators looked at the muscle contractile properties (maximum voluntarycontraction (MVC), peak rate of tension development, peak rate of relaxation, one-halfcontraction time, and one-half relaxation time) of the elbow flexors 6 mm after 1 mm of intensecycling at a fixed load of 5 kg versus a control (i.e. no prior cycling). They found no statisticallysignificant differences in muscle contractile properties after the cycle ergometer bout, butendurance time at 40% MVC was reduced by 25% with prior exercise. After the endurance taskthere was a statistically significant reduction in MVC, peak rate of tension development andpeak rate of relaxation. It was concluded that the elevation of blood L& by intense exercise ofone muscle group reduced the endurance of a second non-exercised muscle group. However, theaforementioned investigations (Pendergast et al., 1983; Yates et al., 1983) did not actuallyinvestigate the effects of AR, but rather showed that increased blood L& and associated changesresult in decrements of performance. The investigators both suggest that the reduction of L&concentration should therefore be beneficial to performance, as increases in L& are detrimentalto performance. This suggestion is more of an anecdotal assertion than scientific fact, butnonetheless provided a conceptual framework for the conviction that AR and hence blood L&clearance is beneficial to performance.Thiriet et al. (1993) investigated the effects of AR and PR on repeated SE. They had 16male subjects perform four cycling bouts to exhaustion at 130%MAP. Each bout was separated25by a 20 mm recovery period of either leg or arm ergometric exercise at 30% MAP or rest. Activerecovery cleared L& faster and maintained work performance more than PR. However, theyalsonoted a non-significant correlation between power output and L& levels, which hasbeenobserved by others (Siebers & McMurray, 1981; Weitman et aL, 1977; Weitman et al., 1979;Weitman & Regan, 1983). Therefore, they concluded that the relationship between power outputand L& is not one of cause and effect. Other researchers have corroborated the finding thatpower output may be maintained to a greater extent with AR compared to PR (Ahmaidi et al.,1996; Bogdanis et al., 1996b; Connolly et al., 2003; Signorile et al., 1993; Spierer et al., 2004).Signorile et al. (1993) examined the effect of AR versus PR on power output during eight 6 ssupramaximal bicycle sprints separated by 30 s. Active recovery consisted of pedaling against 1kg of resistance at 60 rpm while PR consisted of sitting on the bicycle motionless. Mean PP andmean TW performed were statistically significantly greater in the AR protocol. Thisinvestigation used a fixed load for the recovery intensity based on previous work (Weitman etal., 1977), which limits the control of interindividual differences in fitness and work capacity.Biochemical variables were not measured and therefore the interpretation of the data is limitedsolely to performance parameters. Bogdanis et al. (1 996b) compared the effects of recovery typeon performance of two maximal 30 s bicycle sprints separated by 4 mm. Active recoveryresulted in statistically significantly higher MP output compared to PR. The difference in poweroutput could be attributed to the differences observed in the initial 10 s of the sprint. The authorssuggest that the increased blood flow during AR may have increased resynthesis of PCr orallowed an initially faster glycolytic rate as an explanation for the performance improvementbased on results of their previous work (Bogdanis, Nevill, Lakomy, & Boobis, 1994b). Blood Laconcentration did not differ significantly between recovery conditions (Bogdanis et al., 1 996b).Another investigation examined the effects of recovery type on repetitive 6 s bicycle sprintsusing incremental resistive forces separated by 5 mm of active (32% MAP) or passive recoveryin ten male subjects (Abmaidi et al., 1996). The results showed that at the higher resistive forcesthe AR protocol enabled greater maintenance of power and also cleared L& faster than the PRprotocol.Dorado et al. (2004) examined the effects of recovery mode on aerobic and anaerobicenergy yield as well as performance during high-intensity intermittent exercise. Ten trainedsubjects (VO2m of 58 mL.kg’.min’) performed four supramaximal constant intensity cyclingbouts to exhaustion at 110% maximal power output each separated by one of three 5 mmrecoveries. The recoveries were: AR at 20% VO2max (HITA), stretching recovery of the lower26limbs (HITS), or PR (HITP). Performance was 3-4% better and aerobic energy yield was 6-8%greater in the HITA condition. The greater aerobic yield was due to faster V02kinetics and theauthors concluded that this was the source of improved performance in the AR trial. It wasproposed that the faster V02kinetics were a result of either increased blood flow or maintenanceof aerobic regulatory enzyme activation (Bangsbo et al., 1994). It has previously been shownthat aerobic metabolism makes a significant contribution to metabolism during high-intensityexercise (Bogdanis, Nevill, Boobis, & Lakomy, 1 996a) and the authors argued that this was thecase in their investigation (Dorado et al. 2004).More recently, a study investigated the use of a short 3 mm recovery period on Laclearance and power output (Connolly et al., 2003). In congruence with previous work utilizingsimilar work-to-rest intervals (Bogdanis et al., 1996b), it was found that power output on six 15 sbicycle ergometer sprints was greater with AR compared to PR, but L& values did not differwith respect to the recovery used (Connolly et al., 2003). Spierer et al. (2004) examined bothmoderately trained ice hockey players (VO2max of 45.6 mL.kg’.min’) and sedentary (VO2max of36.9 mLkg’ .min’) subjects on their ability to perform serial WAnT interspersed with either 4mm AR at 28% VO2max or PR. Their results showed that PP output did not differ significantlybetween recovery types in both groups. However, sedentary subjects displayed statisticallysignificantly greater MP output and TW values with AR, whereas only TW performed wassignificantly improved in moderately trained individuals with AR. Capillary blood L& differedwith statistical significance in the moderately trained group only when AR was employed. Itshould be noted that there were statistical differences between groups with respect to age,gender, height, and mass in addition to VO2max, which complicates the inter-group comparisonsince the group differences outside of fitness level are a source of uncontrolled variability.Ainsworth et al. (1993) examined the effect of AR duration on blood L& and power in 16male competitive cyclists (VO2max of 67.6 mL.kg’.min’). Following a 45 s bicycle bout subjectsperformed 6, 9, or 12 mm of AR at a fixed resistance of 5.5 kg, after which they immediatelyperformed another 45 s bicycle bout. Results showed that power output was decreased withstatistical significance between bouts during the 6 mm recovery, but was maintained in the 9 and12 mill recoveries. However, no statistically significant differences were observed in the abilityto produce PP in all of the recovery durations. Recovery blood L& was only statisticallydecreased in the 12 mm recovery protocol. It was therefore concluded that in this population 9mm of AR at approximately 30% VO2max was sufficient to restore power output to resting levels27following 45 s of supramaximal cycling. In support of this finding, another investigation inwhich 8 males performed two 30 s bouts of bicycle ergometer work separated by 6 mm of PR,PP and MP output were only 92% and 85% of initial control values (Bogdanis, Nevill, &Lakomy, 1994a). However, this investigation used passive recovery and thereforea directcomparison of results is contentious. Nonetheless, it appears that following maximal workdurations of 30-45 s greater than 6 mm of recovery is necessary for power recuperation.2.6.3 Performance and Active Recovery DurationOne commonality of the aforementioned research on AR and performance that has notfound an improvement in subsequent performance is that the recovery durations were all 15minutes or longer. Therefore, it may be that recoveries of this duration mask any additionalbenefits of an AR that may only be evident in the initial part of the recovery period. Thiscontention is supported by the fact that much of the literature that has shown improvedperformance with AR has used recovery durations of 6 mm or less (Ahmaidi et al., 1996;Bogdanis et a!., 1996b; Signorile et al., 1993; Spierer et a!., 2004). This trend has beenpreviously noted (Franchini et al., 2003). Of the studies reporting improved performance withAR in this literature review only one used a long recovery duration (i.e. 20 mm, ref. Thiriet et a!.,1993). Interestingly, a study that investigated performance on a resistance training (i.e. parallelsquat) task in which exercise sets were separated by 4 mm of cycling or PR it was shown thatAR cleared L& faster and resulted in better performance (Corder et al., 2000). This is inagreement with the aforementioned trend. Also of interest, is the fact that several of the studiesreporting improved performance with AR did not correlated or associated this improvement withL& clearance (Bogdanis et al., 1996b; Connolly et al., 2003; Signorile et al., 1993; Spierer et al.,2004; Thiriet et al., 1993). Therefore, while it appears that a short duration AR may be beneficialto performance it may not be related to the clearance of La and could be a result of increasedblood flow and its effects on subsequent metabolism (Bogdanis et al., 1994b; Bogdanis et al.,1 996b).2.7 SummaryIt has been unequivocally shown that the use of AR can remove L& at a faster rate thanPR. It is proposed that the accelerated clearance rate with AR is a result of heightened bloodflow that serves to circulate L& and provide a fuel source for the working muscles while alsobeing oxidized by resting muscles and other tissues to a lesser extent. While it has beenpostulated that increased L& clearance should be beneficial to subsequent exercise performancethe literature is indeterminate. Active recovery may be only beneficial for short duration28recovery because it can maintain blood flow increasing the aerobic energycontribution toexercise, whereas with longer durations the return to homeostasis may be more similarbetweenrecovery types and result in similar performance.29CHAPTER III: METHODS3.1 SubjectsThe subjects were comprised of a sample of 12 volunteer, trained, male, university-aged(18-35 years) cyclists. An a priori power calculation performed using theG*Powersoftwarepackage(G*PowerVersion 2.0, Germany) was used to determine sample size (Faul & Erdfelder,1992). The analysis was performed with the intent of detecting a 10% decrement in MP outputassuming an average final power output of 800 W with a standard deviation of 50 W. A 10%power decrement was selected because a decrease of this magnitude or less in muscleperformance may be sufficient to limit whole body exercise performance in a competitive setting(Sprague & Mann, 1983). The power output stated above is based on previous researchexamining the performance of competitive road cyclist on a single WAnT (Tanaka, Bassett,Swensen, & Sampedro, 1993) and preliminary pilot data from this laboratory.Subjects were recruited from the University of British Columbia campus and Vancouverarea. All subjects were non-smokers and not under any pharmacological or special dietarytreatment during the investigation. Subjects were defined as trained for this investigation if theirtraining included both a heavy aerobic and anaerobic component. Additionally, subjects wererequired to meet at least three of the following four criteria: currently participating in regularcompetitive level cycling, have PP and MP outputs on the WAnT greater than or equal to 11 and9 W.kg’, respectively, and have a VO2mgreater than 55 mL.kg’.min’.Prior to participation all subjects were informed of potential risks and benefits associatedwith participation and completed a written Informed Consent, approved by the UBC ClinicalResearch Ethics Board (see Appendix X), and a Physical Activity Readiness Questionnaire(PAR-Q). Subjects were required to weigh less than 95 kg, as the resistance load on the Monark(Ergomedic 874E, Monark Exercise AB, Sweden) ergometer becomes less accurate with athletesover this weight (Inbar, Bar-Or, & Skinner, 1996). However, no subjects outside of thisrequirement attempted to participate in the study.3.2 Experimental DesignA randomized counterbalanced within-subjects design was used to evaluate the treatmenteffects. Subjects were randomly assigned to one of three recovery modes (AR, PR, and CAR)and the order in which they performed each trial was counterbalanced in order to control fortreatment order effects.303.3 Facilities and InstrumentationAll testing was completed at the John M. Buchanan Exercise Science Laboratory withinthe University of British Columbia Aquatic Centre. Equipment was calibrated, as permanufacturers’ instructions, prior to testing. Anthropometric measurements of height and weightwere taken for each subject on the first testing day prior to exercise. Additionally, the sum offive skinfolds (biceps, triceps, subscapular, iliac crest, and medial calf) were taken as ameasurement of body composition according to the procedures set out in The Canadian PhysicalActivity, Fitness & Lifestyle Appraisal Manual (CSEP, 1998), using Standard Harpendencalipers (Baty International, UK).3.3.1 Wingate and Sprint TestsPerformance was measured using a repetitive sprint task comprised of five 10 s maximalsprints separated by 30 s of PR. Both the sprints and WAnT were performed on a pan loadMonark Ergomedic 874E (Monark Exercise AB, Sweden) bicycle ergometer. Subjects cycledagainst a set load of 0.09 kg.(kg body mass)’, for the respective test durations, as recommendedfor athletes on the WAnT (Inbar et a!., 1996). In order to calculate power outputs the velocity ofthe bicycle flywheel is determined by way of an optical sensor (SMI OptoSensor, USA) thatrecords pulses from reflective markers fitted to the flywheel. The sensor was interfaced with aPC equipped with SMI POWER Version 5.2.8 software (SMI, USA). The software thencalculates power parameters based on the measured flywheel velocity and belt friction (i.e.applied resistive force). Peak Power and MP were calculated for the WAnT for use as subjectinclusion criteria. Peak Power, MP, and Fl were calculated for each of the five sprints, and TWwas calculated for the entire sprint trial using Microsoft Excel Version 5.1.2600 (MicrosoftCorporation, USA). The SMI POWER (SMI, USA) standard power outputs were used ratherthan the corrected power outputs. The variables calculated were defined as:• Peak power — the highest mechanical power output over 1 s achieved during the sprint.• Mean power — the average power output maintained over the entire 10 s sprint.• Fatigue index — the difference between PP and the lowest 1 s power output divided by PPand expressed as a percentage.• Total Work — the sum of the product of mean power and time across all five sprints.The ability to objectively quantify the capacity for intense activity is one of the mostdifficult components of measuring athletic performance (Inbar et a!., 1996). Since anaerobicATP production is an intracellular process there are no precise methods to quantify the energyrelease, and therefore no direct “gold standard” method of validation (Gastin, 2001; Inbar etal.,311996). Therefore like other measures of anaerobic capacity the validity of this type of sprint taskis contestable. However, it has been stated that “the choice of an anaerobic testdepends on theaims and subjects of a study and its practicability” (Vandewalle, Peres,& Monod, 1987).Therefore, due to practicability and the desire to examine repeathigh-intensity exerciseperformance, the model of five 10 s sprints was chosen as the performance indicator forthisinvestigation.3.3.2 Ventilatory and Gas Exchange VariablesMaximum oxygen consumption was evaluated by an incremental stage bicycle ergometertest, performed on an electronically braked SensorMedics Egrometrics 800 bicycle(SensorMedics, USA) utilizing the SensorMedics Vmax 29 series metabolic measurement cart(SensorMedics, USA). Breath-by-breath values of V02,VCO2 (volume of CO2 produced),VE(minute ventilation) were averaged over 20 s intervals and recorded for analysis. The exactprotocol used was adapted from previous incremental bicycle and treadmill tests (Baldari &Guidetti, 2000; Stegmann et al., 1981). Subjects started at an initial workload of 120 W andperformed 3 mm stages with step increments of 30 W until the attainment of their TAT. Afterwhich, the stage durations were decreased to 1 mm and the step increments were maintained at30 W until exhaustion. The criteria used to determine the attainment of VO2max was operationallydefined as the achievement of any two of the following: volitional fatigue, plateau in V02 (i.e.change<2.1 mL.kg’.min1),90% age predicted maximum HR, respiratory exchange ratio(VCO2/V0)exceeding 1.15, or blood L& concentration greater than 8 mmolL’ (Duncan,Howley, & Johnson, 1997). Subjects were asked to maintain a pedal cadence above 80 rpm whenpossible to facilitate the ease of cycling on the mechanically braked bike, but were allowed topedal at any cadence that was above 60 rpm.The same apparatus was used on subsequent testing days to record ventilatory dataduring the exercise and recovery bouts. Data was again sampled breath-by-breath and averagedover 20 s intervals for analysis.3.3.3 Blood LactateLactate measurements were made using a portable L& analyser (ARKRAY Inc., Japan).Briefly, the finger to be lanced was disinfected with an alcohol pad before a fingertip puncturewas made. The first drop of blood was cleared away (along with any non-evaporated alcohol)with sterile gauze and then a second drop was pressured out to fill a reagent strip via capillaryaction with approximately 5 iL of blood. Lactate in the sample reacts with potassiumferricyanide and La oxidase to form potassium ferrocyanide and pyruvate. A given voltage is32then applied oxidizing ferrocyanide, releasing electrons and creating a current. The current ismeasure amperometrically and is directly proportional to the blood L& concentration of thesample (Pyne, Boston, Martin, & Logan, 2000). Capillary blood L& values have been shown toaccurately reflect arterial blood L& values (Williams, Armstrong, & Kirby, 1992). The LactatePro has been shown to be accurate, reliable and demonstrate a high degree of agreement withother L& analysers (Pyne et al., 2000).3.3.4 Heart RateHeart rate was measured and recorded using a Polar s120 HR Monitor and uploaded to aPC using Polar Infrared Connection (Polar Electro, Finland). Heart rate data was provided every5 s.3.4 Testing ProceduresSubjects attended the lab on six days separated by at least 48 hours. One exception to thisguideline was made for Subject 3 who completed testing days 2 and 3 within 28 hours due to aconflict of schedule. On all testing days subjects were asked to report to the laboratory two hoursafter a suggested snack of a whole wheat bagel and banana. In addition, to control for the effectsof nutritional and exercise status on performance subjects were asked to follow similar dietaryand exercise habits throughout the experiment on both testing and off-days. Furthermore, in the24 hours preceding a testing day subjects were asked to avoid intense physical activity, alcoholintake, and refrain from caffeine intake in the 3 hours preceding a testing session. Prior to alltesting days, subjects were asked to report whether or not they complied with the aforementionedguidelines.3.4.1 Day 1: Anthropometric Measures, VO2,and WAnTOn subjects’ first testing day anthropometric measurements and skinfolds were takenbefore performing a VO2max test (as described above), followed by the WAnT. Bicycle seat andhandle bar height were adjusted to the individuals comfort and recorded for subsequent usethroughout the experiment. Blood L& measures were taken during the VO2max test at the end ofeach 3 mm stage, until the IAT was determined. A final blood L& measure was taken 3 to 4minutes after the incremental test. During this time subjects cycled at 40 W in order to alleviateany discomfort associated with the cessation of intense physical activity. The IAT wasoperationally defined as the workload corresponding to the second L& increase of at least 0.5mmolL1from the previous value (Baldari & Guidetti, 2000). That is, the TAT is the workloadcorresponding to the stage that elicits a second L& increase greater than or equal to 0.5mmolL1.However, in the aforementioned investigation the investigatorsdemonstrated that the33maximal L& steady state (MLSS) was more accurately predicted when the workload from theantecedent test stage was attributed to the blood L& value, rather than the workload of the samestage. Therefore in this investigation the workload used to quantify the IAT was the workloadcorresponding to the stage antecedent to that in which the IAT blood L& value was observed.Additionally the respiratory data collected during the final minute of each test stage wasaveraged and used to calculate the IVT. Specifically,VE/V02was plotted as a function of V02and the level of V02 at whichVE/V02 was the lowest corresponds to the IVT (Baldari &Guidetti, 2001, see Figure 2 for visual representation). The workload corresponding to the stagein which the IVT was found was used to quantify the recovery wattage.Twenty minutesP05t02maxsubjects performed a WAnT. During the 20 mm recoveryperiod subjects cycled at 40 W and were permitted to consume fluids at will. In the last 5 mm ofthe recovery period subjects were allowed to dismount the bicycle ergometer and stretch.Subjects then transferred to the Monark (Ergomedic 874E, Monark Exercise AB, Sweden)bicycle and the seat and handle bar height were adjusted and recorded for subsequent use.Subjects were instructed to start from a “rolling” start, cycling at a light cadence (approximately60-80rpm) against no resistance. They were then given a 10 s and 5 s warning for thecommencement of the test. The SMI POWER software (SMI, USA) was set to have a 3 s countdown which was audibly counted for subjects. Subjects were instructed to achieve maximumpedal cadence by the end of the 3 s count and at this time the pan loaded resistance (0.09 kg.(kgbody mass)’) was applied. Subjects were instructed to remain seated and to attempt to maintainmaximum pedal cadence throughout the entire 30 s period. At the completion of the WAnTsubjects were allowed to cycle at a self selected resistance on either bicycle ergometer to allowfor venous blood return and prevent blood pooling as well as alleviate any discomfort associatedwith the cessation of high-intensity exercise.3.4.2 Day 2: Time to Exhaustion TestOn Day 2, after a warm-up (10 mm at a workload corresponding to 50% of VO2max),subjects performed a TTE ride at an intensity corresponding to 120% MAP. The same bike usedfor the VO2m test was used for this ride and later exercise trials(Egrometrics 800,SensorMedics, USA). Subjects were given verbal encouragement throughout the task and wereinstructed to maintain a cadence over 60 rpm. A verbal warning was given when their cadencefell below 60 rpm and they were allowed a few seconds to bring their cadence back up.Exhaustion was operationally defined as an inability to maintain a cadence above 60rpm, andsubjects were told they could receive up to three warnings before the test would be terminated.34However, in practice all but one subject were unable to bring their cadence back above 60 rpmafter the initial decline and warning. Sixty percent of the TTE was then used for the duration ofthe subjects’ work intervals on the following familiarization and trial days.3.4.3 Day 3: Familiarization TasksFor Day 3 subjects performed familiarizations of the sprint and work tasks in order toensure that they could complete the required intensities and to improve their ability to reproducethe test protocol (Le Panse et al., 2005). After an equivalent warm-up to Day 2, followed by abrief transition to the Monark (Ergomedic 874E, Monark Exercise AB, Sweden) bicycle,subjects performed the sprint familiarization. Identical instructions to the WAnT were given withrespect to the start and countdown. Subjects performed five 10 s sprints against a resistance of0.09 kg.(kg body mass)1,with 30 s of recovery between sprints. During the 30 s recoveriessubjects were instructed not to pedal for the initial 20 s, but were allowed to pedal for the final10 s of recovery leading into the ensuing sprint. Post-sprint task subjects performed 20 mm oflight cycling at a self-selected resistance, between 40-100 W, before performing a familiarizationtrial of the exercise task. The familiarization trial consisted of three square wave bouts at 120%MAP for 60% of the TTE, at that same workload, with 5 mm of cycling at 50 W between boutsat any cadence, provided it was greater than 60 rpm.3.4.4 Days 4 to 6: TestingTesting days (Day 4, 5, and 6) were comprised of a similar protocol to the familiarizationtrial, the only difference being the randomized recovery intensity (i.e. AR, PR, or CAR) over thethree days. Subjects reported to the laboratory rested and hydrated, two- to three- hours postpartum. After an identical warm-up to the previous data collection days, subjects were given ashort period of time (3-5 mm) to allow them to recuperate, mentally prepare, as well as fit themouth piece for respiratory data collection, before commencing the exercise trial. The exercisetrial was similar to the familiarization trial with respect to duration and work intensity, with therecovery intensity varying in addition to the addition of a third recovery period of 14 mm thatseparated the exercise trial from the sprint task (discussed below). The 5 mm recoveries were asfollows on the respective test days:• PR — subjects remained seated and stationary on the bicycle ergometer, but werepermitted to cycle against negligible resistance for five to ten revolutions to preventblood pooling and discomfort every minute.• AR — subjects cycled at an intensity equivalent to the 50% of the difference between theIAT and the IVT (AT) below the IVT (IVT_50%AT). That is, the corresponding workloads35for the IAT and IVT(WIAT and WIVT, respectively) were used to calculate the workloadat IVT_5o%zT (WIvT-5o%AT)from the following equation:WIVT-5O%T = WIVT - Y2(WIAT - WJvT)The use of IVT_50%AT to determine recovery intensity has been previously shown to bethe optimal intensity for L& clearance in soccer players and triathletes during treadmillrunning exercise when compared against three other single intensity recoveries (Baldariet al., 2004; Baldari et al., 2005). Thus, it was selected as the intensity quantification forthis investigation. Evidence exists that recovery intensities for L& clearance betweencycling and running exercise may be different (Belcastro & Bonen, 1975; Bonen &Belcastro, 1976; Davies et al., 1970; Hermansen & Stensvold, 1972). However, the IVT_50%AT intensity relative to VO2mwas 39.3±6.8% and 51.1 ± 4.9% for the soccer playersand triathletes, respectively, which fall within the range of 30-70%VO2m previouslyreported to be optimal for L& clearance. Additionally, an investigation by Boileau et al.(1983), showed that recovery intensity for L& clearance did not significantly differbetween cycling and running exercise, and therefore the IVT_50%AT intensity was deemedappropriate for this investigation.CAR — subjects cycled at an intensity equivalent to the TAT for 2 mm and then the IVT_so%AT for theremaining 3 mm.Blood L& measures were taken immediately after the first two SE bouts and just beforethe second and third exercise bouts (see Figure 3).Following the third exercise bout the subjects recovered for 14 mm before performing thesprint task. This recovery was performed at the same intensity(s) as that performed between theSE bouts. During the PR trial subjects were allowed to dismount the bicycle, but were requiredto remain seated for the initial 8 mm of the recovery period. During the eighth minute subjectsremounted the bicycle so that for the final 5 mm of recovery they could ride at their IVT_50%AT.This was done so that subjects did not begin the sprints cold. Additionally this effectively startedsubjects with similar cardiac outputs for all recoveries as the ended as the same exerciseintensity. For the AR trial subjects cycled for the full recovery duration at their IVT_50%AT. In thecase of the CAR trial the subjects cycled at their IAT intensity for 5 mm and at their IVT_50%ATfor the remaining 9 mm. In all trials post-recovery 2 mm were allotted to allow subjects totransition to the Monark (Ergomedic 874E, Monark Exercise AB, Sweden) bicycle. Therefore, inactuality, subjects underwent 14 mm of the respect AR intensity, with an additional 2 mm of36recovery to allow the bike transition. Approximately fifteen minutesof recovery was selectedbecause it is the typical intermission period for most intermittent sports(e.g. hockey, basketball,soccer). During the recovery after the third exercise bout blood L& measureswere made at the3rd 6th, 9thand14thmm.The final procedure on the testing days was the sprint task. Subjectsperformed five 10 ssprints against a resistance of 0.09 kg.(kg body mass)’,with an identical protocol andinstructions to the familiarization sprint task. Three minutes post-sprinttask a final blood L&measure was taken. After the sprints subjects were recommendedto perform and additionalrecovery to help return the body to homeostasis and relieve any discomfortassociated with theintense sprint tasks. However, this was not mandatory.Heart rate was recorded throughout the testing procedure, during both theexercise boutsand recovery intervals, as well as during the sprint task. Samples were takenevery 5 s duringexercise, and sample points that temporally corresponded to the closest L& sampletime wereused for analysis (i.e. HR1-9). In addition, a HR measure was made at the start of first SEboutand used as a baseline value (HRB). During the sprint task the maximum HR achievedafter eachindividual sprint was selected for analysis. Ventilatory parameters were recorded throughout theexercise bout and recovery periods, but not for the sprint task. These measurements weresampled breath-by-breath and averaged over 20 s. Again, the 20 s average that correspondedtemporally closest to the La sample time was selected for analysis (i.e. V021-8, since ventilatoryparameters were not measured after the 14 mm recovery period). Similar to the HR measures anadditional baseline measure was taken (VO2B). Figure 3 visual depicts the temporal layout of theHR and V02 sample times.Figure 3. Schematic Representation of the Testing Day ProtocolB Li L2 L3 L4 L5 L6 L7 L8 L9Warm- SE1 5 mm SE2 5 mm SE331 6th 9th 14thSprint 3 mmup Recovery Recovery 14 mm Recovery Task PostSprintB, baseline HR and V02 sample time; L1-9, L& (HR and V02)sample times from post-SE 1 to 3 mmpost-sprint task (no V02 measure was made for the L9 time point)373.5 Data AnalysisThe dependent variables that were measured in this investigation were: Blood L&Concentration (mmolL1),PP Output (W), MP Output (W), Fl (%), and TW (J). AdditionallyHR (bpm) and V02 (mLkg’min’) were recorded. Blood La comparisons were made using agroup (3) by time (9) repeated-measures analysis of variance (ANOVA). Similarly, a group (3)by time (5) repeated-measures ANOVA was used to compare parameters from the sprint tests(i.e. PP and MP outputs and Fl). A one-way repeated-measures ANOVA was used to compareTW in the three treatment groups. Heart rate and V02 during the exercise and recovery boutswere assessed using group (3) by time (10 and 9, respectively) ANOVA’s. While HR during thesprint task was assessed using a group (3) by time (5) repeated-measures ANOVA. Statisticalsignificance was set a priori at a level of p 0.05. When the omnibus F-test showed a significantinteraction effect dependent T-tests were used post hoc to determine where differences were,since the repeated-measures within-subjects design for ANOVA in SPSS version 15.0 (SPSSInc., USA) does not produce post hoc tests. Significant omnibus F-tests for the main effects werefollowed up with pairwise comparisons to determine where differences occurred. The Bonferroniadjustment was made to account for multiple comparisons.All values are reported as means ± standard deviations (5 ± SD). Statistical analyses ofANOVA were performed using SPSS version 15.0 for Windows (SPSS Inc., USA) and T-testswere performed with Microsoft Excel Version 5.1.2600 (Microsoft Corporation, USA).38CHAPTER IV: RESULTS4.1 Subject CharacteristicsTwelve trained male cyclists volunteered to participate in this investigation. All subjectscompleted all of the testing protocols. However, four L& values were not obtained due tocomplications measuring the samples in two subjects. In Subject 2 the PR L3, AR Li, and CARL2 values are missing. In Subject lithe PR L4 value is missing. Therefore, in the initial analysisthese subjects were excluded from the blood L& ANOVA, since the default setting for SPSS(SPSS Inc., USA) is to do a listwise deletion for missing data. Since statistical significance wasachieved, despite the smaller sample size, no measures were taken to replace the missing data.Additionally, HR data from Subject 10 on the AR day and Subject 12 on all days was not able tobe uploaded due to technological difficulties. Furthermore, HR could not be electronicallymonitored in Subject 11 due to a morphological anonmaly. Therefore, subjects 10-12 wereexcluded from the HR analysis. Subject’s characteristics and workload and recoverycharacteristics are presented in Table 1 and 2, respectively.4.2 Blood LactateOn each of the Testing Days (i.e. Day 4, 5 and 6) nine blood L& samples were taken.Sample times were: post-exercise bout 1 (Li), pre-exercise bout 2 (L2), post-exercise bout 2(L3), pre-exercise bout 3 (L4), 3 mm post-exercise bout 3 (L5), 6 mm post-exercise bout3 (L6),9 mm post-exercise bout 3 (L7), 14 mm post-exercise bout 3 (L8), and 3 mm post-sprint (L9, seeFigure 3 for visual description).Subject 2 and ii both had missing blood L& values and are therefore excluded from thisanalysis. The ANOVA revealed a significant interaction (groupxtime) effect for the blood L&data (p0.001). Thus, the effects of the recovery group on blood L& differed depending on thesampling time. Larger decreases in blood L& were observed in the AR and CAR protocolscompared to the PR protocol. This effect was more evident in the recovery portion of theprotocol (i.e. L5-8, see Figure 4). Mean differences from L5 to L8 were 4.2, 6.7, and 6.5mmolU’ for PR, AR and CAR, respectively. Targeted dependent T-tests were performed for therecovery and post-sprint blood L& values (i.e. L5-9). T-test showed that during PR blood Lavalues were significantly greater from the L6-8 sample times when compared to AR (pO.O5).Furthermore, PR blood La values were significantly greater than CAR values for all recoverysamples (i.e. L5-8, pO.O5). However, the final blood L& values post-sprint (L9) in both AR andCAR were not statistically different from PR (p>0.05, see Table 3). Differences between the twoactive recoveries were not significantly different, despite the lower blood L& values throughout39the CAR from L5-8 (p>O.05). Post-sprint (L9) blood L& was highest in the PR, followed by ARand then CAR (see Table 3). However, none of these differences were statistically significant(p>O.05).Table 1. Subject CharacteristicsSubjectAge Height Weight So5SVO2m PP MP(yrs) (cm) (kg) (mm) (mLkg’min1)(Wkg1 (Wkg1)1 29.5 176.0 72.7 29.5 71.2 13.7 8.52 21.8 181.5 68.1 31.5 76.5 15.5 11.23 28.8 185.6 77.9 54.4 58.9 13.6 10.24 29.6 182.2 69.8 25.0 75.2 15.2 9.15 27.0 172.2 75.1 41.2 58.1 14.5 9.66 27.1 188.0 87.9 40.1 57.2 16.5 10.67 34.0 181.0 65.3 34.1 65.4 16.8 9.78 30.1 169.6 68.5 45.8 59.5 14.3 9.99 23.8 186.4 72.0 28.5 61.1 13.7 8.510 21.2 181.0 71.6 39.9 61.5 14.1 9.311 25.0 180.3 69.8 43.5 65.7 15.1 9.412 30.9 193.5 89.4 34.3 63.8 15.6 9.0X 27.4 181.4 74.0 37.3 64.5 14.9 9.6SD 3.9 6.7 7.6 8.4 6.6 1.1 0.8So5S, sum of five skinfolds; PP, peak power (on WAnT, Wingate Anaerobic Test); MP, mean power (onWAnT); X, mean value; SD, standard deviationThe main effect for (treatment) group was also significant (pO.OO1). Pairwisecomparisons demonstrated that both AR and CAR groups resulted in significantly lower bloodL& values compared to the PR group (p0.05 and p0.00i, respectively for the former andlatter).40Table 2. Subject Workload and Recovery Characteristics50%AT, 50% of the difference between the TAT and IVT (individual ventilatory threshold) below TVTThe sphericity assumption was violated for the main effect of (sample) time and thereforethe Greenhouse-Geisser correction was applied. The main effect of time on blood L& values wassignificant (p0.001). This demonstrated that the work and recovery protocol intensities weresufficient to induce statistically significant increases in blood L& as well as being appropriate forclearance. Pairwise comparisons revealed where the difference existed between sample timesand Table 4 presents the differences. Blood La levels increased throughout the exercise protocoland peaked at L5 before decreasing during the recovery portion of the exercise protocol. Lactatelevels where again elevated post-sprint task (L9) to an overall maximum across all nine sampletimes.Subject 120% MAP 60% TTE IATIVL50%ATVO2IAT VO2I_5o%T(W) (s) (W)(% max) (W) (% max)1 540 76.5 270 69.6 180 47.72 576 72.4 330 82.3 240 61.73 396 111.2 270 76.3 180 54.44 504 52.4 240 73.9 195 52.05 468 91.4 210 65.1 120 44.76 540 89.4 270 66.1 180 55.57 432 76.8 240 75.9 105 43.18 396 75.4 240 75.5 150 51.39 468 81.9 210 66.7 120 46.910 432 74.5 240 67.6 150 51.311 504 72.9 270 75.9 135 45.012 612 127.6 390 83.1 165 49.0X 489.0 83.5 265.0 73.2 160.0 50.2SD 69.4 19.750., maximum aerobic power; TTE, time to exhaustion; TAT, individual anaerobic threshold; IVT_41Table 3. Mean Blood Lactate ValuesBlood Lactate Sample (mmolL’) PR AR CARLi 5.6+ 1.6 5.6± 1.8 5.4±2.2L2 8.9±2.0 7.8± 1.3 8.2± 1.3L3 12.1 ± 2.1 9.2 ± 2.7 10.6 ± 2.4L4 12.0±3.0 9.9±2.2 10.0±2.1L5 14.4± 1.8 13.6±2.612.4±2.2*L6 13.8 ± 1.8 10.7± 2.7*10.3± 3.0*L7 13.4±3.69.6±3.2* 9.2±3.1*L8 10.3 ± 3.1 6.9± 2.5*5.9± 2.6*L9 14.6± 1.6 13.8±2.3 13.6±2.4X 11.7±3.6 9.’7±3.5 9.5±3.5n = 10, Subjects 2 and 11 are excluded; T-tests were only performed for recovery L& (i.e. L5-9); L1-9,blood L& sample times (see Figure 3)*T-tests significantly different from PR value (pO.O5); Pairwise comparison significantly differentfrom PR (pO.O5); Pairwise comparison significantly different from PR (pO.OO1)Table 4. Mean Blood Lactate Differences for Sample TimeSample Time Mean Blood Lactate (mmoFL’) Significantly Different From (pO.O5)Li 5.6± 1.8 L3-7,L9L2 8.3 ± 1.6 L3-6, L9L3 10.6±2.6 L1-2L4 10.6 ± 2.6 L1-2, L5, L8-9L5 13.5 ± 2.3 Li-2, L4-8L6 11.6±2.9 Li-2,L5,L8-9L7 10.7 ± 3.7 Li, L5, L8-9L8 7.7 ± 3.3 L4-9L9 14.0±2.1 Li-2,L4,L6-8n = 10, Subjects 2 and 11 are excluded42Figure 4. Mean Blood Lactate Values---PRAR—&-CARn = 10, Subjects 2 and 11 are excluded*Significantly different from PR value (pO.O5)Comparing the ten subjects included in the blood L& statistical analysis, eight reachedtheir overall (i.e. among all three testing days) maximum blood L& value on the PR day. Theother three overall maximum values occurred on the AR day, as one subject shared the samemaximum value on both the AR and PR days. Of the two subjects excluded from the analysis,one was the only subject to have their overall maximum blood L& on the CAR day. The otherexcluded subject followed the group trend, having his highest overall value on the PR day. Dailymaximum blood L& values typically occurred at the third minute of recovery (L5), with 5, 8, and6 of the subjects having their daily maximum L& at L5 for PR, AR, and CAR days respectively.In general, the overall highest post-sprint blood L& (L9) predominantly occurred on the PR testday, with 7 of 10 subjects peaking on this day. One subject peaked post-sprint on the AR day andthree peaked on the CAR day (with one subject having the same L9 La value on both the PR andCAR days). Of the excluded subjects, Subject 2 had the same maximum L9 value on the PR andCAR day, while Subject 11 had their overall L9 maximum on the PR day.0EEC.)-J0016. L2 L3 L4 L5 L6 L7 L8 L9Sample Time43The Li -L4 scores were excluded from the determinationof minimum L& values as thesesamples were taken during the fatiguing exercise bout and theinterest for lowest L& values waswithin the 14 mm recovery period. The majority of subjects had their lowestoverall La valueson the CAR day (7 of 10). The other three subjects had their lows on theAR day. Subject 2 and11 had their overall minimum L& values on the PR and CAR day, respectively. Overallminimum L& values were observed at L8 in all subjects (n = 10). Subject 2 (excluded)was theonly participant to have an overall minimum L& value at a sample time other than L8 (i.e. L7).On the CAR day all subjects (n = 10) had their daily minimum L& value atthe L8 sample. Ninesubjects had their daily low at L8 and one at L7 on the PR day. Eight subject’s daily lowsoccurred at L8 and two at L7 on the AR day. Subject 11 had his daily L&minimum at L8 on alldays, while Subject 2 had his daily lows at L7 on the PR and AR days and L8 for the CARday.Of the subjects included in the L& ANOVA, none experienced their overall L& minimumon the PR day, while the majority of maxima (i.e. 8) were achieved on this day. However,Subject 2 (excluded from ANOVA) was an exception to this, as he experienced his overall Laminimum of the PR day. Conversely, no subjects experienced an overall La maximumon theCAR day, while the majority of L& minima occurred on this day. Again, Subject 2 was theexception to this, as he was the sole participant to achieve his overall L& maximum on the CARday. Subject 9 was the only subject to experience their overall maximum and minimum Lavalues on the same day. This occurred on the AR day. Of the eight subjects that achieved theiroverall maximum L& value on the PR day, six also had their overall final (i.e. 3 mm post-sprint)maximum La value too. Subject 7 was the only participant to achieve his overall finalmaximumon the AR day, and interestingly, also had his overall minimum on this day just prior to thesprint task. On the CAR day, three subjects achieved their overall final maximum L& value afterpreviously having their overall minimum L& value at L8. Additionally, Subject 2 achieved hisoverall final maximum L& score on the CAR day (which was the same on the AR day), but didnot experience an overall minimum at L8. Table 5 summarizes the daily and overall maximumand minimum L& values for all subjects.4.3 Sprint Task PerformanceSubjects performed five 10 s sprints, each separated by 30 s of recovery. Each individualsprint was assessed for PP, MP and Fl. In addition, the performance across the sprint task wasassessed by analyzing TW across all five sprints. All subjects were able to complete all fivesprints on each test day. Group means for all sprint task performance variables are presented inTable 6.44Table 5. Group Means for Peak Power, Mean Power, Fatigue Index and Total WorkPP (W) MP (W) FT (%) TW (J)PR 1017.7± 134.4 782.2± 111.7 37.0±9.2 39108.3 ±4852.9AR 1013.6± 145.6 800.1± 114.5*34.2± 11.340003.3±5110.2*CAR 1021.8± 134.4 786.7± 118.0 37.4± 10.6 39335.8± 5022.6*Significantly different from PR value (pO.O5)4.3.1 Peak PowerThe interaction (groupxtime) effect for PP was not found to be significant (p>0.05).Therefore, the effect of time on significantly decreasing PP did not change as a result of thegroup level (i.e. recovery mode). Peak power decreased in all three groups as the number ofsprints performed increased. Table 6 shows the mean PP outputs and Figure 5 graphicallydepicts them.Table 6. Mean Peak Power OutputsPeak Power (W) PR AR CAR1 1067.2±137.1 1054.8±160.1 1072.5±158.12 1046.1± 137.6 1040.7± 130.0 1060.2± 141.53 998.8± 121.1 1000.1± 152.1 1011.0± 126.24 992.1± 145.2 989.2± 151.1 1001.7± 143.95 984.2± 132.4 983.3±143.9 963.6± 113.5The group main effect for PP was not significant (p>0.05). Subjects achieved similar PPoutputs regardless of the recovery intensity. Nonetheless, the group mean PP output was greatestin the CAR group, followed by PR, then AR (see Table 5). The PP output was 4.1 W greaterthan the next closest group mean PP output for each group difference.45Figure 5. Mean Peak Power Outputs0ITable 7. Sprint Number Means for Peak Power, Mean Power, and Fatigue IndexSprint Number PP (W) MP (W) Fl (%)1 1064.8±147.9*35864.5±108.7*2529.8±ii.i*452 1049.0± 132.7*35825.7±997*’34.8± 10.2*453 1003.3± 130.1*12778.6± 102.1*1.2,4536.4± 93*454 994.3± 135.4*1.2748.4± 995*1.339.6±94*35 977.0±127.1*1.2730.9± 101.8*1340.5± 8.8*13*Significantly different from listed sprints (pO.O5)10801060104010201000•PRI AR980 DCAR960940920900A significant main effect of (sprint number) time on PP output was found (p0.001).Therefore, subjects were unable to maintain PP across the sprint task. Pairwise comparisonsshowed where the differences were (see Table 7). Peak power output was significantly greater onthe first two sprints compared to the last three (p0.05). No difference in PP was observedbetween Sprint 1 and 2 or between the last three sprints (p>0.05).1 2 3 4 5Sprint Number46In general the overall maximum PP outputs were achieved in either the first or secondsprint. The exception was Subject 4, who shared the same overall maximum score for both hissecond and third sprint. The majority of overall maximum PP outputs were attained on the CARday (8 of 12). Additionally, three overall maxima were attained on the AR day and one on thePR day.As a general rule, most subjects achieved their highest daily PP output in either the firstor second sprint. Three subjects achieved their daily maximum PP in the third sprint with one onthe AR day and two on the CAR day (one subject shared the same score in the second and thirdsprint on the CAR day) and one in the fifth sprint on the PR day. The other daily maximumvalues were distributed between the first and second sprint (23 and 10, respectively). Seven dailymaxima occurred in the first sprint on the PR and CAR days respectively, and nine in the firstsprint on the AR day. Four daily maxima occurred in the second sprint on the PR and CAR daysrespectively, and two happened in the second sprint on the AR day.Overall minimum PP outputs tended to occur on the PR and CAR day, with five on eachrespectively. The other two occurred on the AR day. In which sprint the overall minima occurredwas more varied than the maxima and displayed no distinct trend. Seven arose in the fifth sprint,with one of these being shared with the second sprint score in Subject 3. Of the seven in the fifthsprint, three occurred on each of the PR and CAR day, respectively, and one on the AR day. Therest of the overall minimum PP outputs were spread over all the other sprints, with one in thefirst sprint, two in the second (one being a shared score), two in the third, and one in the fourth.Daily minimum PP outputs tended to take place in the later sprints, but were evidentthroughout the sprint task. On the PR day six daily minima (two were shared) occurred in thefifth sprint, four in the fourth (one shared), three in the third, and one (shared) in the secondsprint. Five occurred in the fifth sprint on the AR day, five in the fourth, and one in both the firstand third sprints. On the CAR day, seven occurred in the fifth, one in the first, second and fourthsprint, and two in the third. Table 17 summarizes the daily and overall maximum and minimumPP outputs.4.3.2 Mean PowerThe interaction (groupxtime) effect for MP was not statistically significant (p>O.O5).Thus, similar to the effect of time on PP, MP decreased in all three groups as the number ofsprints performed increased. Table 8 shows the mean MP outputs, which are also illustrated inFigure 6.47Table 8. Mean Mean Power OutputsMean Power (W) PR AR CAR1 861.3± 102.9 872.3±114.0 859.7± 118.02 820.3 ± 97.2 834.3 ± 106.1 822.7 ± 103.93 767.9±100.6 791.1±109.5 776.9±103.84 738.3 ± 106.7 757.5 ± 99.2 749.5 ± 100.25 723.1±104.1 744.9±109.1 724.8±99.6The main effect for group MP was statistically significant (pO.O5). The group mean MPwas highest on the AR day, followed by CAR, then PR (see Table 5). Pairwise comparisonsshowed that the significant differences were between the PR and AR MP outputs (pO.O5).Neither of the other two pairwise comparisons (AR vs. CAR and PR vs. CAR) were significant(p>O.OS).The sphericity assumption for the main effect of (sprint number) time was violated andtherefore the Greenhouse-Geisser correction was applied. The main effect of time on MP outputswas significant (pO.OO 1). Therefore, in addition to subjects not being able to maintain PP acrossthe sprint task, they were also unable to maintain MP. Pairwise comparisons showed where thedifferences were (see Table 7). All MP outputs, except on the fourth and fifth sprint, weresignificantly different from all other sprints. The fourth and fifth sprint did not differsignificantly from each other (p>0.05), but were significantly less than the initial three sprints(p0.05). Mean power outputs decreased as the number of sprints completed increased. Eachsubsequent sprint was significantly less than the previous sprint (p0.05), except for the finaltwo sprints.The majority of overall maximum MP outputs were accomplished on the AR day. Sevenoverall maximum MP outputs were achieved on the AR day, three on the PR day, and two on theCAR day. All but one of these occurred in the first sprint, with the exception occurring in thesecond sprint. All daily maximum MP outputs, except for one, occurred in either the first orsecond sprint, with the vast majority (32 of 35) occurring in the first sprint. In the one exceptionthe maximum transpired in the third sprint. On the PR day twelve of the daily maxima happenedin the first sprint and one occurred in the second sprint. Subject11 reproduced the same dailymaximum value for the first and second sprint on the PR day. Ten daily maxima were achieved48in the first sprint on the AR day, one in the second, and one in the third. On the CAR day tendaily maxima were achieved in the first sprint and two in the second.•PRE: ARDCAROn the PR day five of the overall minimum MP outputs occurred. Of these, two occurredin the fourth sprint and the other three in the fifth sprint. Only one overall minimum occurredonthe AR day. It was obtained in the fourth sprint. Sixoverall minimum MP outputs occurred onthe CAR day and they were all in the fifth sprint. On thePR day, three daily minimum MPoutputs occurred in the fourth, and nine in the fifth sprint. Subject 1 sharedthe same dailyminimum MP score on the first and fifth sprint for the AR day. Three subjects had theirdailyminimum in the fourth sprint and nine had it in the fifth. All but one subjecthad their dailyminimum in the fifth sprint on the CAR day. The one anomaly experienced his daily minimumin the fourth sprint.Subject 1 and 4 were the only participants to experience both theiroverall maximum andminimum MP output on the same day (i.e. on the CAR and PR days respectively).On the ARday there were five subjects that experiencedtheir overall maximum MP in addition to also49Figure 6. Mean Mean Power Outputs9008508004-7507006506001 2 3 4 5Sprint Numberachieving their overall final (i.e. fifth sprint) maximum MP. In total there were eight subjectsthat achieved their overall final maximum MP output on the AR day. Table 18 summarizes thedaily and overall maximum and minimum MP outputs.4.3.3 Fatigue IndexThe interaction (groupxtime) effect for FT was not statistically significant (p>0.05).Fatigue index increased in all three groups as the number of sprints increased. The Fl for allthree treatment groups across the sprint times are shown in Table 9 and graphically depicted inFigure 7.Table 9. Mean Fatigue IndexesFatigue Index (%) PR AR CAR1 30.3 ± 9.6 28.4 ± 12.5 30.7 ± 12.02 35.0± 10.4 32.7± 11.0 36.6± 12.03 37.0 ± 7.5 33.7 ± 10.3 38.5 ± 10.04 40.9± 7.4 37.3±11.1 40.7± 9.75 41.8±7.1 38.9±9.9 40.7±9.6The main effect for group for FT was not found to be significant (p>0.05). The groupmean for Fl was greatest in the CAR protocol, followed by the PR then AR protocols. However,the differences were very minute (see Table 5).The sphericity assumption for the main effect for (sprint number) time was violated andconsequently the Greenhouse-Geisser correction was applied. The main effect for time wasfound to be significant (p0.00 1). Fatigue index increased across the sprint task. Pairwisecomparisons demonstrated where the differences occurred (see Table 7). The Fl for the firstthree sprints were significantly less than the last two sprints (p0.05). Conversely, there were nosignificant differences amongst the first three sprints or amongst the final two sprints. Thus, overthe course of the sprint task, subjects developed larger differences between their maximum andminimum power outputs within a sprint.50Figure 7. Mean Fatigue Indexes45.•PRAR20.0 DCAR15. NumberThe trends for maximum and minimum data values for Fl were less discernible than theother performance variables. The overall maximum Fl were relatively evenly distributed amongthe three protocols. Four maxima occurred on the PR day, three on the AR day, and five on theCAR day. Of the four subjects who experienced an overall maximum Fl on the PR day one wasin the fourth sprint and the other three were in the fifth sprint. On the AR day all three occurredin the fifth sprint. Lastly, on the CAR day one occurred in the second sprint, three in the fourth,and one in the fifth. Daily maximum FT tended to occur in the later sprints, but several subjectsexperienced their maxima early on in the sprint task. During the PR trial, two subjectsexperienced their daily maximum Fl in the second sprint, six in the fourth, and four in the fifth.On the AR day, two experienced their maxima in the first sprint, three in the fourth, and seven inthe fifth. During the CAR protocol, one subject had their daily maximum in the first sprint, twoin the second, one in the third, and four in each of the fourth and fifth sprint.Four subjects experienced overall minimum FT on the PR day. Five subjects had theiroverall minimum FT on the AR day and four had theirs on the CAR day. Subject 3 had the sameoverall minimum FT on both the AR and CAR days. On the PR day, two of the overall minima1 2 3 4 551that occurred were in the first sprint and one occurred in each of the second and third sprintsrespectively. Three overall minimum FT occurred in the first sprint on the AR day, and oneoccurred in each of the second and third sprints respectively. On the CAR day the overallminima were divided between the first and second sprint, with two occurring in each.The majority of daily minimum Fl occurred in the first sprint, followed next by thesecond sprint. On the PR day, seven daily minima happened in the first sprint. In the second andthird sprint there were three daily minima that occurred in each (Subject 2 had the same Fl inboth the second and third sprint). During the AR protocol, eight subjects had their dailyminimum FT score in the first sprint. There were two subjects who had their daily minimum FT inthe second sprint, one in the third, and one in the fifth. On the CAR day, nine subjects had theirdaily minimum FT in the first sprint and three had it in the second sprint.Overall initial and final maximum FT values were relatively evenly dispersed among thethree testing days. Table 19 summarizes the daily and overall Fl scores and in which sprint theyoccurred.4.3.4 Total WorkThe one-way repeated-measures ANOVA performed to compare the treatment effects onTW revealed the same results as the ANOVA MP group effect. This is because the TW score issimply an aggregate score of the MP across the sprint trial. Therefore, there were significantdifferences between the treatments with respect to TW (pO.O5). Again, the pairwise comparisonbetween AR and PR was found to be significant (pO.05). The mean values for TW for eachgroup are shown in Table 5. Figure 8 graphically presents the data. The AR group mean TW wasgreatest, followed by the CAR, then the PR. No significant differences existed among AR andCAR, and PR and CAR pairwise comparisons (p>O.05).On an individual basis, seven subjects had their highest TW output on the AR day. Foursubjects had their overall maximum TW output on the CAR day, and only one subject had theirhighest TW output on the PR day. Conversely, six subjects had their overall minimum TWoutput on the PR day, five did on the CAR day, and only one did on the AR day. Table 14summarizes the maximum and minimum TW outputs for each subject.52Figure 8. Total Work40200400003980039600IPR39400 EJAR0DCAR39200390003880038600*Significantly different from PR value (pO.O5)4.4 Heart RateHeart rate was recorded during both the exercise and recovery bouts, as well as duringthe sprint task. During the exercise and recovery bouts HR measures were matched to thecorresponding L& sample points for analysis, with the addition of a baseline measure (HRB)prior to SE1. However, due to technological difficulties several HR files were not able to beuploaded for analysis, while in another subject a HR reading was not obtainable due to thesubject’s (Subject 11) chest morphology. Therefore the exercise and recovery HR ANOVA wascomprised of nine subjects.The maximum HR achieved after each individual sprint was selected for analysis of HRduring the sprint task. In addition to the aforementioned technical difficulties in uploading HRdata, two other HR data sets were excluded from analysis due to erratic values during the sprinttask. Thus the sprint task HR (SHR) data set was comprised of seven subjects.534.4.1 Exercise and Recovery Heart RateThere was a significant interaction (groupxtime) effect for the HR results (pO.OOl).Heart rate responses varied differently over the three recovery intensities for the different sampletimes. Dependent T-tests revealed that HR was greater in both the AR and CAR compared to thePR from the HR2 sample time to HR7 (p0.05). Heart rate was greater in the AR trial comparedto the CAR trial at HR4, but HR was then greater at HR5-6 in the CAR trial compared to the ARtrial (pO.05). Mean HR values are shown in Table 10.Table 10. Mean Exercise and Recovery Heart Rate ValuesHeart Rate (bpm) PR AR CARHRB 115.0± 11.0 117.2± 12.9 115.0± 8.5HR1 173.0 ± 8.8 172.2 ± 10.0 171.9 ± 9.9HR2 119.2± 10.1 139.1± 10.5*141.6±8.3*HR3 175.7±9.8181.1±10.1* 180.6±11.4*HR4 120.9 ± 10.1 148.7± 8.4*146.2±HR5 109.2 ± 9.7 142.4± 93*167.3±HR6 102.2 ± 8.1 139.4± 8.4*156.3±l2.l’HR7 108.2±8.9142.1±9.4* 144.2±11.1*HR8 139.2±8.9 143.7± 11.3 144.4± 12.9HR9 110.3 ± 9.0 112.3 ± 11.4 112.1 ± 6.35127.3 ± 27.0 143.9 ± 22.3 148.0 ± 23.5n 9, Subjects 10-12 were excluded; T-test were performed for all HR (i.e. HRB-9); HRB, HR-Baseline*Significantly different from PR value (pO.O5); significantly different from AR value (pO.05)The sphericity assumption for the group main effect was violated and therefore theGreenhouse-Geisser correction was applied. The main effect for group was significant(p0.001). Pairwise comparisons showed that group mean HR was significantly greater in theAR and CAR versus PR (p0.001), and in CAR versus AR (p0.05). Figure 9 graphicallypresents the mean HR values.54Figure 9. Mean Exercise and Recovery Heart Rate Values60-4-PRAR—&-CARn = 9, Subjects 10-12 are excluded*Significantly different from PR value (pO.O5); significantly different from AR value (pO.O5)The main effect for time was found to be significant (p0.001). Pairwise comparisonsrevealed where the differences between sample times existed. Table 11 shows the sample timemeans and describes the differences and Table 21 presents individual daily and overallmaximum and minimum HR values for the nine subjects evaluated.2001801601408040200HRB HRI HR2 HR3 HR4 HR5 HR6 HR7 HR8 HR9Sample Time55HRB 116.0± 10.6HR1 172.4 ± 9.2HR2 133.1 ± 13.8HR3 179.1±10.3HR4 138.6 ± 15.6HR5 139.9±26.4HR6 132.8 ±24.9HR7 131.6 ± 19.3HR8 142.6± 10.8HR9 112.0±8.8n 9, Subjects 10-12 were excluded4.4.2 Sprint Task Heart RateThe interaction (groupxtime) effect for SHR reached statistical significance (pO.O5).The increase in SHR across the sprint task differed depending on the treatment group. DependentT-tests revealed that SHR was greater in both the CAR compared to the PR after the third andfourth sprint (pO.O5). Mean SHR values are shown in Table 12.Table 12. Mean Maximum Sprint Task Heart RateHeart Rate (bpm) PR AR CARSHR1 167.3 ± 6.6 168.7 ± 5.8 168.0 ± 6.8SHR2 173.1 ± 6.5 175.9 ± 6.5 176.4 ± 6.8SHR3 175.0 ± 6.4 177.3 ± 7.7 178.1± 59*SHR4 175.6 ± 5.1 178.6 ± 7.4 180.1± 74*SHR5 176.1 ± 5.2 179.3 ± 7.3 179.4 ± 7.1173.4 ± 6.5 175.9 ± 7.6 176.4 ± 7.8Table 11. Mean Exercise and Recovery Heart Rate Differences for Sample TimeSample Time Heart Rate (bpm) Significantly DifferentFrom (p0.05)HR1-8HRB, HR2-9HRB, HR1, HR3, HR9HRB-2, HR4-9HRB-1, HR3, HR7, HR9HRB-1, HR3, HR6-7, HR9HRB-1, HR3, HR5, HR8-9HRB-1, HR3-5, HR8-9HRB-1, HR3, HR6-7, HR9HR1-8n = 7, Subjects 7 and 9-12 are excluded*Significantly different from PR value (pO.O5)56The group main effect for SHR was not significant (p>O.05). The group mean for SHRwas greatest in the CAR protocol, followed by the AR then PR protocols. However, thedifferences were very small.The main effect for time was found to be significant (pO.OOl). Maximum HR valuespost-sprint increased across the sprint task. Pairwise comparisons demonstrated where thedifferences occurred (see Table 13). Mean SHR steadily climbed over the course of the sprinttask. The SHR for the first sprint was significantly less than all other values (p0.05). After thesecond sprint maximum HR was significantly greater than the first sprint, but less than the lasttwo sprints (p0.05). Heart rate after the third sprint was only significantly different form theSHR1 value (p0.05). Heart rate after the last two sprints was significantly greater than after thefirst three sprints (pO.O5). The SHR for all three groups across the sprint times are graphicallydepicted in Figure 10. Table 22 presents individual daily and overall maximum and minimumSHR values for the seven subjects evaluatedTable 13. Mean Sprint Task Heart Rate Differences for Sample TimeSprint Number Heart Rate (bpm) Significantly DifferentFrom (pO.05)SHR1 168.0±6.1 SHR2-5SHR2 175.1 ± 6.4 SHR1, SHR4-5SHR3 176.8 ± 6.5 SHR1SHR4 178.1 ± 6.7 SHR1-2SHR5 178.3 ± 6.4 SHR1-2n = 7, Subjects 7 and 9-12 are excluded57Figure 10. Mean Sprint Task Heart Rate1851800.. 175t 170165160n 7, Subjects 7 and 9-12 are excluded4.5 Volume of Oxygen ConsumedThe interaction (groupxtime) effect for the V02 scores was significant (pO.OO 1).Responses of V02 to the exercise and recovery protocol varied differently over the threetreatments across the sample times. Dependent T-tests revealed that V02 in both the AR andCAR protocols was significantly greater than the PR protocol at the V02 sample, and fromV024-7 (pO.0O1). Volume of 02 consumed during CAR was greater than AR at the V025 andV026 sample times (p0.O0l). Mean V02 was lower during the PR protocol from VO2B toV027, except at the V021 and V023 samples. At the V028 sample the mean V02 during PR wasactually significantly higher than during AR (pO.O5), and greater than during the CAR(p>O.O5).Mean V02 was higher in the CAR protocol than in the AR protocol at all measuresexcept at baseline (VO2B) and pre-exercise bout 3 (V024). Mean V02 values are shown in Table14.1 2 3 4 5Sprint Number58Table 14. Mean Volume of Oxygen Consumed ValuesVolume of Oxygen Consumed (mL.kg’.min’)PR AR CARVO2B13.6 ± 3.0 15.1 ± 4.1 14.8 ± 3.9V021 56.5 ± 6.8 57.0 ± 7.1 57.8 ± 6.8V02 14.3 ± 4.9 36.5± 6.1*377± 8.0*V02358.9±6.5 60.5±7.4 61.6±8.8V024 13.6±4.038.6±6.1* 38.2±6.7*V02510.6± 1.7 36.5±6.6*5149*tV026 8.0± 1.634.3±6.4*40082*tV02711.1 ± 3.2 32.9± 6.6*34.6± 6.8*V02833.0±6.431.7±6.0*31.9±7.3524.4± 19.7 38.1 ± 14.2 40.9± 15.4T-test were performed for all V02 (i.e. VO2B-8)*Significantly different from PR value (pO.OO 1); significantly different from AR value (pO.O5)The sphericity assumption for the main effect of group was violated and therefore theGreenhouse-Geisser correction was applied. The effect was then found to be significant(p0.00 1). Pairwise comparisons showed that all three groups were significantly different withrespect to group mean V02 scores (p0.001). Volume of 02 consumed was greatest in the CARprotocol, followed by AR then PR.The sphericity assumption for the main effect for time was violated and consequently theGreenhouse-Geisser correction was applied. The V02 main effect for time was found to besignificant (p0.001). Pairwise comparisons revealed where the differences between sampletimes existed. Table 15 shows the sample time means and describes the differences. Figure 11graphically presents the mean V02 values. Table 23 presents individual daily and overallmaximum and minimum V02 values for all subjects.59VO2Bv021V02V023V024V025V026V027V0280).-jE•0a)E00C.)a)0)0II0a)E0>14.5 ± 3.657.1 ± 6.729.5 ± 12.660.4 ± 7.530.1 ± 13.132.8 ± 18.227.5 ± 15.326.2 ± 12.232.2 ± 6.4V021-8VO2B,V022,V024-8VO2B-1, V023,V025VO2B-1, V024-8VO2B-1, V023,V026-7VO2B-4, V026-7VO2B-1, V023-5, V028VO2B-1, V023-5, V028VO2B-1, V023,V026-7Table 15. Mean Volume of Oxygen Consumed Differences for Sample TimeSample Time Mean Volume of Oxygen Consumed SignificantlyDifferent From (pO.O5)(mL.kg1.min’)Figure 11. Mean Volume of Oxygen Consumed Values70.—PRAR30.0—&-CAR20.010.00.0VO2B V021 V022 V023 V024 V025Sample Time*Significantly different from PR value (p0.O5);tsignificantly different from AR value (pO.O5)V026 V027 V02860CHAPTER V: DISCUSSION5.1 Subject CharacteristicsThe mean age (27.4 yrs) of the subjects tested in this investigation was similar to that ofStamford et a!. (1981) and Dodd et a!. (1984), but older than that of more recent investigations(Baldari et al., 2004; Baldari et al., 2005; Gmada et al., 2005). Furthermore, the subjectsinvestigated displayed greater VO2max scores than those reported by Stamford et al. (1981), Doddet al. (1984), and Gmada et al. (2005), but slightly lower than the populations investigated byBaldari et al. (2004; 2005). This was expected as the two early investigations did not use trainedpopulations. Interestingly, the subjects had VO2max scores that were reasonably higher than thetrained group examined by Gmada et al. (2005). This is attributed to the criteria utilized todetermine training status in the respective investigations. However, the group did exhibit similarVO2max,threshold and MAP data to those reported in other groups of trained cyclists (Faria,Parker, & Faria, 2005; Tanaka et al., 1993).Compared to Gmada et al. (2005) workloads at 120% MAP were substantially higher(489.0 ± 69.4 vs. 310.0 ± 14.0 W (trained) and 280.0 ± 15.0 W (untrained) respectively). The60% TTE duration was shorter than the trained group (83.5 + 19.7 vs. 102.0 ± 20.0 s), but longerthan the untrained group (73.0± 21.0s). These differences may be explained by differences inthe parameters used to define training status, as well as differences in the protocol used toachieve VO2m. During the VO2m protocol in the study by Gmada et a!. (2005) subjects wererequired to pedal at a set cadence (60 rpm) which is suggested to be more economical, but lowerthan preferred cadences of trained cyclists (Marsh, Martin, & Foley, 2000). The only cadencerestriction in the current investigation was that subjects could not drop below 60 rpm. This mayhave had some effect on the VO2max and, more particularly, MAP scores. Though the majorcontributor to the differences is more likely directly related to fitness levels.5.2 Blood LactateThe changes observed in mean blood La during the recovery portion of the exercise boutwere as anticipated. That is, mean blood L& was lowest in the CAR trial at the end of therecovery period, albeit only slightly less than the AR trial. Mean blood L& was always higher inthe PR protocol. However, the differences observed between clearance rates in the AR and CARprotocols were non-significant, and thus it cannot be said with any certainty that chance alonecould not account for the differences. Nonetheless, blood L& concentration was lower at allsample points during the 14 mm recovery period for CAR. Furthermore, the fact that blood Lawas lowest in the CAR trial at the L5 sample showsthat L& likely peaked fastest during CAR.61This is in agreement with the suggestion put forth by Stamford et al. (1981) and also agrees withthe findings of Gmada et al. (2005).Blood L& almost always reached a minimum at the L8 sample time, with the exceptionof three cases in the ten subjects analyzed over all the testing days. This suggests that L& valueswere still decreasing at the14t1imm of recovery. Analysis of the final L& scores at the end of therecovery period renders this more plausible, as the values are still sufficiently above restinglevels. However, due to the experimental protocol design, this was not to be investigated.Recently, Baldari et al. (2004; 2005) reported that during a 30 mm recovery period, significantdecreases in L& did not occur after the20thmm of recovery. However, decreases in L& in theirinvestigation were expressed as percentages, whereas the current investigation used absolutevalues. When expressed as percentages of maximum mean values, L& values at the end ofrecovery are substantially higher (72, 51, and 48% for PR, AR and CAR respectively) in thisstudy than those reported by Baldari et al. (2004; 2005) at 15 mm of similar intensity recovery(approx. 20%, (2004); and 12-25% (2005)). It therefore follows that blood L& was likely stillsignificantly decreasing after 14 mm of recovery and would require a longer recovery time toreach baseline levels after similar intensity work. Blood La values did however decrease tosimilar absolute values as those reported by Gmada et al. (2005). This difference is probably dueto the type of exercise performed, as Gmada et a!. (2005) used an intermittent exercise protocolwhich resulted in higher overall L& values, similar to this investigation, compared to the singlehigh-intensity bout employed by Baldari et al. (2004; 2005).As such, the finding that blood La clearance was greater with an AR protocol is inagreement with numerous other investigations (Baldari et al. 2005, Dodd et al., 1984; Gmada etal., 2005; McAinch et al., 2004; Spierer et al., 2004; Siebers & McMurray, 1981; Stamford et al.,1981). Among all the subjects analyzed, blood La was always lowest across the three testingdays in either the AR or CAR trial. Therefore, the findings are in complete agreement with thevast majority of findings that show blood La clearing faster with AR. Investigations that do notshow improved L& clearance with AR have used shorter recovery periods, much less than that ofthe present study (Dorado et al., 2004; Spencer et a!., 2006). Such short durations appear tonotallow enough time for L& levels to decrease substantially.It is now currently believed that the major fate of La is oxidation(Gladden, 2003). Thisis especially true during exercise, when as much as 75% of L& is oxidized, with the remainderbeing disposed through gluconeogenesis (Brooks, 2007). During high-intensity exercise La ispredominantly produced in the glycolytic muscle fibres and then is shuttled to adjacent and62remote oxidative muscle fibres, as well as other tissue sites, such as the heart and liver. DuringAR the maintenance of a lower metabolic power output, compared to the previously higherpower output during exercise, provides an energy demand that is met by a large contribution ofL& metabolism (i.e. oxidation, Bangsbo et al., 1994; Rontoyannis, 1988). Additionally, themetabolic power demand results in higher cardiac output and hence, higher blood flow, which isbelieved to contribute to largescale L& shuttling to more remote bodily locations. The collectiveoutcome is a greater clearance of blood L&.5.2.1 Combined Active Recovery and Lactate ClearanceStamford et al. (1981) initially suggested that a recovery intensity that decreased inrelation to a decreasing blood L& concentration may clear blood L& faster than a single intensityrecovery. Dodd et al. (1984) and Gmada et al. (2005) have previously examined this, withconflicting results. The current study is in agreement with the latter two, in that CAR was able toclear L& at a rate at least equal to AR performed at a single intensity. However, results did notconfirm Gmada et al.’s (2005) finding that CAR was able to clear La faster than AR in a trainedpopulation and to a lesser extent in an untrained population. Differences in findings between thecurrent investigation and those of Gmada et al. (2005) could be related to subject fitness leveland/or recovery intensity. The trained group in the study by Gmada et al. (2005) had a meanVO2max of 56.5 ± 3.5mL.kg’•min’, compared to 64.5 ± 6.6 mL•kg1•min’ in this study.Additionally, while recovery intensities in Gmada et al.’s (2005) work were based on individualthresholds, the workloads were determined relative to ventilatory thresholds minus 20% VO2max(specifically VT1 and VT2). The authors selected these workloads because they would beroughly equivalent to 35% and 65% of VO2max; both which had been previously used for Laclearance analysis in other investigation (Dodd et al., 1984; Stamford et al., 1981). Recoveryintensities in this investigation were quantified relative to IAT and IVT, determined via bloodL& analysis and ventilatory data (respectively), and recently examined in a similar population fortheir effectiveness for L& clearance (Baldari et al., 2005). Furthermore, we felt that recoveryintensities based on the AT determined with blood L& would be more accurate than solely fromventilatory data since the measure is more direct. It is important to have a recovery intensity thatdoes not surpass the AT and result in a significant increase in L& production in order to facilitateL& clearance with AR (Dodd et al., 1984).Relative to VO2max, recovery intensity in this study was higher than that of Gmada et al.(2005). Volume of 02 consumed at VT2 was 61.0 ± 4.5 and 54.5 ± 6.0% VO2m, and at VT1was 37.5± 5.0 and 33.5 ± 4.5%VO2mfor trained and untrained subjects, respectively.63Conversely, V02 at IAT andIVL5O%AT in the present investigation were 73.2±6.1 and 50.2 ±5.3% VOmax, respectively. Accordingly, it may be that CAR did not result in significantlygreater La clearance than AR because the IAT workload may have resulted in substantialproduction of L& within the muscle as the workload was higher than Gmada et al. (2005), whichmay have limited clearance from the blood. Interestingly however, it was observed that L& waslowest at the L5 sample point in CAR, so it seems that the TAT workload was at a sufficientintensity to clear La quickly enough to have an earlier peak. Despite the early peak, it seems thatCAR did not incur a significant advantage to overall La clearance, above that obtain with AR.It appears that the protocol used to determine the TAT in this investigation was adequate,as there was no evidence of an increase in blood L& in the CAR trial. However, it may be thatthe workload was below the AT. Nonetheless, the workload could not have been much lowerthan the AT since subjects V02 at IAT was sufficiently high. Therefore the treadmill protocoladopted from Baldari et al. (2000) and modified for use on a bicycle ergometer seems to be validfor determination of the IAT.5.3 Sprint Task PerformancePerformance results on the sprint task followed the hypothesized trends with respect toPP, but did not fulfill the other predictions. Across the three testing days, no significantdifferences were observed in PP output or FT. Mean power outputs was significantly greater inthe AR group compared to the PR group. Additionally, TW was significantly greater during ARcompared to PR.5.3.1 Peak PowerPeak Power did not significantly differ amongst the recovery interventions. However,over the course of the five sprints, subjects fatigued and PP significantly dropped. As a trendamong individuals, subjects tended to achieve their highest PP on the CAR day. These occurredin either the first or second sprint. Conversely, the highest PP in the final sprint tended to occuron the AR and PR days.The finding that PP was not significantly affected by recovery in this investigation is inagreement with several other studies (Ainsworth et al., 1993; Spierer et al., 2004; Weitman,Stamford, Moffatt, & Katch, 1977). Ainsworth et al. (1993) demonstrated that as little as 6 mmof AR at 80 W was sufficient to restore 5 s PP output on a 45 s bicycle sprint task. While Spiereret al. (2004) showed that PP on repeat 30 s WAnT in both trained and untrained subjects was notsignificantly different when interspersed with 4 mm of either PR or AR at 28% VO2max. Basedon these findings, it was hypothesized that 14 mm of recovery (with an additional 2mm64transition period, totaling 16 mm) would be more than adequate to allow complete restoration ofPP output in this study. Then from this point the sprint task would be identical, regardless of therecovery trial, and thus no differences in PP were expected on the latter sprints.Recent investigations have shown that AR can actually be detrimental to performance ofsprint tasks when compared to PR (Dupont et a!., 2004; Dupont, Moalla, Matran, & Berthoin,2007; Spencer et al., 2006). However, these investigations used very short recovery durations(15 s and 21 s, respectively), and therefore cannot be directly compared to the present study.There are likely different mechanisms responsible for changes in performance over such shortdurations compared to longer durations. It was suggested that AR impaired performance in theaforementioned investigations by limiting PCr resynthesis via competition for limited02supplies (Spencer et al., 2006). However, any potential limitations to PCr resythesis in thisinvestigation did not cause any observable detrimental effect to PP performance in either of theactive recoveries.Peak power output, when assessed over a short duration, is primarily controlled byenergy release from free ATP and the cycling of the PCr system. Indeed, PCr resynthesis hasbeen strongly correlated with subsequent sprint performance (Bogdanis, Nevill, Boobis,Lakomy, & Nevill, 1995). Both free ATP and PCr energy sources are quickly depleted duringhigh-intensity exercise, yet the half-time for PCr resynthesis is short, approximately 21-60 s(Harris et al., 1976; Yoshida & Watari, 1993; Bogdanis et a!., 1995). Accordingly, maintenanceof PP output requires adequate replenishment of PCr. As maintenance of PP output was observedin the current study, it follows that PCr levels were adequately replenished in all threerecoveries. Thus, during 14 mm recovery, there seems to have been ample time to replenish PCrlevels, despite a significant 02 demand to the working muscles in both the AR and CAR.Previously, it has been reported that AR can result in decreased oxyhemoglobinloxymyoglobinrecovery as well as prolong PCr resynthesis when a short (15 s to 2 mm) recovery period is used(Dupont et al., 2007; Spencer et a!., 2006; Yoshida, Watari, & Tagawa, 1996). Oxygencompetition between working muscle and the aerobic process of PCr repletion did not appear tobe a factor over the longer recovery period in this study. It may be that 02 competition effectswere dispersed over the extended recovery period and were thus nullified. That is to say, despiterecovery intensities ranging from the IAT (73.2 + 6.1% V02m) to the IVT_50%AT (50.2 ± 5.3%VO2max), whichimposed substantial V02 demands, it seems the overall recovery duration wassufficient to allow potentially limited PCr repletion over along enough time period to result inadequate replenishment. However, as PCr levels were notactually measured in the current65investigation, their successful repletion can only be inferred from subject’s ability to achieve PPoutputs equivalent to their baseline values. During the 30 s recovery periods between the fivesprints PCr levels likely depleted, and this is evident in the significant main effect for time. Inter-sprint recoveries were equivalent across testing days and therefore this effect was similar on alldays and is assumed to have had no discernable effect on the treatment groups.Peak power was operationally defined as the highest 1 s mechanical power output duringeach individual sprint. Therefore, it may be that due to the operational definition of PP the sprinttask was not sensitive enough to find statistical differences in the assessment of fatigue. It ispossible that any potential effects of energy metabolism on PP output were masked by thecriteria used to determine PP. That is, subjects may have been able to reproduce PP for 1 sdespite physiological changes that would not allow them to maintain those power outputs over alonger duration. Though it is worth mentioning that the cyclist tested were significantly trained,as well as motivated, and thus it is more likely that they would have been able to reproduce theirperformances with greater reliability.A 1 s duration was selected for the determination of PP as the proportion of the totalsprint (10%) is most similar to the proportion of typical time, 5 s (16.7%), used to determine PPin a standard 30 s WAnT. Though, it should be noted that the measurement precision is lower(approx. ± 1.7%) with a shorter sample time for PP (SMI POWER, 2000). Furthermore, flywheelinertia was not considered in the calculations of power output. Lakomy (1986) showed thatduring a WAnT maximal power output was achieved before peak velocity and was 3 0-40%greater than power output at peak velocity. Therefore, it may be that power outputs reported inthis study are lower than the power outputs actually achieved. However, as subjects wereallowed to start sprints from a rolling start, the effects of not considering flywheel inertia inpower calculations were reduced. Additionally, as all sprints were started in a similar matter, anyerror incurred became systematic and would not have compromised results with random error.5.3.2 Mean PowerMean MP output during AR was significantly greater than during PR. This appeared tobe a result of a greater ability to maintain power output in thelatter sprints in the AR trialcompared to the PR trial. As the difference between MP scores became more prominent in thelast three sprints. Additionally, MP decreased significantly over time within a given sprint task.At the individual level, maximum MP over the three days tended tohappen in the AR trial.Furthermore, the majority of the initial and final maximum MP outputs occurredduring the ARtrial. Concurrent with these trends, subjects tended to experience their minimum MP outputs on66either the CAR or PR days. Thus, in this investigation AR showed a strong tendency towardmaintenance of power output during the sprint task, compared to the other two recovery modes.Several other researchers have noted a greater ability to maintain performance with theuse of an AR (Ahmaidi et al., 1996; Bogdanis et al., 1996b; Connolly et al., 2003; Corder et al.,2000; Signorile et al., 1993; Spierer et al., 2004; Thiriet et al., 1993). Of the aforementionedinvestigations, only several have noted benefits to MP specifically with an AR (Ahmaidi et al.,1996; Bogdanis et al., 1996b; Spierer et al., 2004). Ahmaidi et al. (1996) found that AR resultedin higher MP outputs at high braking forces compared to PR during a repeat force-velocity testwith increasing loads. The observed increased power performance with AR was associated witha decreased plasma L& concentration. The authors suggest that the greater L&clearance mayhave resulted in improved power outputs by reducing the amount of H accumulation, which hasbeen previously shown to inhibit glycolysis. While the finding that AR recoveryresulted inimproved MP output is in agreement with the current investigation, the interpretation of why isnot. In this study AR and CAR both resulted in enhanced L& clearance compared to PR.However, despite a L& clearance rate that was equivalent to AR with CAR, no performancebenefit was observed in the CAR trial. Therefore, the performance benefit observed in the ARtrial cannot be solely attributed to enhanced La clearance.Bogdanis et al. (1996b) noted greater MP output on a repeat 30 s sprint task separated by4 mm, when AR was used compared to PR. The improvement was notassociated with a lowerblood L& concentration or higher blood pH. These findings arevery similar to this investigation,with respect to the improved performance being dissociated fromL& clearance. The authorssuggest four possible mechanisms for the improvedperformance with AR: (1) greater PCrresynthesis, (2) lower muscle L& and [Hj, (3) increasedaerobic contribution to energy supply,and (4) changes in mechanical efficiency from increasedmuscle water content; all of which havethe potential to be affected by blood flow (Bogdanis et al., 1996b).Previously it has been shownthat during the initial 10 s of a 30 s sprint (approx. 45% of the TWof the sprint) a large portionof the ATP demand is supplied through anaerobicmetabolism (Bogdanis et al., 1996a).Specifically, in the initial 10 s PCr accounted for 34% andglycolysis 42% of the energy supply.Since the noted performance benefits in Bogdanis etal. ‘s (1 996a) investigation were attributed toa greater power output in the initial 10 sof the sprint, it was hypothesized that AR may haveeither enhanced PCr resynthesis, or increasedthe initial glycolytic contribution to the energysupply via H removal. Nevertheless, despitethis supposition, more recent works, with recoverydurations varying from 15 s to 15 mm, haveshown a decreased muscle oxygenation (Dupont et67al., 2004; Dupont et a!., 2007) and PCr resynthesis (McAinch et a!., 2004; Spencer et a!., 2006)with AR compared to PR. These findings imply that PCr resynthesis is impaired with AR, ratherthan enhanced. Thus it may be more plausible to infer that the improvement in performancenoted by Bogdanis et a!. (1 996a) was likely due to an increased initial glycolytic contribution tothe energy demand. It is possible that a similar mechanism would be responsible for theimproved performance noted in this investigation.Muscle L& concentration was not determined in this investigation, but it has beenpreviously shown that changes in plasma L& and muscle La are independent of one another(McAinch et al., 2004). Thus, the finding that the two AR intensities in this investigationresulted in lower blood L& concentrations has no direct bearing on the muscle L&concentrations. Furthermore, investigations have reported both higher (McAinch et a!., 2004;Peters-Futre et a!., 1987) and lower (Bangsbo et al., 1994; Spencer et al., 2006) muscle L&concentrations with AR. Therefore, a postulation as to what the effects of the recovery intensitiesused in this study were on muscle L& cannot be made. However, it can be hypothesized thatmuscle pH would have been higher in the active recoveries as AR has been shown to increasemuscle pH (Sairyo, Ikata, Takai, & Iwanaga, 1993; Sairyo et al., 2003) as well as blood pH(Siegler, Bell-Wilson, Mermier, Faria, & Robergs, 2006). A potentially lower [Hj in the musclemay have contributed to improved performance via a reduced inhibition of glycolytic enzymesand consequently greater glycolysis in the AR trial (Ahmaidi et aL, 1996; Karisson, Hulten &Sjodin, 1974). Slightly contrary to this statement is the fact that Siegler et a!. (2006) did not findany performance benefits with AR despite an increased blood pH. However, blood pH is notnecessarily indicative of muscle pH, and it may be that a decreased muscle pH results inimproved performance.Numerous investigations have shown that with repeat sprint tasks the aerobiccontribution to energy supply increases with the number of sprints performed (Bogdanis et al.,1996a; Gaitanos, Williams, Boobis, & Brooks, 1993; Dorado et al., 2004; Trump, Heigenhauser,Putman, & Spriet, 1996). When AR is performed between the sprints the subsequent aerobiccontribution is greater than with PR (Dorado et al., 2004). The increase in aerobic contributionhas been attributed to faster V02 kinetics (Dorado et a!., 2004; Spriet, Lindinger, McKelvie,Heigenhauser, & Jones, 1989), similar to those observed when a warm-up is performed prior tohigh-intensity exercise (Bangsbo et al., 1994). Dorado et al. (2004) concluded that AR enhancedwork capacity during high-intensity intermittent exercise by increasing the aerobicenergy yieldvia faster V02 kinetics and a longer working time. Though the precise mechanism bywhich AR68enhances work capacity was unclear. It may be that the improved performance in the AR trial inthis investigation was a result of expedited V02 kinetics too. However, ventilatory data was notmeasured during the sprint task, and therefore it cannot be determined for certain if this was infact the case. At the V028 sample (i.e.14thmm recovery) the V02 was highest in the PRprotocol, followed by the CAR then AR protocols. This seems contrary to expected outcomesince V02 should be lower during PR as the metabolic demand is minimal. However, theexercise and recovery protocol design had subjects complete the last 5 mm of the 14 millrecovery at the IVT_50%ATh in order to give them a ‘warm-up’ prior to the sprint task, as well asto minimize the differences in pre-sprint starting conditions with respect to HR, blood flow, andV02,by having all three recoveries finish at the same workload. In actuality, the ‘warm-up’ inthe PR trial resulted in a significantly greater V02 (33.0 ± 6.4 mL.kg’.min’) at the end ofrecovery (V028) compared to AR (31.7 ± 6.0 mL.kg’.min1).It may be that the addition ofexercise and increased V02 may have resulted in 02 competition between energy supply forexercise and the restorative processes of recovery. This contention is further support by thedifferences in the HR7 and HR8 values for PR and AR (108.2 ± 8.9 vs. 142.1 ± 9.4 bpm,pO.OS;and 139.2 ± 8.9 vs. 143.7 ± 11.3 bpm, p>0.05, respectively). From the9thto14thmm of recoveryduring PR HR and V02 increased drastically (11.1 ± 3.2 to 33.0 ± 6.4 mL.kg1.mmn’) whereas inAR HR was relatively steady while V02 was gradually decreasing (32.9 ± 6.6 to 31.7 ± 6.0mL.kg’.min’). Thus it would seem 02 extraction would be greater in the PR trial at this timesince overall V02 was on the rise but close to the values from the AR and CAR trials, while HRwas lower. The further uptake would be a result of the added exercise stimulus since anyrestorative processes would have already been in operation prior to the additional workload.Thus, it would appear that the V02 kinetics may very well have been slower in the PR trial, sinceit has been previously shown that V02 kinetics are faster when the 02 content of arterial blood iselevated (Balsom, Ekblom, & Sjodin, 1994).Two possible mechanisms suggested for faster V02 kinetics are: increased blood flow toexercised muscle group and/or greater maintenance of aerobic regulatory enzyme activationlevels (Bangsbo et al., 1994; Dorado et al., 2004). As to why only AR recovery resulted inimproved MP output in this investigation remains unclear. To our knowledge this is the onlyinvestigation to have examined the effects of a two-tiered intensity recovery on subsequentperformance. It seems plausible that both the CAR and AR would both maintain leg blood flow.Furthermore, leg blood flow during the PR recovery would have been close to the two active69recoveries at the start of the sprint task since all subjects finished at least the last 5 mm of the lastrecovery period cycling at their respective IVT_SOO,’OIXT workloads. Though, throughout the greaterportion of the last recovery (i.e. 9 mm of the 14 mm) leg blood flow would have beensubstantially lower in the PR trial compared to the two AR trials. Thus, while reduced leg bloodflow could account for the absence of a performance benefit in the PR trial, it does not providean explanation for the lack of a benefit in the CAR trial. The higher intensity portions of theCAR (at IAT) may have been too intense to allow sufficient recuperation, despite a greater bloodflow. This would have then had to have had a carry-over effect into the following recoveryperiod, as the remainder of the recovery period was performed at the same workload as the ARtrial. It is unlikely that any carry over effects would have had to do with PCr levels, as theduration at the IVT_50%AT recovery intensity would have allowed sufficient PCr resynthesis. Theelevated intensity may have had an effect on blood or muscle pH levels, or the hydroelectricbalance of the muscle by changingNatKpump activity (Bangsbo et al., 1992). Similarly theremay have been some form of carry-over effect in the CAR trial with respect to oxidative enzymeactivation levels. Again, the higher intensity recovery may have caused physiological changes,such as a decreased pH, that would have potentially limited oxidative enzyme activation.However, the aforementioned arguments are speculative and further research is needed tosubstantiate the claims.Lastly, it has been suggested that water shifts from the blood to the muscle, as seenduring intense sprint exercise, may increase intramuscular pressure and alter mechanicalefficiency (Bogdanis et al., 1 996b). Large increases in total muscle water from intense exercisehave previously been reported (Sjogaard & Saltin, 1982). The shifts in water are likely driven bychanges in osmolarity due to the production of metabolites and increases in blood pressure(Bogdanis et al., 1996b). The elevated intramuscular pressure over that of blood pressure mayoffset vasodilation and restrict local blood flow to certain areas of the muscle (Bogdanis et a!.,1 996b). A faster removal of such metabolites (e.g. L&) may help to reduce the osmolarityimbalance and restore homeostatic conditions more rapidly and reduce muscular inefficiency.Notwithstanding to these findings, there is some evidence to the contrary. In a veryapplied study Franchini et al. (2003) used a similar duration recovery (15 mm) to examine theeffects of a prior judo combat match on repeat upper body WAnT performance. No differencesin performance were observed in this investigation between the different recoveries.Franchini etal. (2003) note that previous investigations finding performance benefits with AR versus PR, ingeneral, used a shorter recovery duration (i.e. 6 mm or less). Interestingly, this study is then one70of few investigations finding improved performance with an AR recovery over a duration greaterthan 6 mm. One major difference between this investigation and that by Franchini et a!. (2003) isthat the current investigation exercise modalities were similar between the fatiguing work bouts,recovery, and performance task (i.e. all performed on bicycle ergometers). In the investigationby Franchini et al. (2003), subjects were fatigued during a simulated judo combat, recoveredrunning, and had their performance assessed by repeat upper body WAnT. Thus, directcomparisons between the studies are limited due to changes in the exercised muscle groups aswell as the intensities used. There is similar trend throughout the literature that limits betweenstudy comparisons since there are a wide variety of experimental designs that have been used toassess the effects of recovery intensity on performance (e.g. exercise intensity/durationltype,recovery intensity/durationltype, etc.).5.3.3 Fatigue IndexThere were no significant differences in Fl amongst the recovery groups, contrary to theprediction that differences in Fl would be inverse to MP. As expected FT increased over thenumber of sprints performed, demonstrating a larger difference between the PP and minimumpower outputs. Interestingly, the mean FT was lower for all sprints in the AR trial, indicating atrend towards greater maintenance of power output. Despite being evident as a significantlygreater MP output in the AR trial, the trend of a lower Fl in the AR trial was not statisticalsignificant.Individual scores for FT showed less distinct trends than the other performance taskvariables. The amount of subjects who had their daily and overall maximum Fl scores wasrelatively evenly distributed amongst the three testing days. This was also the case for theminimum Fl scores as well as the initial and final maximum scores. Two possible explanationscan account for this amount of variance among the individual scores. Firstly, it has been shownthat performance decrement and fatigue indices scores inherently have large variations, even intrained populations, and thus should be interpreted cautiously (Glaister et al., 2007; McGawley& Bishop, 2006). Secondly, it is possible that the FT data did not reach significance for similarreasons described for PP. That is, the operational definitions for PP and minimum power used 1 saverages, which may not have been sensitive enough to detect statistical differences. Again, the1 s duration for PP, and also minimum power, was selected to minimize the proportion of thesprint that each variable comprised. However, the shorter time comes at a cost of reducedprecision for the measurement (SMI POWER, 2000). Decrement scores have been suggested tobe more reliable for repeat-sprint exercise compared to Fl scores (Glaister,Stone, Stewart,71Hughes, & Moir, 2004). As such, it is worth noting that assessment of fatigue across the sprinttask (TaF) was analyzed using the formula described by Fitzsimons et al. (1993) andrecommended by Glaister et al. (2004) and did not show statistical significance. This formulauses MP power to assess the amount of decrement from an ideal power output to an actual poweroutput and therefore avoids the problem of reduced precision that the 1 s average may haveintroduced to the FT score. The main limitation to this formula is the assumption that maximumpower output occurs on the first sprint (Glaister et al., 2004). As this criterion was not met, FTwere presented in the results. Interestingly, despite the use of MP (i.e. a 10 s versus a 1 saverage) the TaF score was still not significantly different between groups. This lends moresupport to the first interpretation, that a lack of statistical significance was due to the inherentvariability in measures of fatigue, rather than the second interpretation. The TaF formula andscores (see Table 24) are presented in Appendix TX.Many studies examining performance after active or PR have not included a measure offatigue. This is partly due to the fact that several investigations have used TTE tests as theirperformance criterion (Dorado et al., 2004; McAinch et al., 2004; Siegler et al., 2006). Otherinvestigations have simply not reported a measure of fatigue (Gaitanos et al., 1993) or used adesign that did not allow assessment of fatigue by way of Fl or decrement scores (e.g. Ahmaidiet al., 1996). Bogdanis et al. (1996b), Signorile et al. (1993), and Spencer et al. (2006) allreported fatigue scores, and did not find any significant changes to fatigue after AR. Bogdanisand colleagues (1996b) used FT as their measure of fatigue, whereas Signorile et al. (1993) usedfatigue rate (i.e. power decrement over time, Ws’), and Spencer et al. (2006) used a workdecrement score (Fitzsimons et al., 1993). Furthermore, more similar to this study, Bogdanis eta!. (1996b) and Signorile et a!. (1993) did not find statistical differences in their measures offatigue despite improved power outputs with AR. Conversely, Spencer et al., (2006) did not findstatistical differences in work decrement, but found a reduced power output with AR. Thesimilar lack of change to the fatigue measures is likely due to the greater variability associatedwith the measure of fatigue. In contrast, Spierer et al. (2004) found that AR resulted in a reducedfatigue index per bout (i.e. FT/# of bouts) during AR compared to PR in sedentary subjects butnot in moderately trained hockey players. Congruent with this, sedentary subjects achievedhigher MP outputs with AR whereas there was no significant difference in MP output betweenrecoveries in the hockey players. Differences in the findings from Spierer et al. (2004) comparedto the other investigations are likely due to methodologicaldifferences. Specifically, the otherinvestigations performed a fixed number of sprints, whereas subjects in thelatter investigation72performed serial WAnT until exhaustion (i.e. inability to complete the test) or until power outputwas reduced to less than or equal to 70% of the first sprint.5.3.4 Total WorkTotal work demonstrated the same results as MP, which is expected, as TW is theaggregate of MP scores. That is, contrary to the hypothesized results, AR in fact resulted in thegreatest TW followed by CAR then PR. Differences were only significant between AR and PRTW scores. However, CAR may result in greater TW than PR, but these findings cannot say withcertainty whether the improvement was a result of chance alone.Among individual subjects the majority (seven) had their overall maximum TW outputon the AR day. That was followed by the CAR day (four) then the PR day (one). Consistent withthis trend is the fact that most (six) of subjects had their overall minimum TW output on the PRday, followed by the CAR day (five), then the AR day (one). Interestingly, Subjects 3 and 4, theexceptions to the trend, experienced their overall minimum and maximum on the AR and PRdays respectively, and had the other extreme score default to the CAR day. The effect of theCAR on TW appears to be quite varied as an almost equal number of subjects experience TWmaxima and minima on this day (four and five, respectively).The exact mechanism by which AR resulted in improved TW remains unclear, althoughit is obviously due to the same factors proposed for the improved MP output. Thus, it seems thatthere is an interaction between maintenance of blood flow to the working muscle and an optimalintensity with which to allow restorative processes to take place. An alternative interpretationwould be that there may be an optimal intensity that allows improved metabolism onsubsequentexercise rather than effecting restorative processes. In either case, thevariance in individual TWoutcomes may be an artifact of the procedures used to determinethreshold intensities. Since,workloads during the VO2max test were increased by 30W per stage, the thresholds could only bedetermined accurately within a 60 W range. Therefore, it could be thatsome of the subjectsperformed better in the CAR trial because their IATworkload was on the lower end on thatrange, whereas others may have performed worse becausethe workload may have been too high.Differences in relative workload intensities may havesubsequently altered the aerobiccontribution to metabolism by changing the chemicalenvironment within the muscle and henceoxidative enzyme activation levels (Balaban,1990). Or conversely, it may be that the glycolyticcontribution to metabolism was hindered via anincreased acidity (Spriet et al., 1989), sincemild-intensity recovery has been shown to reduceintracellular pH levels (Sairyo et al., 2003).However, neither of these suppositions can besupported of refuted from the present study73results, and further research is necessary to clarify the mechanism for improved work capacityduring AR.Two other investigations have noted improved TW with AR compared to PR (Signorileet al., 1993; Spierer et al., 2004). Interestingly, in the investigation conducted by Spierer andcolleagues (2004), both sedentary and moderately trained subjects performed more TW with ARcompared with PR despite no significant differences in MP output in the trained group. This islikely the result of the criteria used to determine the cut-off point for exercise bouts performed.Subjects performed bouts until they were unable to achieve 70% of the PP outputfrom the firstsprint bout. This resulted in three moderately trained subjects performing an extra sprint bout onthe AR day. In contrast, a recent investigation found no significant difference in TW performedbetween active and PR, despite a greater power decrement and lower finalPP during AR(Spencer et al., 2006). Similarly, Franchini et a!. (2003) measured TW performed butdid notfind any significant differences between active and PR. Other investigations have used TTEtrials as their performance indicator (Dorado et a!., 2004; Dupont et al., 2004; Dupont etal.,2007; McAinch et al., 2004) and therefore are not relevant for a direct comparison. However, itcould be argued that a longer TTE is indicative of more TW, but it is not known whether or notthis would hold for a repeat sprint task.5.4 Heart Rate and Volume of Oxygen ConsumedHeart rate and V02 data were collected as measures of exerciseintensity, to allowcomparisons of the recovery workloads throughout the exercise andrecovery periods as well asprior to the initiation of the sprint task. Additionally,HR was measured to provide an indirectand crude measure of blood flow, albeit total body bloodflow. Despite the varying recoveryintensities resulting in different metabolic demands,the final 5 mm of the 14 mm recoveryperiod was performed at the same intensity in all threerecovery protocols. This was an attemptto standardize the pre-sprint physiological conditions.Assessment of HR and VO2 at this samplepoint allowed the determination as to whether or not this goal wasachieved.5.4.1 Exercise and Recovery Heart RateAs expected mean HR values were different among thethree recovery intensities duringthe SE bouts and recovery periods. MeanHR was greatest during the CAR trial, followed byAR, then PR. This was to be expectedsince the recovery intervals performed during the CARwere at a higher intensity for 2 mm of the 5mm recovery periods, and 5 mm of the 14 mmrecovery period compared to AR, as wellas for the entire recovery intervals compared toPR.Similarly, the intensity during AR recovery intervalswas higher throughout the entire recovery74periods compared to PR. This demonstrates that the amount of work performed prior to eachsprint task was different between recovery conditions and had a significant physiological effect.Mean HR after the first SE bout (HR1) was highest in the PR trial, but there were nosignificant differences between the three recovery trials. This was to be expected since theworkloads were the same across all three recovery trials and subjects performed equivalentwarm-ups on all testing days. However, after the second SE bout (HR3) the effect of PR on HRbecame evident. The lack of activity during the PR interval resulted in a significantly lower HRafter the SE2 bout (HR3) compared to the other two recoveries. The lower HR value at the startof the PR SE2 bout (HR2) prevented the HR from reaching the same peak values as in the ARand CAR protocols. Heart rate prior to SE3 (HR4) was slightly greater in the AR protocolcompared to the CAR protocol, which in turn were both significantly greater than the PRprotocol. It is likely that this small difference is a result of a slower pedal cadence in the CARprotocol during the higher intensity portions. Subjects were only required to keep their cadenceabove 60 rpm, but were allowed to cycle at whatever speed they found comfortable.Consequently, while not systematically observed, anecdotal observations suggest that subjectshad lower cadences during the higher workload periods of the CAR, as several subjects werewarned to maintain their cadence above 60 rpm. The slower cadences apparently allowed for alower HR during the first 2 mm of the recovery interval that carried over into a slightly lowerfinal HR at the mm of recovery.During the final recovery period mean HR followed the expected trends, with the highestvalues occurring in the CAR trial. At the end of recovery period (HR7) HR values were notsignificantly different from each other. This provides some evidence thatthe equivalentworkload during the final 5 mm of the 14 mm recovery period was successful in standardizingthe pre-sprint conditions. Therefore it is quite likely that subjectswould have began each sprinttask with a comparable cardiac output and blood flow tothe legs on each testing day. Thus, itmay be that differences observed in performanceare related to changes that occurred earlier inthe recovery period. The sprint task performance wasnot related to HR pre-sprint. Thus, thesprint task performance did not appear to be heavily controlled by pre-exercisecardiac output orblood flow factors.5.4.2 Sprint Task Heart RateDuring the sprint task, HR did not differ significantly betweengroups. Mean HR acrossall five sprints did however mirror the trendobserved during the SE and recovery period. TheCAR SHR was highest, followed by AR, andthen PR. This suggests that there was some75residual effect on HR from the SE bouts and recovery period to the sprint task. Interestingly, thegreater amount of TW performed in the AR trial did not result in a significant change in HRcompared to the other recoveries. The differences in performance on the sprint task appeared tobe independent of HR. This is likely due to the fact that energy metabolism during high-intensityshort duration exercise is predicated by local muscle factors, rather than systemic attributes.5.4.3 Volume of Oxygen ConsumedMean V02 throughout the SE and recovery period was greatest in the CAR trial,followed by AR, then PR. This was a result of the higher recovery intensities and hence greateramount of work performed in the two active recoveries prior to the sprint task. As expected, thisagain demonstrates that the amount of work performed prior to each sprint task was differentbetween recovery conditions and had a significant physiological effect.The first and second SE bouts caused a similar V02 peak in all three recovery trials.After the first 5 mm recovery interval (V022), V02 was similar between the two activerecoveries, which were both greater than the PR V02.Despite a substantially greater workloadduring the initial 2 mm of the recovery interval in the CAR, equivalent workloads for the final 3mm of the interval resulted in a similar V02 value at the V02 sample during to the AR trial.This finding was similar to the HR data. However, contrary to the HR scores atthe same samplepoint, V02 scores post-SE2 (V023) were not significantly different between recoveries.Leadinginto the third SE bout (V024), V02 showed the same trend as the previous bout, with theexception that V02 was slightly greater in the AR trial compared to the CAR trial. Thedifference is negligible and likely due to the summation of breaths over the 20 s sample periodfor V02 data. At the V025 sample, V02 was significantly higher in theCAR trial compared tothe other two recoveries, since subjects were still riding at their IAT workload at this time.Active recovery V02 was in turn significantly greater than PR V02,as subjects were working attheir IVT_50%AT workload compared to seated rest. Although the difference was less than theprevious sample, V02 remained significantly greater in theCAR at the V026 sample timecompared to the other recoveries, in spite of the reduced workload.Obviously there was a lag inV02 to accommodate the new workload. At the9thmm of recovery (VO27) the differences inV02between the two active recoveries were nolonger significant. Fascinatingly, the addition ofIVT_50%ATworkload to the PR trial at the9thmm of recovery resulted in a substantial increase inV02,to the point that the PR V02 wassignificantly greater than the AR V02 at the V028sample. Though the difference is hardly substantial,it perhaps reflects a lack of metabolic76efficiency with the onset of exercise in the PR, compared to greater efficiency in the AR from asustained effort.Thus, while the HR and V02 data demonstrate that the SE bouts provoked similarphysiological responses among the three testing days, it is apparent that the overall physiologicaleffects throughout the exercise and recovery period are different. This was to be expected, asobviously the workloads between the three recoveries were not equivalent. Interestingly, theleast amount of work prior to the sprint task (i.e. PR trial) did not result in the best performance,as one might logically reason. In fact, it was the middle amount of work performed pre-sprint(i.e. AR trial) that resulted in the best performance, as measured by TW performed.5.5 Practical SignificanceActive recovery has been suggested to result in superior recovery from exercisecompared to PR (Ahmaidi et al., 1996; Bogdanis et al., 1996b; Spierer et al., 2004). However,the empirical evidence of this is more equivocal than the common perception. The belief that ARis beneficial to subsequent performance appears to result from historic belief that L& is a causeof fatigue in addition to the finding that AR does in fact clear La faster than PR. From apractical standpoint in performance athletics, AR would only be beneficial if it in fact didtransmit some sort of improvement to performance, regardless of the effect on L& concentration.Furthermore, the effect on performance would need to impart a significant competitiveadvantage. The results from this investigation showed that the AR recovery employed over thetwo 5 mm and one 14 mm recovery intervals resulted in statistically significantly more TWduring five 10 s sprints interspersed by 30 s, when compared to PR. However, conditions in alaboratory setting are different from those in an athletic competition. Specifically, when dealingwith sports with multiple repetitive high-intensity bouts within one competition (e.g. hockey,football, soccer, basketball), a favourable and successful outcome is rarely determined purely bytotal work capacity. The unpredictable nature of the activities is determined by a combination ofwork capacity, physical fitness, skill, and motivation, to name a few. Similarly, in morefitnessdriven competitions (e.g. track, cycling, swimming), work capacity is not the sole factordetermining success. Though, a greater work capacity would likely increase the chances for asuccessful outcome and thus is a desirable attribute.Interestingly, the data obtained in this study appear to show practical significance whenthe differences in mean MP betweengroups are converted from power outputs to velocities.Using an on-line bicycle speed and powercalculator (Zom, 2005), differences in mean MPwattage demonstrated that the averagesubject tested would have gone 10 kmhr’ faster in the77AR trial compared to the PR trial and 8.1 kmbr’faster than the CAR trial. The CAR trial wouldhave had a velocity 3.1 kmhf1 faster than the PR trial. Over 50 s of total sprint time, thesevelocities would correspond to distances of 138.9, 112.5 and 43.1 m, respectively, assuming thatthe mean MP (i.e. differences in velocity) was maintained. However, these calculations aresomewhat contrived as they do not consider changing conditions, but nonetheless demonstratethe potential for application to competition. For example it cannot be determined from thisexperiment whether these effects would hold over an event like an individual pursuit (4000m), orbe relevant in the final sprint to the finish line of a longer distance event.78CHAPTER VI: CONCLUSION6.1 ConclusionsThis study adds further knowledge to the wealth of literature surrounding the use of ARand its effects on subsequent performance. The following was concluded based on the results ofthe study:a. Active and CAR both cleared blood L& significantly faster than PR.b. Active recovery resulted in greater TW performed on the five 10 s sprints via a greatermaintenance of MP in the latter sprints compared to PR.c. Despite similar decreases in blood L& concentration between AR and CAR, nosignificant performance benefits were observed in the CAR trial. Therefore the improvedperformance in the AR trial appears to be independent of blood L& clearance.d. Active recovery at a moderate intensity (i.e. approx. 50% VO2m) may be an effectiverecovery intervention for recovery intervals of approximately 15 mm when subsequenthigh-intensity intermittent exercise requires the maintenance of power output.Therefore, this investigation confirms that a CAR, utilizing a moderate-to-high-intensityfollowed by a moderate-intensity of exercise, can successfully clear blood L&. However, theintensities used in this investigation for the CAR did not impart any significant clearance benefitabove that of a single intensity moderate AR. And furthermore, did not statistically improveperformance above that achieved from PR. Thus, for similar exercise requirements and recoverydurations it appears that a moderate intensity AR is most beneficial. This study provides moreevidence that L& is not a causative factor in the development of fatigue and that benefit of AR toperformance is not directly related to the faster clearance of La. Additionally, it provides supportfor the use of an AR to promote improved performance over moderate recovery durations (i.e.approx. 15 mm). However, further research is needed to confirm the effect of AR onperformance over this recovery duration as the literature is somewhat divided, as well as todetermine the exact mechanism by which AR is beneficial.6.2 Recommendations for Future ResearchFuture research areas for the continued acquisition of knowledge regarding AR, lactatekinetics, performance and fatigue are diverse. While it is likely that future research endeavourswill remain subdivided and specific, it is important for the resultinginterpretations to remainunified and generalized to facilitate further discussion and dissemination.796.2.1 Performance CriteriaIt is imperative that future research into the effects of AR incorporates some form ofperformance assessment. Anecdotal evidence of improved performance or logical reasoning thatincreased blood L& clearance should prevent fatigue (e.g. Gisolfi et al., 1966) can longer be thebasis for the notion that AR is beneficial to performance. There must be empirical evidence of aperformance benefit that can only come through objective assessment of performance variables.6.2.2 Active versus Passive Recovery and Duration DependencyGiven that recent investigations have demonstrated improved performance with PR overshort duration sprint and recovery intervals (Dupont et al, 2004; Dupont et al., 2007; Spencer etal, 2006), further research is still required to elucidate the time frames as well as intensities atwhich active or PR is most beneficial. Specifically, active recoveries of a moderate duration (i.e.ranging from 3-20 mm) have shown equivocal findings as to whether they are beneficial ordetrimental to performance. Therefore, future research should focus on illuminating thecircumstances and intervals over which active or PR is most appropriate. Particularly thereproducibility of some of the previous works should be tested using larger sample sizes toconfirm previous results.6.2.3 MechanismsThe mechanisms by which AR is beneficial are still undetermined and further studiesdelving into the mechanisms are needed. Similarly, as the mechanisms of muscular fatigue stillremain elusive, it follows that any insight into methods to maintain or improve performance willbe limited. As such, it follows that further research into the mechanisms of fatigue are neededand will lead to new ideas and interpretations of the processes of recovery, specifically, how orwhy AR is beneficial.The development, utilization and refinement of new technologies will play a pivotal rolein new research. Particular, Magnetic Resonance Spectroscopy (MRS) looks to be a promisingtool as it allows for non-invasive and real-time measurement of the working muscle intracellularmetabolism (Sairyo et al., 2003). Specifically, further research focused on the role of P1 and{H+] via MRS looks to be intriguing. Additionally, MRS technology may alsoprove to be usefulfor the assessment of muscular blood flow.6.3.3 Suggested Modifications and AdditionsFurther research using similar investigative models to the one employed in this studylook to benefit from the addition of more blood measures as well asthe inclusion of muscle80measures. Metabolites of key interest would be L&, H, Pi, and Ca2,in addition to examine theeffects of temperature as well as the mediation of acid-base status via Po2.81ReferencesACSM. (2006). ACSM’s Guidelinesfor Exercise Testing and Prescription(7thEd.). Baltimore:Lippincott Williams & Wilkins.Ahmaidi, S., Granier, P., Taoutaou, Z., Mercier, J., Dubouchaud, H., & Prefaut, C. 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Daily and Overall Maximum and Minimum Blood Lactate ValuesSubject 1 2 3 4 5 6 7 8 9 10 11 12PR Max. l4.8 16.3 15.1 l3.21715.6 l5.O l5.6 l’7.2 l4.3 l5.O ll.8Time3 2 7 5 4 5,6,77 5 5 5 6 3Mm. 7.8 7.6 13.2 4.7 12.9 12.8 12.1 9.3 14.3 14.7 8.85.3Time8 7 8 7 8 8 8 8 8 8 8 8Final15.6* 16.9* 15.1* 15.3* 15.9*15.7 14.814.4* 15.8*13.416.2* 10.7*AR Max. 11.1 15.6 l7.& 11.4 13.4 l6.O 14.6 12.0 l7.2 13.2 17.2 11.2Time5 6 5 5 5 7 5 5 5 5 5 3Mi 2.8 9.0 10.0 7.1 6.2 9.2 8.3 5.1 7.6 6.0 5.2 4.2Time8 7 7 7 8 8 8 8 8 8 8 8Final 11.6 15.2 13.3 14.4 13.1 16.815.8*13.4 17.0 11.9 13.9 10.2CAR Max. 13.4 l9.6 13.8 10.0 14.4 15.2 14.9 11. 15.2 12.8 12.4 11.1Time5 7 3 5 3 5 5 3 5 5 5 3Mm. 5.6 14.0 6.6 3.2 3.8 6.1 10.3 4.0 10.6 5.1 4.8 4.1Time8 8 8 8 8 8 8 8 8 8 8 8Final 14.616.9* 15.1*12.9 10.6 16.0 14.3 11.6 15.016.6*12.8 9.2Subjects 2 and 11 had two and one missing data point, respectively; Overall maximum blood La;Overall minimum blood L&;*Overall final maximum blood L&93APPENDIX IITable 17. Daily and Overall Maximum and Minimum Peak PowersSubject 1 2 3 4 5 67 8 9 10 11 12PR Max. 1113 1105 1012 1179 1050 l359 975 982 1055894 942 1290Sprint 2 5 1 1 1 2 1 21 1 2 1Mm. 991 10459071060 936 1189 847859:920 759 904 1142Sprint 3 4 2, 5 5 4, 5 55 5 4 4 3 3Initial 1068 1081 1012 1179w 1050 1328 975 951 1055894w 923 1290Final1023*1105907*1060 936 1189 847 859926*817929*1212AR Max. 1010 1189 977 1135 1057 1320 lO34 1013 1023 894985 l342Sprint3 1 1 1 1 1 2 1 2 11 1Mm. 856 1057 794 1048 969 1143 905 890 862 791 904 1228Sprintl 4 3 5 4 5 5 5 5 4 44Initial 856 1189 977 1135 1057 1320 911 1013 978 894985 1342wFinal 9521147*822 10481023*1143905* 890*862 811929* 1267*CAR Max. ll52 1141 lO68 ll8S IO’77 1312 901 lOY7 ll39 9S2 1010 1337Sprint I 1 2 2, 3 1 1 3 1 1 2 1 2Mm. 10101032: 9071109190211073 850 884888178587311149Sprint3 2 3 5 5 5 5 5 5 1 5 4Initial 1152 1141 914 1135 1077 1312 878 1037w 1139 785 1010w 1290Final 1017 1093 8921091*902 1073 850 884 888843*873 1157Overall maximum PP; Overall minimum PP; Overall initial maximum PP;*Overall final maximumPP94APPENDIX IIITable 18. Daily and Overall Maximum and Minimum Mean PowersSubject 1 2 3 4 5 6 7 89 10 11 12PR Max. 818 878 9l9814 8651039 696 809 932 821 730 1014Sprinti 1 1 1 1 1 1 1 1 1 11,2Mm. 792 853 741 668 734 802 586 615 689 569 675 913Sprint5 4 5 5 4 5 5 5 5 4 5 5Initial 818 878 919 814 865 1039 696 809 932 821 730 1014Final 792 860 741 668 739 802 586 615 689 597675 913AR Max. 844 933 888 791 8621111r822 923830 7’75 1033Sprint3 1 1 1 1 1 2 1 1 1 1 1Mm. 796 875 696 672 759 827 610 630 709 650 669 976Sprintl,5 5 4 5 4 5 5 5 5 4 5 5Initial 796 933 888 791 862 1111 707w 822w 923 830 775 1033wFinal796*875 751672* 761* 827*610630* 709* 652* 669* 976*CAR Max. 894 921 916 757 839 1079 686 817939806 743 1018Sprinti 1 2 1 1 1 1 1 1 2 1 1Mi786885 777 676 712 799 611 592 708 638 635 872Sprint5 5 4 5 5 5 5 5 5 5 5 5Initial894921 873 757 839 1079 686 817 939 750 743 1018Final786885* 784*676 712 799611*592 708 638 635 872Overall maximum MP; Overall minimum MP; Overall initial maximum MP;*Overall finalmaximum MP95APPENDIX IVTable 19. Daily and Overall Maximum and Minimum Fatigue IndexesSubject 1 2 3 4 5 6 7 8 9 10 11 12PR Max. 41.6 36.6 31.3 56.2 38.1 47.2 46.4 46.9 4O.345747.O 42.7Sprint2 5 4 4 4 4 2 4 5 5 5 4Mm. 35.7 27.6 13.2 47.6 25.3 32.0 40.7 24.5 21.3 18.0 35.8 34.9Sprint3 2,3 2 1 2 1 1 1 1 1 1 3thitial 38.0 28.5 16.0 47.6 25.6 32.0 40.7 24.5 21.3 18.0w 35.8 35.2Final 38.4 36.627.9*55.9 36.046.1*44.8 44.340.3*457*47.0*38.7AR Max. 28.4 38.9 19.4 57.1 38.8 46.0 4’7.l 48.4 32.7 36.5 43.0 40.4Sprint5 5 1 5 5 4 5 4 4 5 5 1Mlii. 11.3 25.6 11.5 48.4 28.0 28.1 34.0 32.7 9.9 14.4 37.5 38.3Sprintl 2 3 1 1 1 1 1 1 1 2 5Initial 11.3 32.0 19.4 48.4 28.0 28.1 34.0 32.7 9.9 14.4 42.4 40.4Final 28.438.9*18.8 57.138.8*42.647.1*46.9 30.6 36.5 43.0 38.3CAR Max. 47.l 33.1 32.3 64.6 34.9 41.7 41.7 S4.2 39.9 42.0 44.4so3rSprint4 5 4 4 2 5 4 5 3 4 1 2Min. 35.2 25.7 11.5 50.0 31.9 27.3 34.6 34.3 26.6 7.4 32.4 35.8Sprintl 2 1 1 1 2 1 1 1 1 2 1Initial 35.2 28.6 22.8 50.0 31.9 28.2 34.6 34.3 26.6 7.4 44.4 35.8Final40.5*33.1 11.558.9*32.1 41.7 41.254.2*34.8 42.0 44.342.6*Overall maximum Fl; Overall minimum Fl; Overall initial maximum Fl;*Overall final maximum Fl96APPENDIX VTable 20. Individual Total Work Outputs and Maxima and MinimaSubject PR AR CAR1 39890 40730 4l42O2 43320 4492O 447903 40870 39500 4.l55O4 36’74O 36330 361105 394004OOlO384406 46180 4’72AO 467507 32190 33’72O 319908 347303532O335009 39880 41150 4ll’7O1033570356003562O11 351703572O3464012 47360 4.98OO 46050Overall maximum TW; Overall minimum TW97APPENDIX VITable 21. Daily and Overall Maximum and Minimum Exercise and Recovery Heart RateValuesSubject 1 2 3 4 5 6 7 8 9PR Max. 178 180 170 170 185 160 176 172 192Time 1,3 1,3 3 3 3 1 3 3 3Mi 97 99 96 94 108 102118t96 110Time 6 6 6 6 6 6 6 6 6Initial 178w 180 167 166 177 160 175 166 188Final 107 102 107 104 116 112119*99 127AR Max. 179 l9l1’73174 186 l6& 179179 201Time 3 3 3 3 3 3 3 3 3Mm. 119 150 140 141 129 130 138 138 144Time 2 2 2 5, 6 5, 6 2 6, 7 7 6Initial 170 180w 164 169 179 161w 167 167 193wFinal 96 111110*101 112113*116115* 137*CAR Max. l8& 188 169 l’78 l9O l6&183175 2OlTime 3 3 3 3 3 3 5 3 3Mm. 133 154 141 149 129 136 136 131 149Time 2,7 2 2 4 2 2 2 8 2Initial 177 176 160 166 181 159 172167c0189Final113* 119* 110* 105* 117*110 115 106 124n 9, Subjects 10-12 were excluded; Initial, FIR at HR1; Final, HR at HR9; Overall maximum HR;Overall minimum HR; Overall initial maximum HR;*Overall final maximum HR98APPENDIX VIIMm. 166 167162Sprint 1 1 1Initial 166 167 162Final 176 176 171AR Max. 178 190 171Sprint 5 3, 5 3, 5Mi 165 178 163Sprint 1 1 1Initial 165 178 163wFinal 178190*171CAR Max.l8l 193 1’76Sprint 4, 5 4 4Mm. 168 179 162Sprint 1 1 1Initial 168 179w 162Final181* 190* 173*174 176 157 1691 1 1 1174 176 157 169178185*169 178178 184 l’7O l844,5 5 5 4,5171169:162 1731 1 1 1171 169 162 173178 184170* 184*l83 l8Sl7O1754 5 3,4,5 4,5173 170 159 1651 1 1 1173 170 159 165182* 185* 170*175Table 22. Daily and Overall Maximum and Minimum Sprint Task HeartRate ValuesSubject 1 2 3 4 5 6 8PR Max. 176 177 171 180 l8S 169 178Sprint 4, 5 3 3, 4, 5 3 5 5 5n = 7, Subjects 7 and 9-12 are excluded; Initial, HR at SHR1; Final, HR at SHR5; Overall maximumSHR; Overall minimum SUR; Overall initial maximum SHR;*Overall final maximum SHR99APPENDIX VIII4 5 6 7 8 9 10 11 1259.4 56.5 54.7 61.0 54.9 53.6 59.7 58.5 64.03 3 3 3 1 3 1 1 1,36.6 9.7 10.2 11.1 12.3 13.9 15.8 6.6 16.06 6 6 6 6 6 6 7 651.7 54.7 50.6 59.3 54.9w 46.5 59.7 58.8 64.038.525.1* 30.2*29.1 30.2 26.835.8*377*31.5*60.6S6.S 60159.2 56.5 56.56O.O55.7 65.33 3 3 1 3 1,3 3 1 138.3 24.0 29.3 26.8 28.6 23.3 31.1 29.9 29.58 8 8 6 7 7 8 8 657.6 50.9 52.7 59.2 54.3 56.5 50.6 55.7 65.338.3 24.0 29.330.2* 31.1*27.3 31.1 29.9 29.968.2 54.1 57.8 63.7 51.853t59.2 6l.O 6S.’73 3 3 3 3 3 3 3 142.4 24.6 29.6 26.5 28.4 31.0 31.3 27.1 23.87 8 8 2 8 8 8 8 8Table 23. Daily and Overall Maximum and Minimum Volume of Oxygen ConsumedValuesSubject 1 2 3PR Max. 67.6 73.0 S2.2Time 1 3 3Mm. 13.19.1:8.7Time 6 7 6Initial 67.6 63.4 46.8Final 33.7 48.4 28.5AR Max. ‘73.S 75.8 50.1Time 3 3 3Miii. 31.4 47.1 30.2Time 8 6 8Initial 70.0 65.9 45.7Final 31.4 47.6 30.2CAR Max. 70.1 82.3 51.0Time 3 3 3Miii. 36.4 48.6 32.3Time 8 8 8Initial 69.2 69.5 48.8w 57.0 52.8 53.6 55.7 51.3 54.7 57.9 58.0 65.7Final36.4*48.632.3* 42.5*24.6 29.6 27.4 28.431.0*31.3 27.1 23.8Initial, V02 at V021; Final, V02 at V028; Overall maximum V02; Overall minimum V02; Overallinitial maximum V02;*Overall final maximum VO2100APPENDIX IXSprint Task Fatigue FormulaFatigue = the percentage decrement scoreFatigue = 100 — [(Total power output ± Ideal power output) x 100]WhereTotal power output = sum of MP outputs from all sprintsIdeal power output = the number of sprintsxMPmaxTable 24. Sprint Task Fatigue ScoresSubject PR AR CAR1 2.5 3.5 7.32 1.3 3.7 2.73 11.1 11.0 9.34 9.7 8.1 4.65 8.9 7.2 8.46 11.1 15.0 13.37 7.5 8.2 6.78 14.1 14.1 18.09 14.4 10.8 12.310 18.2 14.2 11.611 3.6 7.8 6.812 6.6 3.6 9.559.1±5.1 8.9±4.2 9.2±4.1101


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