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Effects of respiratory muscle fatigue on exercise performance in healthy females Shoemaker, Andrea Paula 2003

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EFFECTS OF RESPIRATORY M U S C L E FATIGUE ON EXERCISE P E R F O R M A N C E IN H E A L T H Y F E M A L E S by A N D R E A P A U L A S H O E M A K E R B.H.K. The University of British Columbia A THESIS SUBMITED IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE in THE F A C U L T Y OF G R A D U A T E STUDIES (School of Human Kinetics) We accept this thesis as confirming to the required standard THE UNIVERSITY OF BRITISH C O L U M B I A October 2003 © Andrea Paula Shoemaker In presenting this thesis in partial fulfilment of the requirements for an advanced degree at the University of British Columbia, I agree that the Library shall make it freely available for reference and study. I further agree that permission for extensive copying of this thesis for scholarly purposes may be granted by the head of my department or by his or her representatives. It is understood that copying or publication of this thesis for financial gain shall not be allowed without my written permission. Department of tiUrTljJ fW£77CS The University of British Columbia Vancouver, Canada Date / K M / 4 I/JO'2, DE-6 (2/88) Abstract The respiratory system has not been traditionally considered a limiting factor in exercise performance however, several studies have demonstrated that respiratory muscle fatigue (RMF) occurs following high-intensity exercise as well as prolonged submaximal exercise. In order to investigate R M F as a limiting factor in exercise performance fatigue was induced in ten healthy female participants (Age = 2 6 . 8 ± 2 .0 yrs; height = 165 .7 ± 4.5 cm; weight = 57 .3 ± 7 .6 kg; V 0 2 m a x 4 3 . 3 ± 4 .7 mL-kg'-min" 1, range 3 5 . 8 to 4 9 . 5 mL-kg"'-min"'). Subjects were required to visit the lab on six separate occasions. Three test days served as control conditions where R M F was not induced and baseline measures of spirometry and exercise performance were measured. On the remaining three test days, R M F was induced and the subsequent effects on exercise performance were measured. Maximal test of aerobic capacity was performed on two of the six test days and on the remaining 4 test days participants performed tests of endurance performance. Subjects were instructed to breathe at 7 0 % of their maximal voluntary ventilation (MVV) for 15-minutes to induce RMF. Following induction of R M F exercise performance was measured on an electronically braked cycle ergometer. Ventilation during the hyperpnea task equaled 7 2 to 7 5 % M V V on the three days that R M F was induced. The induction of R M F did not significantly alter maximal aerobic power (p = 0 . 1 1 1 ) , although, exercise was ceased at a significantly lower peak heart rate (p = 0 . 0 0 2 ) and peak minute ventilation (p = 0 . 013 ) . Ratings of perceived exertion for the respiratory muscles muscles were significantly increased following the induction of R M F (p = 0 . 0 0 3 ) . Endurance performance (time to exhaustion) was reduced from 4 0 8 . 0 ± 8 4 . 9 seconds to 3 2 0 . 3 ± 71 .5 seconds following the induction of R M F (p = 0 . 0 0 2 ) without any associated changes in ii VO2, heart rate, or minute ventilation. The reduction seen in endurance performance time supports the hypothesis that a decreased time to exhaustion is seen with the induction of RMF. Maximal oxygen consumption did not decrease and therefore cannot support the hypothesis that VC_ max will be reduced following R M F induction. Respiratory muscle fatigue appears to be a limiting factor in exercise performance in healthy females. iii Table of Contents Abstract ii List of Tables V List of Figures vii List of Abbreviations viii Acknowledgements ix Introduction 1 Methods 6 Subjects 6 Experimental protocol 7 Maximal Voluntary ventilation 7 Maximal aerobic power 7 Respiratory muscle fatiguing task 9 Tests of endurance performance 10 Statistical analysis 11 Results 13 Discussion 29 References 36 Appendix A. Review of respiratory anatomy and exercise physiology 45 Appendix B. Respiratory muscle fatigue 50 Appendix C. Table-Individual subject data 73 Appendix D. Pilot study data , 83 Appendix E. Rating of perceived exertion Borg 10-point scale 92 iv List of Tables Table 1. Descriptive characteristics and baseline (resting) spirometry values. Table 2. Physiological parameters during a maximal cycle ergometer test to exhaustion. Table 3. Endurance Performance Test. Physiological parameters during constant load (80% of maximum power output) exercise to exhaustion. Table 4. Best time of Endurance Performance. Physiological parameters at maximal exercise during constant load (80% of maximum power output) exercise to exhaustion. Table 5. M V V at baseline, and following voluntary hyperpnea and exercise. Ventilation during voluntary hyperpnea task. Table 6. Summary of the reported effects of respiratory muscle fatigue (RMF) on exercise performance and/or R M strength and endurance. Table 7. Participant Characteristics. Table 8. Resting lung volumes of participants. Table 9. Ventilatory parameters at peak exercise. Individual subject data. Day 1. Table 10. Ventilatory parameters at peak exercise. Individual subject data. Day 2. Table 11. Ventilatory parameters at peak exercise. Individual subject data. Day 3. Table 12. Ventilatory parameters at peak exercise. Individual subject data. Day 4. Table 13. Ventilatory parameters at peak exercise. Individual subject data. Day 5. Table 14. Ventilatory parameters at peak exercise. Individual subject data. Day 6. Table 15. Performance at peak exercise. Individual data. Day 1. Table 16. Performance at peak exercise. Individual data. Day 2. Table 17. Performance at peak exercise. Individual data. Day 3. Table 18. Performance at peak exercise. Individual data. Day 4. Table 19. Performance at peak exercise. Individual data. Day 5. V Table 20. Performance at peak exercise. Individual data. Day 6. Table 21. Ventilation in Litres per minute during the 15-minute voluntary hyperpnea task. Individual subject data. Table 22. Maximal voluntary ventilation at rest, following hyperpnea task and exercise of of all participants. Table 23. Individual subject data, menstrual cycles (day). Table 24. Individual subject data, handgrip strength before and after the induction of R M fatigue. Table 25. Pilot data: Individual subject descriptive data. Table 26. Resting lung volumes before and after 15-minute hyperpnea task, individual subject data. Table 27. Maximal voluntary ventilation before and after the 15-minute hyperpnea task, individual subject data. Table 28. Percent drop in M V V , FEV], and F V C following 15-minute hyperpnea task, individual subject data. vi List of Figures Figure 1. R M Fatiguing Task Set-up Figure 2. Flow Chart of Experimental Protocol Figure 3. Mean values for oxygen consumption during maximal cycle ergometer test ( V O 2 max test) with and without prior induction R M fatigue. Figure 4. Mean values for heart rate (FfR) during maximal exercise ( V O 2 max test) with and without prior induction of R M fatigue. Figure 5. Mean values of minute ventilation during maximal cycle exercise (V02max test) with and without prior induction of R M fatigue. Figure 6. Mean values of carbon dioxide production during maximal cycle exercise ( V O 2 max test) with and without prior induction of R M fatigue. Figure 7. Mean values of %Sa0 2 during maximal cycle exercise (V02max test) with and without prior induction of R M fatigue. Figure 8. Mean values of duty cycle ( T I / T T O T ) during maximal cycle exercise (V02max test) with and without prior induction of R M fatigue. Figure 9. Mean values of oxygen consumption during constant load exercise (TTE @ 80% max) with and without prior induction of R M fatigue. Figure 10. Mean values for heart rate (FfR) during constant load exercise (TTE @80% max) with and without prior induction of R M fatigue. Figure 11. Mean values of minute ventilation during constant load exercise (TTE @ 80% max) with and without prior induction of R M fatigue. Figure 12. Mean values of carbon dioxide production during constant load exercise (TTE @ 80% max) with and without prior induction of R M fatigue. Figure 13. Mean values of %Sa0 2 during constant load exercise (TTE @ 80% max) with and without prior induction of R M fatigue. Figure 14. Mean values of duty cycle ( T J / T T O T ) during constant load exercise (TTE @ 80% max) with and without prior induction of R M fatigue. Figure 15. Absolute change in M V V following 15-minute hyperpnea task on test day 1, 3, and 4. Figure 16. Absolute change in M V V following maximal and constant load exercise on test days 1, 5, and 6. vii List of Abbreviations a alpha A N O V A analysis of variance B f breathing frequency BPNS bilateral phrenic nerve stimulation CMS cervical magnetic stimulation DC duty cycle DI dyspnea index E E L V end-expiratory lung volume EPT endurance performance test FEV, forced expiratory volume in 1 second FEF25-75% forced expiratory flow at 25% to 75% of F V C F E F m a x maximal forced expiratory flow F V C forced vital capacity HG hand grip HR heart rate IC inspiratory capacity IFR inspiratory flow rate IRL inspiratory resistive loading MD? maximal inspiratory mouth pressure M V V maximal voluntary ventilation NS non-significant PFT pulmonary function testing Pdi max maximal diaphragmatic pressure P| max maximal inspiratory pressure PO power output RER respiratory exchange ratio R M respiratory muscle RMF respiratory muscle fatigue RMT respiratory muscle training RPE rating of perceived exertion %Sa0 2 percent arterial oxyhaemoglobin saturation SVC sustained ventilatory capacity TTE time to exhaustion TV tidal volume V E minute ventilation V 0 2 rate of oxygen consumption V E / V 0 2 ventilatory equivalent for oxygen V C 0 2 rate of carbon dioxide production V E / V C 0 2 ventilatory equivalent for carbon dioxide V 0 2 max maximal oxygen consumption w v v max maximal power output viii Acknowledgements I am so grateful to have had the opportunity to work with Dr. Don McKenzie, he is a wonderful teacher and an amazing human being. I cannot begin to express the amount of respect I feel for him. Don, thank-you so much for sharing your lab and your wisdom with me I could not have asked for a more inspiring teacher and mentor. I would also like to thank Diana Jespersen for always helping me without hesitation. I would not have made it through this without your help, thank-you so much Diana. I will also say thank-you to my committee members Dr. Darren Warburton and Dr. Bi l l Sheel for all their help and suggestions. Thank you Darren for your help when I first began my Master's I truly learned a great deal from you. Lastly, I would like to thank my family for their endless support and comforting words. I love you very much. ix Introduction Exercise places many demands on the pulmonary system. The major function of the respiratory system during exercise is to provide the working muscles with oxygen (O2) and to remove excess carbon dioxide (CO2) via the circulatory system. During exercise, large volumes of O^need to be delivered to and utilized by the working muscles, and during maximal exercise this value can increase up to 20 times normal O2 uptake. Matching O2 supply and demand is accomplished in three ways. Firstly, the number of capillaries that are open increases to allow for greater perfusion and gas exchange (Hlasta, 2001). Consequently, at maximal exercise intensities this causes mixed venous PO2 content to fall below resting values (<20%) and increases mixed venous P C 0 2 levels to greater than 80mmFfg (Sheel, 2002), therefore placing extreme importance on alveolar to arterial gas exchange. Secondly, an increase in cardiac output helps to achieve oxygen delivery, and allows an increased blood flow through the lungs to pick up more O2 (Hlasta, 2001). As another challenge to the pulmonary system, this increased cardiac output results in considerably less time for the pulmonary capillaries to accomplish the required gas exchange. Thirdly, in order for a precise regulation of alveolar PO2 and P C 0 2 , alveolar ventilation must increase more than 20 times the resting values at maximal exercise (Sheel, 2002). Fortunately, a healthy respiratory system is capable of accomplishing this overwhelming task of force development, but it is crucial that the physiological cost to provide sufficient ventilation not be too great. Breathing pattern and duty cycle must also be precisely controlled. It is imperative that the respiratory and cardiovascular system responses to exercise are coordinated and precisely matched to the increase in metabolic requirements, and required gas exchange. The potential importance of respiratory muscle fatigue or more specifically 1 inspiratory (diaphragm) muscle fatigue has become well recognized and for exercise physiologists it has become a concern as a limiting factor in exercise performance. The diaphragm is a highly oxidative, densely capillarized muscle, composed of approximately 55% slow oxidative type I (fatigue resistant) fibres; therefore the human diaphragm is traditionally considered capable of withstanding fatigue. This holds true in most cases, as during exercise to exhaustion at intensities less than or equal to 80% of VC_ max the diaphragm in normal healthy individuals usually does not fatigue. Respiratory muscle fatigue has been documented to occur at end-exercise following high-intensity endurance exercise, as demonstrated with bilateral phrenic nerve stimulation (Johnson et al, 1993). During high-intensity endurance exercise, high levels of ventilation need to be sustained, the increased diaphragmatic activity required to generate these levels of ventilation could by itself produce diaphragmatic fatigue (Mador et al, 1996). This is cause for concern as the diaphragm is the primary muscle of inspiration as well as the most effective pressure generator for increasing alveolar ventilation. If the diaphragm is subject to fatigue following prolonged submaximal exercise and high-intensity short-term exercise, as it has been demonstrated by many authors (Loke et al, 1982; Johnson et al, 1993; Mador and Dahuja, 1996; Ker and Schultz, 1996) it is possibly a limiting factor in exercise performance. Given the demands on the respiratory system during heavy exercise, competition between respiratory and peripheral locomotor muscles for 0 2 delivery may exist, and this hypothesis is supported by demonstration of reduced leg blood flow under conditions of increased respiratory work (Harms et al, 1997). Thus exercise hyperpnea may impose a cost to the balance between central and peripheral oxygen demands, and reduce exercise 2 performance. The causes of fatigue remain somewhat unclear; they are complex and probably involve simultaneous changes at various sites within both the central nervous system and the muscle itself (Roussos and Moxham, 1985). Techniques or methods used to induce and/or quantify respiratory muscle fatigue may include having the subject inspire against a resistive load, phrenic nerve stimulation, voluntary hyperpnea, or exercising at a percent of maximal work capacity (VC_ max) to exhaustion. Mador, Rodis, and Diaz (1996) investigated whether or not diaphragm fatigue could be induced following hyperpnea at levels equal to or greater than 60% of 12-s M V V until task failure. The majority of the subjects demonstrated a 10% or greater reduction in transdiaphragmatic pressure. Mador and coworkers concluded that voluntary hyperpnea to task failure can reliably produce long-lasting fatigue of the diaphragm. Bai and his colleagues (1984) found similar results in their study and concluded that respiratory muscle fatigue induced by prior ventilatory work (short-term near-maximal normocapnic hyperpnea) impaired ventilatory muscle function and may limit endurance at high levels of ventilation. In order to investigate whether respiratory muscle fatigue is a limiting factor in exercise performance several authors have unloaded the respiratory muscles during exercise and observed the effect on performance. Exercise performance is improved, it may suggest that respiratory muscle fatigue has an effect on exercise performance. Aaron et al, (1985) examined the effect of helium/0 2 breathing on human performance in a group of rowers and found that exercise time increased by 40%. Harms and his colleagues (2000) also unloaded the respiratory muscle in attempt to observe the effects on exercise performance. They also supported the hypothesis that exercise performance 3 is affected by diaphragm fatigue but at work intensities greater than 90% VO2 max-Through techniques of loading the respiratory muscles (inspiratory resistive breathing) studies have shown that by fatiguing the diaphragm subsequent exercise performance is reduced. Mador and Acevedo (1991) induced diaphragm fatigue in their subjects using a resistive breathing protocol and measured subsequent high-intensity exercise performance. Exercise time was reduced following diaphragm fatigue and the authors concluded that respiratory muscle fatigue does indeed impair exercise performance. Other authors have been interested in the effects of ventilatory work on subsequent exercise, although increased ventilation is one of the most readily observed physiological responses to exercise, it is relatively unclear how severely this hyperpnea stresses the respiratory muscles. Martin, Heinzelman, and Chen (1982) compared short-term maximal running performance in nine subjects with and without prior ventilatory work (150-min sustained maximal ventilation) intended to decrease respiratory muscle endurance. They found that short-term running performance was reduced following the ventilatory work compared to the control group. Studies involving training of the respiratory muscles have provided evidence to support the idea that respiratory muscle fatigue impairs exercise performance, while other studies have shown no effect. Training of the respiratory muscles usually involves resistive training or hyperpnea protocols that result in an increase in respiratory muscle strength and endurance. Boutellier and his coworkers (1992) have demonstrated increases in respiratory muscle strength and endurance as well as modest increases in cycling performance in both healthy sedentary and active subjects. Although still being a controversial area in exercise physiology the results may indicate a respiratory limitation to exercise performance. 4 Investigation of respiratory muscle fatigue and its effects on subsequent exercise performance is a valid and major concern among exercise physiologists. Voluntary hyperpnea at a level equal to or greater than 60% of M V V represents a non-invasive, reliable method to induce respiratory muscle fatigue and can be demonstrated by a significant decrease in M V V values following the hyperpnea task (Mador et al., 1996). This type of voluntary hyperpnea task mimics the experience of the R M during submaximal exercise, without the entire effects of whole body exercise. The effects of a 15-minute hyperpnea task at >70% M V V on subsequent exercise performance (endurance performance and exercise capacity) has not been investigated previously. Most studies have used small sample sizes, no control group and an inspiratory resistive loading (IRL) protocol to induce fatigue of the respiratory muscles. Results of the proposed study will provide additional knowledge on respiratory muscle fatigue and the implications on exercise performance. If R M fatigue is indeed found to be a limiting factor in exercise performance, implications for respiratory muscle training will be of importance for both athletes as well as in a clinical setting for rehabilitation of patients. Hypotheses 1. Exercise performances, maximal aerobic power (VC^max) will decrease following the induction of respiratory muscle fatigue. 2. Endurance performance, defined by time to exhaustion at 80% V 0 2 max intensity, will decrease following the induction of respiratory muscle fatigue. 5 Methodology Subjects Ten healthy female subjects were recruited for this study from the University of British Columbia campus and Vancouver recreational and competitive athletic teams. A power calculation based on mean vales of maximal voluntary ventilation before and after a voluntary hyperpnea task from pilot data collected for this study was used to determine the number of subjects required (n=7.4 @ 80% power; a >0.05). A secondary power calculation was also performed (n=10 @ 80% power; a >0.05) using mean vales of endurance performance time before and after the induction of fatigue, provided in a study by Dodd and his colleagues (1989). Subjects were included if they were between the ages of 18 to 35 years, nonsmokers, without a history of pulmonary or respiratory disease and if they were recreation ally fit or competitive athletes (V0 2max < 35 mL-kg^-min"1 to >50 iriL-kg"1 -min"1). Subjects were required to perform standard pulmonary function testing to determine lung function. For all testing periods (days), subjects were required to abstain from exhaustive exercise for 24 hours prior to testing, refrain from ingestion of alcohol or caffeine for 12 hours, and food or liquids other than water for 2 hours before the testing period. Subjects received consistent verbal encouragement throughout all exercise tests and the respiratory muscle fatiguing task. Each subject completed a Physical Activity Readiness Questionnaire (Par-Q) prior to testing. Subjects rated their sensations of breathlessness and leg discomfort throughout the testing protocols using the Dyspnea Index (DI) Borg (10-point) scale (please see Appendix E for details). Menstrual phase was recorded for each subject on each test day (for details please see Table 22). 6 E X P E R I M E N T A L P R O T O C O L Ethics approval was attained from the University of British Columbia Clinical Ethics Review Board. The subjects were provided with a written description of the testing procedures prior to the first testing session. Following written informed consent, the subjects were asked to complete 6 testing sessions. A l l testing sessions took place at the Exercise Physiology Laboratory located in the Allan McGavin Sports Medicine Centre at the University of British Columbia. During the first testing session (day 1), descriptive subject data was collected (age, height, weight). Spirometry measures that were performed (Medgraphics CPX-D Metabolic Cart, St. Paul, Minnesota) included: forced vital capacity (FVC), forced expiratory volume in one second (FEV|), forced expiratory flow at 25% to 75% of F V C (FEF 2 5_ 7 5 % ) , and maximal voluntary ventilation (MVV). Maximal Voluntary Ventilation (MVV) On test day 1, the subjects became familiarized with the M V V breathing endurance test. The M V V maneuver requires the subject to as best they can breathe as quickly and deeply as possible for a 12-second period, and maximal ventilation (L-min"1) is extrapolated. The test was repeated until 3 consistent values within 5% of each other were obtained. The highest maximal ventilation achieved was used to determine the level at which the subjects breathed during the voluntary hyperpnea task. Maximal Aerobic Power (V0 2 max): Day l(control) and Day 2 Five minutes following the familiarization period the subjects engaged in an incremental exercise test to evaluate V0 2 max. For attainment of V0 2 max, the subjects warmed-up on an electronically braked cycle ergometer (LODE Excalibur, Groningen, the Netherlands) for 3 minutes at a self-selected power output. A l l subjects then 7 performed an exercise test to exhaustion using a ramp protocol beginning at 75-W and increasing by 25-watts min"1 to exhaustion. VO2 max was accepted upon the basis of reaching three of the four following criteria: (1) ±10% of the age-adjusted maximum heart rate, (2) RER value of 1.1 or greater, and/ or (3) VO2 plateau (<150 ml-min"lz) with increasing power output and/ or (4) volitional fatigue. Heart rate was monitored during the test and recorded every 15 seconds using a telemetric heart rate monitor (Polar Vantage X L , Finland). During exercise the subjects breathed room air through a low resistance, two-way non-rebreathing valve (Hans Rudolph). Ventilatory parameters were measured for the duration of the test using a 5-L mixing chamber for collection of expired gases. Average ventilatory and gas exchange parameters were recorded every breath and averaged over 15-seconds using a computerized system (Physio-Dyne, Flo IT). Inspired ventilation was measured with a flow meter (Physio-Dyne, Flo LT). Percent arterial oxyhaemobglobin saturation (%Sa02) was measured using ear oximetry and reported every 15-seconds (Ohmeda Biox 3740 pulse oximeter). In order to increase ear lobe perfusion, the pinna was rubbed with a vasodilatory nicotine cream (Finalgon, Boehringer Ingelheim). Dyspnea Index scores (leg and respiratory effort) using the Borg scale were recorded once every minute of exercise. Maximal voluntary ventilation was measured at 3- and 5-minutes post-exercise. Following the aerobic fitness test, the subjects had the opportunity to become familiarized with the respiratory muscle fatiguing equipment to be used in the following testing sessions. Please see Figure 2 for flow chart of experimental protocol. Protocols for the 5 remaining test days were randomly assigned for each participant. Test day 2 (experimental condition) began with the subjects performing a 8 M V V maneuver, the highest of 3 consistent values (within 5%) was used to calculate 70% M V V used in the respiratory muscle (RM) fatiguing task. Subjects underwent the 15-minute R M fatiguing task (details to follow). In order to ensure the subjects were fully motivated hand grip (HG) strength was measured before and immediately after the induction of R M fatigue. The subjects gripped a hand dynamometer (Lafayette Instrument Co) with maximal strength using their dominant hand for approximately one second. Hand grip strength measurements were repeated twice for each trial to ensure maximal strength was achieved, the highest value was recorded. Immediately following the R M fatiguing task the subject's M V V was measured (@ 1- and 2-minutes post fatigue) to ensure R M fatigue had occurred. After the last M V V measurement the subject immediately underwent a VC^max test (same as dayl). Maximal voluntary ventilation was measured at 3- and 5-minutes post-exercise. Respiratory Muscle Fatiguing Task On test days 2, 3, and 4 the subjects engaged in a 15-minute hyperpneic R M fatiguing task before engaging the exercise protocols. While wearing a noseclip the subjects breathed through a low resistance 2-way non-rebreathing valve (Hans Rudolph) receiving air from a Douglas Bag with a known gas concentration (21% O2, 5% CO2, and balance nitrogen). Gas was warmed and humidified via a 30-L plastic container filled (~2-L) with warm water. The subjects were instructed to breathe at a ventilation level equal to or greater than 70% of their M V V for 15-minutes (see Figure 1). The target ventilation was achieved through visual feedback of ventilation (L-min) on a computer monitor (Physio-Dyne System, Flo II), and encouragement was provided verbally throughout 9 Figure 1. R M Fatiguing Task Set-up Endurance performance exercise (80% peak power output): Test days 3, 4 (experimental) and days 5, 6 (control) Experimental test days 3 and 4 proceeded as day 2; measuring M V V and inducing R M fatigue using similar protocol as above. This test was repeated twice in order to reduce intrasubject variability. Hand grip strength was again measured before and immediately following the induction of R M fatigue. Maximal voluntary ventilation was measured post induction of R M fatigue at 1- and 2-minutes, followed immediately by an endurance performance test (EPT). The EPT was conducted at a power output corresponding to the workload at 80% VC^max obtained on day 1. This test was performed on the same cycle ergometer as day 1 set at a constant workload to exhaustion. During the first minute of exercise the workload was increased incrementally until the 80% VC>2max workload was reached. Heart rate, %SaC>2, ventilation and gas exchange variables were measured. Dyspnea index (DI) and leg discomfort scores were also recorded each minute during exercise. Time to exhaustion (TTE) was recorded at the point at which the subject reached volitional fatigue and ceased exercise, or when the 10 subject could no longer maintain 40 rpm on the cycle ergometer. Maximal voluntary ventilation was measured at 3- and 5-minutes following exercise. Test days 5 and 6 were used as control conditions and did not involve the induction of R M fatigue. The subjects were required to do an EPT as described for test 3 and 4. Heart rate, DI and leg discomfort, %SaC>2, ventilation and gas exchange parameters were recorded. Maximal voluntary ventilation was measured previous to exercise and at 3- and 5-minutes post exercise. Figure 2. Flow Chart of Experimental Protocol D a y l Descriptive Data Day 2 Spirometry & M V V VO?max M V V Familiarization: R M Fatigue Days 3 & 4 H G h~H M V V h-W EPT h-W M V V Days 5 & 6 M V V _. EPT M V V w • Statistical Analysis Mean differences in maximal voluntary ventilation (MVV), before and after the induction of respiratory muscle fatigue were analyzed using one-way analysis of variance (ANOVA) with repeated measures; statistical significance was set at a < 0.05. A 11 Tukey's HSD post hoc measure was used to make multiple comparisons among the treatment means and to determine where the significant differences exist. A repeated measures paired t-test was performed on aerobic test values from day 1 and day 2; statistical significance was set at a < 0.013, the Bonferroni correction method was used for the comparison of multiple t-tests; exercise and ventilatory parameters were compared. A repeated measures paired t-test was also used to compare mean differences among the endurance performance tests control versus experimental conditions (days 3, 4, 5, and 6). The best test of endurance performance (TTE) and corresponding exercise and ventilatory parameters of either experimental test day 3 or 4 was used and compared to the best endurance performance test of control day 5 or 6 (the worst endurance performance tests were omitted, i.e. shortest TTE). Statistical significance was set at a< 0.013 using the Bonferroni adjustment. A one-way analysis of variance with repeated measures was used to compare within and between group differences in arterial oxygen desaturation, heart rate, and cardiorespiratory variables during exercise (0%, 25%, 50%, 75%, and 100% of maximum TTE) before and after the induction of R M fatigue. Pairwise comparisons were used to locate where the significant differences existed. 12 Results Descriptive characteristics Ten healthy female participants completed the study. Mean descriptive and baseline spirometry values can be seen in Table 1. Group means for peak maximal cycle ergometer exercise parameters for test days 1 and 2 can be seen in Table 2. Peak constant load (80% of maximum power output) exercise parameters for endurance performance test days 3, 4, 5, and 6 can be seen in Table 3. A l l individual subject data can be seen in Appendix C. Table 1. Descriptive characteristics and baseline (resting) spirometry values. Values are mean ± SD; yrs, years; cm, centimeters; kg, kilograms; F E V i , forced expiratory volume in one second; F V C , forced vital capacity; F E V i / F V C , ratio of F E V i to F V C ; 25- 75%, percent of forced expiratory volume occurring between 25 and 75% of the curve; F E F m a X i maximal forced expiratory flow in litres per second. Exercise Parameters Maximal Aerobic Power (VChmax): Day 1 (control) versus Day 2 (experimental) Maximal exercise values from the VC_ m a x test on day 1 are shown in Table 2. Subjects demonstrated aerobic capacity values from 1.72 to 3.26 L-min*1 (35.8 to 49.5 mL-kg^-min"1), mean values were 2.47 ± 0.41 L-min"1 (43.3 ± 4.7 mL-kg^-min"1). This represents a modest range of fitness levels, from low to moderately trained females. The respiratory exchange ratio (RER) during the V02max test exceeded 1.10 in all but two n = 10 Age, yrs Height, cm Mass, kg F E V i , litres F V C , litres F E V j / F V C , percent F E F m a x , L-sec 1 26.8 ±2.0 165.7 ±4.4 57.2 ±7.5 3.27 ±0.56 3.89 ±0.56 83.6 ±4 .1 6.68 ± 1.23 13 subjects. Peak heart rate within 10% of predicted (226-age) was achieved in all subjects (McArdle et al, 1996). Maximal exercise was indicated by volitional fatigue. Maximal exercise values from the VO2 max test on day 2 are also displayed in Table 2. Following the induction of respiratory muscle (RM) fatigue subjects demonstrated aerobic capacity values from 1.68 to 2.96 L-min"1 (34.7 to 49.5 mL-kg" '•min'1), mean values were 2.33 ± 0.41 L-min"1 (40.7 + 4.7 mL-kg"1-min"1). During the V 0 2 max test on day 2, 8 of the 10 subjects did not achieve RER values higher than 1.10. A peak heart rate within 10% of predicted (226-age) was achieved in all but 4 subjects. Table 2. Physiological exercise parameters during a maximal cycle ergometer test to exhaustion. D a y l Day 2 Non-RMF R M F HR, bpm 185 ±4.6 179.1 ±4.7 * V E , L-min" 1 102.1 ± 15.7 92.4 ± 12.3 * V 0 2 , L-min' 1 2.47 ±0.41 2.43 ± 0.64 VO2, mL-kg^-min"1 43.3 ±4.7 40.7 ±4.7 ' V C 0 2 , L/min 1 2.73 ±0.48 2.46 ± 0.46 R E R 1.13 ±0.06 1.06 ±0.07 * IFR, L-min" 1 2.74 ±0.51 2.59 ±0.35 Sa0 2 , percentage 95.26 ±3.72 96.33 ±2.14 V E / V 0 2 , L-min 1 41.62 ±6.48 40.3 ±7.13 V E / V C 0 2 , L - m i n 1 36.87 ±3.67 38.09 ±5.55 * Denotes a significant different between trials. Values are mean ± SD; HR, heart rate in beats per minute; V E , minute ventilation in litres per minute; VO2, maximal rate of oxygen consumption in litres per minute; VO2 max> maximal rate of oxygen consumption in milliliters per kilogram per minute; V C O 2 , rate of carbon dioxide production in litres per minute; RER, respiratory exchange ratio; inspiratory flow rate in litres per minute; arterial oxygen saturation in percentage; oxygen ventilatory equivalent in litres per minute, carbon dioxide ventilatory equivalent in litres per minute. 14 Pulmonary gas exchange Ventilatory parameters V E , V C 0 2 , VO2, and RER were measured. A repeated measures paired t-test was performed on aerobic test values from day 1 and day 2. A significant difference was not seen in maximal oxygen consumption (p=0.111). Peak heart rate was significantly different between day 1 and day 2 (185 ± 4.6 versus 179 ± 4.7bpm; p=0.002). Peak minute ventilation was also significantly reduced (p=0.013), from 102.1 ± 15.7 L-min"1 on day 1 to 92.3 ± 12.2 L-min 1 on day 2. Inspiratory flow rate (IFR) was not significantly different between the two test days (p=0.390). A one-way analysis of variance with repeated measures was used to compare differences in exercise variables between R M fatigue and non-RM fatigue trials throughout maximal exercise; significance was set at a < 0.05. Heart rate, minute ventilation, carbon dioxide production, oxygen consumption, percent arterial oxygen saturation, and duty cycle during maximal exercise (0%; exercise start, 25%, 50%, 75%, and 100% of maximal exercise time [Tm a x]) were considered. No significant differences were identified for oxygen consumption, carbon dioxide production, duty cycle, or percent arterial oxygen saturation at the start of exercise, throughout exercise or at 100% TTE in the V 0 2 max test. A significant interaction effect was identified within the trials for heart rate (p=0.014), and ventilation (p=0.028). A significant reduction was seen in heart rate 100% T m a x as mentioned previously. Minute ventilation was significantly higher at 50% of T m a x following the induction of respiratory muscle fatigue (p= 0.047). Mean handgrip strength on day 2 increased from 32.1kg before the hyperpnea task to 32.4kg after the induction of R M fatigue. 15 Figure 3. Mean values for oxygen consumption during maximal cycle ergometer test (VO2 max test) with and without prior induction R M fatigue. 0 -I , , 1 1 0% 25% 50% 75% 100% Percent of endurance performance (%Tm a x) Figure 4. Mean values for heart rate (FIR) during maximal exercise (VC_ max test) with and without prior induction of R M fatigue. 20 -0 -I 1 1 1 1 0% 25% 50% 75% 100% Percent of endurance performance (%Tm a x) Denotes a significant difference between groups at corresponding T, 16 Figure 5. Mean values of minute ventilation during maximal cycle exercise (VC_ max test) with and without prior induction of R M fatigue. 0% 25% 50% 75% 100% Percent of endurance performance (%Tm a x) * Denotes a significant difference between groups at corresponding T, Figure 6. Mean values of carbon dioxide production during maximal cycle exercise (VC_ m a x test) with and without prior induction of R M fatigue. 3200 -, 0% 25% 50% 75% 100% Percent of endurance performance (%Tm a x) 17 Figure 7. Mean values of percent arterial oxygen saturation (%SaC_) during maximal cycle exercise (VO2 max test) with and without prior induction of R M fatigue. 0% 25% 50% 75% 100% Percent of endurance performance (%Tm a x) Figure 8. Mean values of duty cycle (TJ/TTOT) during maximal cycle exercise (VC_ test) with and without prior induction of R M fatigue. 0.40 -I , , , , 0% 25% 50% 75% 100% Percent of endurance performance (%Tmix) Endurance performance exercise (80% peak power output): Day 3, 4 versus 5 (control), 6 (control) Maximal exercise values from the constant load exercise test on days 3, 4, 5, and 6 are shown in Table 3. Subjects demonstrated group VC_ m a x values on days 3, and 4 following the induction of R M fatigue of 2.25 and 2.20 L-min"1 (r=0.862), time to 18 exhaustion on these days was 317.1 and 295.0s (r=0.775), peak heart rate values were 179.3 and 176.8 bpm (r=0.428), peak minute ventilation values were 94.5 and 99.6 L-min"1 (r=0.390), respectively. Subjects demonstrated mean aerobic capacity values on days 5 and 6 of 2.26 and 2.47 L-min"1 (r=0.633), peak heart rate values 182.0 and 179.8 bpm (r=0.461), and peak ventilation values 98.9 and 96.0 L-min"1 (r=0.432), respectively. Subjects demonstrated a group mean endurance performance time on day 5 of 375.0 and 368.9s (1-0.544) on day 6. Table 3. Endurance Performance Test. Physiological parameters at maximal exercise during constant load (80% of maximum power output) exercise to exhaustion. Day 3 Day 4 Day 5 Day 6 R M Fatigue R M Fatigue N o n - R M Fatigue Non-RM Fatigue T T E , seconds 311.10 ± 75.22 295.30 ± 80.01 375.00 ±76.66 368.90 ± 13.17 HR, bpm 179.3 ±3.8 176.8 ±5.5 182.0 ±3 .1 179.8 ±4.9 V E , L-min' 1 94.5 ± 12.4 99.6 ± 12.5 98.9 ±9.5 96.0 ± 10.5 V 0 2 , L - m i n 1 2.25 ±0.5 2.20 ±0.3 2.26 ±0.3 2.47 ±0.3 VO2, mL-kg^-min"1 48.25 ±7.6 48.58 ±9.0 49.35 ± 10.2 46.20 ± 5.8 V C 0 2 , L-min' 1 2.52 ±0.51 2.55 ±0.40 2.44 ± 0.49 2.55 ±0.39 R E R 1.06 ±0.08 1.04 ±0.08 0.98 ±0.09 0.99 ± 0.07 IFR, L-min 1 2.85 ±0.42 2.89 ±0.48 2.89 ±0.29 2.74 ±0.33 % S a 0 2 96.53 ± 1.68 96.30 ± 1.27 95.51 ± 1.84 93.26 ±2.85 V E / V 0 2 , L-min 1 40.22 ±4.17 40.83 ±5.32 41.07 ±4.47 37.97 ±6.39 V E / V C 0 2 , L-min' 1 38.49 ±4.51 39.80 ±5.90 41.86 ±7.29 38.50 ±5.90 Values are mean ± SD; TTE, time to exhaustion in seconds; HR, heart rate in beats per minute; V E , minute ventilation in litres per minute; V 0 2 , maximal rate of oxygen consumption in litres per minute; VO2 max, maximal rate of oxygen consumption in milliliters per kilogram per minute; V C 0 2 , rate of carbon dioxide production in litres per minute; RER, respiratory exchange ratio; IFR, inspiratory flow rate in litres per minute; arterial oxygen saturation in percentage; oxygen ventilatory equivalent in litres per minute, carbon dioxide ventilatory equivalent in litres per minute. 19 Table 4. Best time of Endurance Performance. Physiological parameters at maximal exercise during constant load (80% of maximum power output) exercise to exhaustion. Best E P T Best E P T Day 3/4 Day 5/6 R M F N o n - R M Fatigue T T E , seconds 320.30 ±71.54 408.00 ± 84.90 HR, bpm 178.5 ±4.5 182.0 ±2.5 V E , L/min 96.59 ± 11.21 99.29 ±8.11 V0 2 , L/min 2.28 ±0.43 2.31 ±0.28 VO2, mLkgmin 42.15 ±5.24 44.20 ± 3.28 V C O 2 , L/min 2.54 ±0.49 2.49 ± 0.43 R E R 1.06 ±0.08 0.98 ±0.06 IFR 2.91 ±0.42 2.94 ±0.30 %Sa02 96.32 ± 1.46 95.22 ±2.16 V E / V 0 2 , Lmin 10.62 ±3.97 40.27 ±4.61 V E / V C 0 2 , Lmin 38.68 ±4.26 40.79 ±5.26 Values are mean ± SD; TTE, time to exhaustion in seconds; HR, heart rate in beats per minute; V E , minute ventilation in litres per minute; V 0 2 , maximal rate of oxygen consumption in litres per minute; V 0 2 m a x , maximal rate of oxygen consumption in milliliters per kilogram per minute; V C 0 2 , rate of carbon dioxide production in litres per minute; RER, respiratory exchange ratio; IFR, inspiratory flow rate in litres per minute; arterial oxygen saturation in percentage; oxygen ventilatory equivalent in litres per minute, carbon dioxide ventilatory equivalent in litres per minute. A repeated measures paired samples t-test on test days 3, 4, 5, and 6 was performed to identify significant differences among the test days. Statistical comparisons of aerobic test parameters were made between the best endurance performance time of day 3 or 4 and the best TTE achieved on day 5 or 6; significance was set at a<0.013, the Bonferroni adjustment method was used for the comparison of multiple t-tests. Subjects performed a mean best TTE of 325.2 ± 75.4s following the induction of R M fatigue and a mean best TTE for day 5 of 408.0 ± 84.9s demonstrating a significant difference between the two test days (p= 0.002). A significant difference was not seen in oxygen consumption (p= 0.066), peak minute ventilation (p= 0.267), peak heart rate (p= 0.021), 20 or mean inspiratory flow rate (p=0.800). Mean HG strength decreased minimally from 32.3kg to 32.2kg following the breathing task. A repeated measures A N O V A was used to analyze differences among exercise variables throughout exercise with and without the prior induction R M fatigue (RM fatigue versus non-RM fatigue trials). The variables from the best endurance performance times of experimental test days 3 and 4, and control test days 5 and 6 were compared. Heart rate, minute ventilation, carbon dioxide production, oxygen consumption, percent arterial oxygen saturation, and duty cycle during constant load (80% Pmax) exercise (0%, 25%, 50%, 75%, and 100% of maximal TTE) were considered. No significant changes were seen between the two trials for heart rate, oxygen consumption, duty cycle or percent arterial oxygen saturation at rest or during the exercise test. Minute ventilation was significantly lower (p=0.049) at the start of exercise between the two groups. Carbon dioxide production was also significantly different (p=0.050) at the start of exercise; no significant differences were seen in CO2 production beyond that time. Figure 9. Mean values of oxygen consumption during constant load exercise (TTE @ 80% max) with and without prior induction of R M fatigue. 0% 25% 50% 75% 100% Percent of endurance time (%Tm a x). 21 Figure 10. Mean values for heart rate (FIR) during constant load exercise (TTE @80% max) with and without prior induction of R M fatigue. 40 -20 -0 -• 0% 25% 50% 75% 100% Percent of endurance time (%Tm a x) Figure 11. Mean values of minute ventilation during constant load exercise (TTE @ 80% max) with and without prior induction of R M fatigue. c 0% 25% 50% 75% 100% Percent of endurance time (%Tm a x) * Denotes a significant difference between groups at corresponding T, 22 Figure 12. Mean values of carbon dioxide production during constant load exercise @ 80% max) with and without prior induction of R M fatigue. Figure 13. Mean values of percent arterial oxygen saturation during constant load exercise (TTE @ 80% max) with and without prior induction of R M fatigue. 00 100. 99 98 97 96 95 94 93 92 R M fatigue Non-RM fatigue 0% 25% 50% 75% 100% Percent of endurance time (%Tm a x) 23 Figure 14. 80% max) 0.70 -^ 0.65 -O fc; 0.60 -_T 0.55 -CJ >, ° - 5 0 " 3 Q 0.45 -Mean values of duty cycle (TJ/TTOT) during constant load exercise ( T T E @ with and without prior induction of R M fatigue. 0.40 — R M fatigue -w—Non-RM fatigue 0% 25% 50% 75% Percent of endurance time (%T™X) 100% R E S P I R A T O R Y M U S C L E F A T I G U E 15-minute voluntary hyperpnea task Throughout the 15-minutes of voluntary hyperpnea (induction of R M fatigue) occurring on test days 2, 3, and 4, mean average ventilation values were equal to 96.63 ± 17.82 Lmin" 1 , 96.64 ± 21.46 L-min"1, and 93.65 ± 24.17 L-min"1, respectively (Table 4). These values correspond to 72.8 ± 6.7%, 74.5 ± 6.0%, and 71.7 ± 11.8% of baseline M V V on test days 2, 3, and 4, respectively. Maximal voluntary ventilation Mean maximal voluntary ventilation (MVV) on day 1 before exercise or the voluntary hyperpnea task (baseline) was 128 ± 22 L-min"1, 3-minutes following exercise M V V had increased to 133 ± 22 L-min"1, and 5-minutes post exercise M V V had nearly returned to baseline (127 ± 22 L-min"1). On day 2 of testing, baseline M V V for the group was 132 ± 27 L-min"1, 1-minute and 2-minutes following the induction of respiratory 24 muscle (RM) fatigue M V V had decreased to 114 ± 30 L-min"1 and 118 + 26 L-min"1, respectively. M V V was still reduced at 3-minutes post-exercise (125 ± 23 L-min"1) and 5-minute post-exercise (125 + 26 L-min"1). Baseline M V V values from day 1 and day 2 proved to be reproducible with an r = 0.841. Mean baseline M V V on day 3 was 131 ±27 L-min"1, at 1- and 2-minutes following the voluntary hyperpnea task M V V decreased to 118 ± 29 L-min"1 and 116 ± 27 L-min"1, in that order. At 3 and 5-minutes post-exercise M V V was still reduced to 127 + 28 L-min"1 and 125 + 29 L-min"1, respectively. On day 4 M V V baseline values were recorded and provided a group mean of 131 ± 26 L-min"1", M V V values decreased by a mean of 14 ± 8 L-min"1 and 17 ± 10 L-min"1 for the group at 1 and 2-minutes following the induction of R M fatigue. M V V was still reduced at 3 and 5-minutes post-exercise by 7 ± 8 L-min"1 and 9 ± 10 L-min"1, respectively. M V V values were reproducible for days 3 and 4 at 1-minute (r= 0.957) and 2-minutes (r=0.944) following the induction of R M fatigue. Baseline M V V values for both days 5 and 6 were 132 ± 28 L-min"1, this value dropped to 131 ± 26 L-min"1 on day 5 and to 128 ± 24 L-min" 1 on day 6 at 3-minutes post-exercise. At 5-minutes post-exercise M V V values were at 129 ± 27 L-min"1 and 127 ± 27 L-min"1 on days 5 and 6, respectively. 25 Table 5. M V V at baseline, following voluntary hyperpnea and exercise. Ventilation during voluntary hyperpnea task. Day 2 Day 3 Day 4 M V V (baseline) (L min"1) 132 ± 27 131 ± 2 7 131 ± 2 6 M V V 1-minute p o s t - R M fatigue (L min' 1) 114 ± 3 0 * 118 ± 2 9 * 117 ± 2 5 * M V V 2-minute p o s t - R M fatigue (L min"1) 118 ± 26* 116 ± 2 7 * 114 ± 2 5 * M V V 3-minute post-exercise (L min' 1) 125 ± 23 127 ± 28 124 ± 2 5 M V V 5-minute post-exercise ( L m i n 1 ) 125 ± 2 6 125 ± 29 122 ± 26 V E during 15-minute hyperpnea task (Lmin ' 1 ) 96.6 ± 17.8 96.6 ±21.5 93.7 ±24.2 V E during 15-minute hyperpnea task ( % M W ) 7 2 . 8 ± 6.7 74.53 ±6 .0 71.7 ± 11.8 * Denotes a significant different difference from baseline M V V . Values are mean ± SD; M V V in litres per minute; V E in litres per minute; V E in percent of baseline M V V . A repeated measures A N O V A was used to analyze the effects of the voluntary hyperpnea task on M V V ; significance was set at a < 0.05. On day 2 M V V was significantly reduced from baseline values at 1-minute (p=0.003) and 2-minutes (p=0.000) following the voluntary hyperpnea task, a significant difference was not seen at 3-minutes (p=0.115) and 5-minutes (p=0.152) post-exercise ( V 0 2 max test). At 1- and 2-minutes post-hyperpnea M V V had significantly decreased on day 3 (p=0.003 and p=0.000, respectively). A significant difference was not found following the constant load exercise (80% P m a x ) at 3- or 5-minutes. Following the induction of R M fatigue on day 4 M V V was significantly reduced from baseline at 1-minute (p=0.005) and 2-minutes (p=0.004) post-fatigue, whereas a significant difference was not seen at 3-minutes (p=0.142) and 5-minutes (p=0.290) post-exercise (80% Pmax)- Individual data can be seen in Appendix C. 26 Figure 15. Absolute change in M V V following 15-minute hyperpnea task on test days 1, 5, and 6. Figure 16. Absolute change in M V V following maximal and constant load exercise on test days 2, 3, and 4. Denotes a significant difference from baseline values. 27 Dyspnea Subjects rated the level of dyspnea and leg discomfort they felt throughout exercise once every minute and at the end of exercise using the Borg 10-Scale. Following the induction of R M fatigue on test day 2 during VO2 max test, nine of the ten subjects rated their breathing discomfort, at maximal exercise higher than that on day 1. Leg discomfort was rated higher at maximal exercise following the induction of fatigue in 7 of the ten subjects. Six subjects reported chest tightness and an increased difficulty of breathing throughout exercise especially at maximal exercise following the hyperpnea task, three subjects reported strong sensation of inability of getting enough air into their lungs. Eight of the ten subjects reported increased sensation respiratory effort as the reason for ceasing exercise with prior induction of R M fatigue whereas only one subject stopped exercise because of respiratory related reasons when R M fatigue was not induced prior to the exercise test. The dyspnea index and leg discomfort rating scores were significantly increased following the induction of R M F (p=0.000 and p=0.038, respectively). When fatigue was induced prior to the endurance performance test, seven of the ten subjects reported an increased sensation of respiratory effort with the induction of R M fatigue. Eight subjects ceased exercise due to leg discomfort when R M fatigue was not induced, whereas, when R M fatigue was present seven of the ten subjects reported increased respiratory and leg discomfort as the reason to quit the exercise test. Significant differences for the ratings of perceived exertion for neither the legs (p=1.00) nor respiratory muscles (p=0.394) were found following the induction of respiratory muscle fatigue. 28 Discussion The major findings of this research study were as follows: the induction of respiratory muscle fatigue caused (1) a significant decrease in cycle time to exhaustion during the endurance performance test and, (2) significant changes in physiological parameters such as heart rate, minute ventilation at the end of the maximal aerobic capacity assessment. The findings from this study indicate that R M fatigue may impose a limitation on exercise performance in normal healthy females. Respiratory Musc le Fatigue A 15-minute voluntary hyperpnea task equal to 70% of the participants M V V was chosen to induce respiratory muscle fatigue. This method of inducing R M fatigue was similar to the method employed by Mador and his associates (1996) who demonstrated that R M fatigue occurred in ten healthy males following a 10-minute hyperpnea task equal to their 60% M V V . Mador et al. measured transdiaphragmatic pressure (Pdi) during bilateral supramaximal phrenic nerve stimulation, a method considered to be the most direct and reliable procedure to assess diaphragm strength. A pilot study conducted in our laboratory identified this hyperpneic method of inducing R M fatigue as significant and reliable [for details please refer to Appendix D]. Hamnegard et al. (1996), measured transdiaphragmatic twitch pressure using cervical magnetic stimulation (CMS) following 2-minutes maximal isocapnic ventilation and found a 13% reduction in diaphragm strength. Other authors have stated that maximal sustainable ventilation decreases with time and that ventilation levels equal to 55-80% of M V V can be maintained for approximately 15-minutes. The inability to maintain high levels ventilation is thought to be related to the development of R M fatigue (Fitting, 1991). 29 Ventilation during the voluntary hyperpnea task on the three different days ranged from 93 to 97 L-min"1 or 72 to 75% of M V V . On average, a 10-14% reduction in M V V was seen on all three days in which R M fatigue was induced. The decrease in M V V was found to be significantly different from baseline values, and the reductions were found to be reproducible among the testing days. Therefore we are confident in this method of inducing R M fatigue based on our pilot work and previous research findings. Following exercise only, M V V increased from pre-exercise values by 4% following the maximal aerobic capacity test, and decreased by 1-3% following cycle to exhaustion tests; these changes were insignificant. The decline in M V V could be attributed to motivational factors, peripheral muscle contractile failure (peripheral fatigue), or a reduction in central motor drive (central fatigue). We made considerable efforts to maintain high levels of motivation by choosing only highly motivated subjects and by continually encouraging the subjects throughout the M V V maneuver. Exercise Parameters Test of Maximal Aerobic Power (V02max): Day l(control) versus Day 2. The induction R M fatigue did not significantly alter oxygen consumption during the last minute of maximal exercise, albeit, peak minute ventilation decreased 9.5% and exercise was terminated at an overall lower heart rate. The decrease in peak minute ventilation and heart rate without an associated decrease in V02maxmay be attributed to the decrease in exercise time. The respiratory quotient at end exercise (1.06 ± 0.07) was significantly reduced following the induction of fatigue compared to the control trial (1.13 ± 0.06), suggesting that skeletal muscle effort was not the same for each trial 30 Various authors have used mean inspiratory flow as an indicator of respiratory drive (Mador and Acevedo, 1996; Gardner and Meah, 1989). This variable was also not significantly different following the induction of R M fatigue compared to control indicating that the degree of respiratory effort was similar after the induction of R M fatigue, compared to the control trial. The induction of R M fatigue did not significantly alter VO2 max even though exercise duration was less following the induction of R M fatigue. An increased sensation of respiratory discomfort is the likely cause of early cessation of exercise. Subjects were asked to rate the level of dyspnea and leg discomfort they felt throughout exercise once every minute and at the end of exercise upon fatigue on scale of 1 to 10 (1= no discomfort at all; 10= maximal discomfort). Dyspneic scores and leg effort scores were significantly increased following the induction of R M fatigue. Six of the ten subjects complained of chest tightness and increased difficulty to breath throughout, as well as at the end of the exercise test following the hyperpnea task. Eight of the ten subjects rated their breathing effort higher than leg effort at the end of exercise following the induction of R M fatigue. Endurance performance exercise (80% peak power output): Day 3, 4 versus 5 (control), 6 (control). The results of this study indicate that R M fatigue is a limiting factor in exercise performance. Exercise performance was defined by endurance performance time (EPT) or time to exhaustion (TTE). EPT during the constant load (80% Pmax) exercise test was reduced by 2 2 % following the induction of R M fatigue, although no significant changes were seen in VC_, peak heart rate, minute ventilation or inspiratory flow rates during the last minute of exercise. Our findings are in partial agreement with a previous study by 31 Martin et al., (1982) who observed a 14.5% drop in treadmill run endurance performance time but also found that exercise was ceased at a significantly lower peak minute ventilation, peak oxygen consumption, and peak heart rate following the induction of R M fatigue. In contrast, Dodd and his colleagues found that the induction of R M fatigue via 10-minutes of volitional isocapnic hyperpnea had no effect on 85% peak power output to exhaustion cycle exercise performance or pulmonary function. In response to the latter study, discrepancy between the results it is likely that the ventilation during the volitional hyperpnea task was not sufficient to induce R M fatigue. It was previously stated that at maximal exercise ventilation attains approximately 70% of M V V (Fitting, 1990), whereas, Dodd and his Colleagues had their subjects breathe at a ventilation level equal to only 85% of maximal exercise ventilation, a level possibly insufficient to induce R M fatigue. Mador and Acevedo (1991) found a 23% decrease in exercise performance (90% VO2 max), they also found a significant decline in VO2, V E , and heart rate following inspiratory threshold loading when compared to control. It is possible that the different methods of inducing R M fatigue may have caused the discrepancy in our results, although, it is most likely that the higher intensity exercise and therefore shorter exercise duration caused the significant reduction in peak V 0 2 , V E , and heart rate. Endurance performance time in the present study lasted considerably longer when compared to the Mador et al., 1991 study performed at 90% VO2 max exercise. A test of endurance performance at an exercise level equal to 80% VO2 max exercise was chosen to increase the likelihood that volitional fatigue occurred due to respiratory limitation as well as lower limb fatigue rather than leg fatigue alone, as the legs tend to fatigue rapidly on high intensity cycle tests. We chose the hyperpnea method of inducing R M fatigue, as it more 32 closely resembles that of the hyperpnea experienced during exercise. Contractile fatigue of the respiratory muscles, namely the diaphragm is a likely explanation for the decrease in exercise performance, as Mador and his colleagues (1996) showed following a volitional hyperpnea task (60% M V V ) lasting approximately 8-minutes caused a significant reduction in transdiaphragmatic pressure. The decrease in Pdi max was long lasting and indicative of peripheral contractile fatigue. It is likely that contractile failure is not the sole explanation for the reduction in EPT via the induction of R M F rather it is more likely that a multifactorial process is involved and more research is warranted. Motivation was an important factor in this study, as mentioned previously only highly motivated subjects were included in this study, equal and consistent verbal encouragement was provided throughout the exercise tests. Verbal encouragement was given on regular time intervals and the same words of encouragement were used on all test days and subjects. Handgrip strength was measured before and after the induction of fatigue to determine if centrally mediated fatigue had occurred and to ensure equal levels of motivation before and following the breathing task. For most subjects handgrip strength increased or remained the same following the breathing task. Mean handgrip strength on day 2 greater following the induction of R M fatigue. On the EPT day mean HG strength decreased slightly following the breathing task. The endurance performance tests were also repeated twice to ensure that maximal effort was achieved in at least one of the test days, the worst performance time for each trial was discarded and the best EP times were analyzed. We feel confident that our subjects were equally motivated to perform exercise all test days we used for our data analysis. 33 Dyspnea Eight of the ten subjects tested had an increased sensation of respiratory discomfort during exercise following the induction of R M fatigue, and attributed both leg and respiratory discomfort as the reason for ceasing exercise. Whereas, when fatigue was not induced, only one subject complained of respiratory discomfort as the reason to stop cycling. Eight subjects had higher RPE for the leg muscles and the remaining two subjects had equal ratings for leg and R M discomfort when respiratory muscle fatigue was not induced. Increased sensation of R M discomfort appears to be an important factor in the early cessation of endurance performance exercise following the induction of fatigue. Conclusion In summary, these data illustrate that 15-minutes of voluntary hyperpnea has a detrimental effect on exercise performance during constant load exercise in healthy moderately trained females. Exercise performance was reduced from 408.0 ± 84.9 s to 320.0 ±71.5 s following the induction of fatigue. Maximal oxygen consumption was unaffected with an associated decrease in heart rate and minute ventilation during the last minute of the VO2 max test with the induction of fatigue. The fact that the induction of R M fatigue caused a decrease in exercise performance without an associated decrease in oxygen consumption has important implications to exercise performance and possibly supports research in favor of respiratory muscle training (RMT). Future Research According to the results of the present study and various others, the respiratory muscles have proven to be a possible limiting factor in exercise performance, and 34 therefore support research aimed to improve strength and endurance of the respiratory muscles. The implementation of R M T in athletic training regimes could possibly increase exercise endurance performance by decreasing sensations of respiratory discomfort at maximal exercise via the increase or improvement of respiratory muscle endurance. 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Journal of Applied Physiology, 87(2): 643-651. 43 Wragg, S., Aquilina, R., Morgan, J., Hamnegard, C , Green, M. , Moxham, J., (1992). Diaphragm fatigue following maximal ventilation in man. American Reviews of Respiratory Disease, 145: A147. Yan, S., Similowski, T., Gauthier, A . P . , Macklem, P . T . , & Bellemere, F., (1992). Effect of fatigue on diaphragmatic function at different lung volumes. Journal of Applied Physiology. 72: 1064-1067. 44 Appendix A : Review of the Literature: Review of Respiratory Anatomy and Physiology and Exercise 1.0 The Muscles of Respiration In order to thoroughly discuss the effects of respiratory muscle fatigue on exercise performance it is necessary to review the basic anatomy and physiology of the respiratory muscles. The muscles of respiration serve to change the pressure within the lungs (pleural pressure), thus leading to differences between the pressure within the gas phase of the alveoli and the pressure outside the body (Hlastala and Berger, 2001). These pressure differences result in airflow. The muscles of respiration rely on the central respiratory control system for their rhythmic activation, although they have no inherent rhythm associated with them. The respiratory muscles are embryologically, morphologically, and functionally skeletal muscles. They are mixed muscles made up of the combinations of the three principle fiber types found in all skeletal muscles. The human diaphragm consists of approximately 55% slow-oxidative (type I) fibres, whereas the remainder of the fibres consist of equal proportions of fast oxidative glycolytic (type IJA) fibres and fast glycolytic (type UB) fibres (NHLBI Workshop Summary, 1990). Muscles of respiration can be divided into two groups, inspiratory and expiratory muscle groups. The recruitment of these two muscle groups varies greatly between at rest and during exercise conditions. 1.1 Muscles of Inspiration The mechanical process of pulmonary ventilation is achieved by rhythmically changing the pressure in the thoracic cavity so that it drops slightly below atmospheric pressure and draws air in, then rises slightly above atmospheric pressure and expels this 45 air (Roussos and Macklem, 1997). Inspiratory muscles are used to elevate (expand) the chest cavity and force the diaphragm downward to increase the thoracic volume (decrease pressure). Inspiration is an active process involving contraction of the inspiratory muscles. The primary muscle of inspiration is the dome-shaped diaphragm, separating the abdominal and thoracic cavities. The overall force length characteristics of the diaphragm depend on its two main components, the costal and crural parts, and how they are linked. The diaphragm attaches to the vertebral column and to the circumference of the lower thoracic cage. The diaphragm bulges towards the thoracic cavity and the contraction of this muscle pulls down the central part, acting like a piston to increase the volume of the thoracic cavity, resulting in an increase in intraabdominal pressure and subsequent expansion of the ribcage. Other muscles of inspiration include the external intercostals; they contract during inspiration to pull the ribs forward and upward, thus increasing thoracic volume. The external intercostals muscles attach adjacent ribs and slope downward and forward. When the respiratory system is pushed to the limits of its reserve (i.e. during intense exercise), accessory muscle recruitment becomes necessary. The accessory muscles of inspiration include the sternocleidomastoid and the scalene muscles, which are attached to the first two ribs and the sternum. Only the diaphragm and external intercostals are active during normal quiet breathing (Mahler and Loke, 1981). 1.2 Muscles of Expiration The collective purpose of the expiratory muscles is to decrease thoracic volume (which drives up intrapleural pressure) and thereby force gas out of the lungs quickly (Mador and Tobin, 1992). Normal expiration during quiet breathing is an energy-saving 46 passive process that requires no muscular contraction. It is achieved by the elasticity of the lungs and thoracic cage— the tendency to return to their original dimensions when released from tension (Roussos and Macklem, 1997). When demands are placed on the respiratory system the expiratory muscles must be recruited to reduce the respiratory time and thereby increase the number of breaths per minute (Mahler and Loke, 1981). The expiratory muscles recruited to achieve expiration when there is an increased demand for O2 uptake and CO2 removal (i.e. during exercise) includes the rectus abdominus, transverse abdominus, internal obliques, external obliques, and internal intercostals. The rectus abdominus pulls down on the lower ribs while it compresses abdominal contents to push upward on the diaphragm. The internal and external obliques as well as the transverse abdominus are capable of joining in to serve this function as in forced expiration. The internal intercostals pull ribs backward and down, decreasing thoracic volume (Mador and Tobin, 1992). 1.3 Respiratory Muscle Bioenergetics As mentioned previously, at rest, inspiration is an active process whereas expiration is a passive one. Respiratory muscle contraction during moderate and heavy exercise differs significantly than at rest. With exercise, both inspiration and expiration are active processes that require considerable amounts of metabolic work. Elastic work is used for lung expansion during inspiration and elastic recoil via the aid of expiratory muscles overcomes the elastic work done on the chest during expiration. The response to exercise requires coordination of the respiratory and cardiovascular systems. Exercise increases the demand for O2 and the production of CO2 by increasing the activity and the demands of skeletal muscle. To supply the increased O2 and remove excess CO2, three 47 primary physiological changes must take place: (1) increased alveolar ventilation, (2) increased cardiac output, and, (3) redistribution of cardiac output to enhance perfusion of exercising muscles (Hlastala, 2001). At rest and during light exercise, the oxygen requirement of breathing is small, averaging 1.9 to 3.1 mL of oxygen per Litre of air breathed, or approximately 2-4% of the total energy expenditure. As breathing rate and tidal volume increase, as in moderate to heavy exercise, the energy cost rises to between 2.1 and 4.5 mL of O2 per Litre of ventilation (Mahler, Snyder, and Loke, 1980). During exercise that elicits aerobic power (VC^max), as much as 8 to 11% of the total oxygen uptake is required for respiratory muscle work in untrained individuals and as much as 15 to 16% of VO2 max and of maximal cardiac output in highly fit individual (Harms et al, 1998; Mahler, Snyder, and Loke, 1980). In ordinary active individuals, the cardiovascular system limits V0 2 max. While overall ventilation can increase by approximately 20-fold during maximal exercise, the heart increases its output by only five times that of its normal resting output. The increase in cardiac output during exercise is due to large increases in heart rate and small increases in stroke volume (Mahler and Loke, 1981). During exercise, redistribution of blood flow is an important adaptive cardiovascular mechanism that increases perfusion of exercising muscles and skin. The blood flow to the respiratory muscles therefore also increases during exercise. 2.0 Respiratory Limitations to Exercise A major function of the respiratory system during exercise is to provide the working muscles with oxygen via the circulatory system. The respiratory system may fail directly or indirectly in this vital function and thus may limit exercise. Indirect failure 48 would occur if any additional oxygen provided by an increase in ventilation were taken up by the ventilatory muscles, thus depriving the rest of the body of O2. A study has recently shown, by unloading the respiratory muscles, that the respiratory muscle work experienced under normal physiological conditions at maximal exercise exerts two types of effects on the cardiovascular response: (1) a substantial percentage of the cardiac output (up to 14-16%) is directed to the respiratory muscles to support their metabolic requirements (Harms et al, 1998) and (2) and blood flow to the working locomotor muscles is decreased due to sympathetically controlled vasoconstriction. Sheel et al., (2001) demonstrated using Doppler ultrasound techniques that leg blood flow decreased and limb vascular resistance increased following fatiguing inspiratory work. Direct failure would occur if the lung and chest wall were to fail to provide sufficient ventilation to oxygenate the blood adequately or if inefficiency of gas exchange were to lead to arterial hypoxemia (Bye et al, 1984). Lastly, although the ventilation might be temporarily adequate, the onset of respiratory muscle fatigue could eventually cause ventilation insufficiency and arterial hypoxemia. Past investigation of respiratory factors limiting exercise has been examined in terms of possible limitations arising from the function of pulmonary gas exchange, the energetics of respiratory muscles, the respiratory mechanics, and the development of respiratory muscle fatigue. The purpose of this review and the following review will focus on the development of respiratory muscle fatigue as a limiting factor in exercise performance or capacity. 49 Appendix B : Respiratory Muscle Fatigue The National Heart, Lung, and Blood Institute defines muscle fatigue as a condition in which there is a reduction in the force-generating capacity of the muscle, resulting from muscle activity under load that is reversible by rest. Respiratory muscle fatigue occurs at different sites between the brain and the diaphragm and can be divided into three categories: contractile fatigue, transmission fatigue, and central fatigue (Mador, Rodis and Diaz, 1996). Although several other respiratory muscles are recruited during whole-body exercise (i.e. sternocleidomastoid, external intercostals, and scalene muscles), the diaphragm is the primary inspiratory muscle and the most effective pressure generator for increasing alveolar ventilation and thus provides the best index of respiratory system function. Therefore, respiratory muscle fatigue, when mentioned in this review, will be referring mainly to diaphragmatic fatigue. According to Roussos et al, (1979), diaphragm fatigue occurs when the diaphragm generates pressure greater than 40% of maximum whereas fatigue of the inspiratory muscles occurs if the pleural pressure developed exceeds 50 to 70% of the maximum pressure. Fatigue also has been determined to occur more readily at low inspired oxygen concentration (Roussos et al, 1979) or when subjects breathe at higher lung volumes (Roussos and Macklem, 1977). In experimental circumstances, when loading the respiratory muscles, two main determinants of respiratory muscle fatigue are the ratio of pressure developed in inspiratory muscles to their maximal capacity (P/Pmax) and the duty cycle of the inspiratory muscles (Ti/Ttot): fatigue occurs above a certain threshold of intensity and 50 duration of contraction in the various inspiratory muscles (Roussos and Macklem, 1977). The force generating capacity of the diaphragm decreases at higher lung volumes, indicating end-expiratory lung volume as another important factor in diaphragm fatigue (Smith and Bellemere, 1987). End expiratory lung volume may be actively increased by persistent contraction of the inspiratory muscles, as in asthma. Thus, fatigue occurs with lower inspiratory pressures when end-expiratory lung volume is actively increased (Fitting, 1991). Respiratory muscle fatigue, with respect to energetics, is determined by efficiency, which is determined by the balance between the energy demand and the energy supplied, and by the ratio of external power produced to energy consumption rate (Fitting, 1991). Another possible important determinant of fatigue is the ratio of velocity of muscle shortening to maximal velocity, particularly during unimpeded breathing (Fitting, 1991). 3.0 Measures and/or Detection of Respiratory Muscle Fatigue The potential importance of respiratory, chiefly inspiratory, muscle fatigue has become well recognized, therefore the importance of reliable measurement techniques to assess respiratory muscle fatigue are also increasingly important. In order to understand fatigue mechanisms, several tests have been developed to measure the change from a non-fatigued, unloaded state to a fatigued state after a load has been applied. Such tests may include measurements of the pressures generated by the respiratory muscles, these include maximal inspiratory mouth pressure or Pi max, and transdiaphragmatic pressure (P_ m a x ) . Unfortunately, when interpreting Pi m a x , and P d i m a x , submaximal efforts (poor motivation) cannot be distinguished from central fatigue this may pose a problem with critically i l l patients, as well as with healthy normal subjects. 51 Other tests that are used to assess respiratory muscle fatigue include those that measure diaphragmatic or other inspiratory muscle electrical activity (power spectral analysis and integrated electrical activity and pressure development [Ed/Pdi])- These tests that quantify the electrical activity of such muscles also present some limitations in that they are influenced by changes in spatial relationships between the recording electrodes and the muscle. The cellular mechanisms responsible for the shifts in the power spectrum remain unknown, which casts doubt on the sensitivity and specificity of this technique. The measurement of P d j requires the placement of esophageal and gastric balloon catheters and its magnitude is dependent on the geometry of the respiratory system in addition to the contractile state of the diaphragm. To assess fatigue of the diaphragm specifically, supramaximal/bilateral phrenic nerve stimulation ( B P N S ) , i.e. measurement of twitch transdiaphragmatic pressure (P_i, t w ) and P d / Pdi max frequency curves, is currently regarded as being the most objective measure of diaphragm fatigue. These tests aim to define the capacity of the diaphragm to generate pressure independent of central control mechanisms. Another test used to assess diaphragm fatigue is the twitch-occlusion test. This measures the increase in P d j when a twitch is superimposed on the naturally activate diaphragm, to assess the degree of motor unit recruitment through central pathways. The previous tests mentioned are mostly invasive, uncomfortable for the subject, and impractical for a field setting. Therefore less invasive measures are needed even though a decrease in Pdi, tw is an unequivocal measure of diaphragm fatigue. One noninvasive measure to determine whether respiratory muscle performance is reduced proceeding exercise is to examine the ability of the respiratory muscles to generate 52 maximum force (strength) through measuring P i m a x and maximal expiratory pressures (PE m a x ) . Another method to evaluate respiratory muscle performance is to carry out short or long term respiratory endurance tasks, for example, maximal voluntary ventilation (MVV) or sustained ventilatory capacity (SVC). The changes in maximal flow tasks can also be investigated, e.g. forced expiratory volume in one second (FEVi) and forced vital capacity (FVC). Loke and Virgulto (1982) demonstrated that M V V was reduced in some subjects after running a marathon; Pi m a x and P E max were also reduced post marathon in this study, while other studies reported that M V V remained unchanged after similar endurance competitions (Hill et al, 1991, and Chevrolet et al, 1993). Studies have shown reductions in F E V i and mean expiratory flow (Hill et al, 1991, Mahler et al, 1980, and Miles et al, 1983) whereas in other studies these values remained unchanged (Loke et al, 1982, Chevrolet et al, 1993, Maron et al, 1979, and Nava et al, 1992). 3.1 Possible Mechanisms/ Causes of Respiratory Muscle Fatigue Although a high density of slow twitch fibres makes the diaphragm resistant to fatigue, respiratory muscle fatigue has been demonstrated on volitional tests following both prolonged submaximal exercise (Loke et al, 1982; Ker and Schultz, 1996) and heavy short-term exercise (Johnson et al, 1992). The causes of fatigue are complex and involve simultaneous changes at various sites within both the muscle (peripheral) and the central nervous system (CNS). According to the NHLBI Workshop Summary (1990), fatigue is likely to be the result of a dynamic process in which compensatory mechanisms are overwhelmed in a closed-loop system consisting of central motor drive, peripheral impulse propagation, excitation/contraction coupling, depletion of energy substrates and/or metabolite accumulation, and feedback modulating reflexes. 53 The condition in which muscle force generation during sustained or repetitive contraction becomes limited due to a decline in motoneuronal output is referred to as "central fatigue". By comparing the forces generated by a truly maximum voluntary to a maximum electrically stimulated contractions, an assessment of central fatigue is possible (Bigland-Ritchie et al, 1979). Although the diaphragm is a skeletal muscle, central control of the diaphragm differs from that of limb skeletal muscles (Luo et al, 2001). McKenzie et al. (1992) showed that central fatigue was more important in the diaphragm than that of limb muscle. McKenzie and his colleagues showed evidence of the development of central diaphragmatic fatigue during repeated maximal and submaximal diaphragmatic contractions. Bellemere and Bigland-Ritchie (1987) found that central fatigue played an important role in the reduced performance of the diaphragm during inspiratory resistive loading (IRL). They also found that motor drive to the diaphragm decreased progressively during repeated maximal breathing efforts. In another study it was found that electromyographic (EMG) amplitude recordings were reduced during IRL trials (Luo et al, 2001). This reduction of the diaphragm E M G responses indicates decreased central respiratory drive because LRL breathing does not cause failure of neuromuscular transmission (Bellemere & Bigland-Ritchie, 1987). Controversy still exists in the literature if central respiratory fatigue actually occurs or if it is a safety mechanism preventing complete contractile failure, further studies are required to fill in the gaps in the literature. Peripheral fatigue refers to failure at the neuromuscular junction or distal to this structure, and defined to be present when muscle force output or velocity decreases in response to direct electrical stimulation. This type of fatigue can result because of 54 alterations in the neuromuscular junction (NMJ), changes in propagation of the action potential along the sarcolemmal membrane or the t-tubules, changes of excitation-contraction coupling or due to other alterations in the muscle cell (e.g. alterations in metabolism, changes in contractile proteins). Peripheral fatigue can be further classified as "high" or "low" frequency fatigue. Aldrich (1987) suggested that loss of force at low frequencies represents an impairment of muscle at excitation-contraction coupling, whereas a decline in high frequency force generation is thought to suggest an alteration in N M J transmission, a reduction in action potential propagation into the t-tubular system, or a reduction in sarcolemmal membrane excitability (Aldrich, 1987; Bazzy and Donelly, 1993). Low frequency fatigue can occur in isolation, whereas high frequency fatigue is always associated with some alterations in muscle force generation at lower frequencies. Force generation in response to high frequency stimulation remains unimpaired in the presence of pure low frequency fatigue, thereby indicating that the contractile proteins are still capable of generating maximal force provided that sufficient calcium is released by the sarcoplasmic reticulum (SR). Therefore, a reduced level of calcium availability due to alterations in SR function or a reduction in calcium sensitivity of the myofilaments at submaximal calcium levels may represent the impaired force generation at low frequencies of stimulation. (American Thoracic Society, 2002) Unfortunately, the explanation for the impaired calcium release by the SR during contractions is not well understood. Low frequency fatigue has been demonstrated in the sternocleidomastoid and diaphragm muscles of normal subjects breathing against high resistive loads (Westerbald et al, 1990; Moxham et al, 1981) and during sustained maximal ventilation for 2-minutes (Wragg et al, 1992). 55 There are also metabolic factors and chemical changes to consider with the occurrence of muscle fatigue. If the chemical energy available to muscle or the ability of the muscle to utilize this energy becomes impaired, the muscle will fail as a force generator. Babcock et al. (1995) postulated that the effects of locomotor muscle activity, such as competition for blood flow distribution and/or extracellular fluid acidosis, in conjunction with a contracting diaphragm accounted for most of the exercised-induced diaphragm fatigue. Ward and co-workers (1992) concluded that increased diaphragm blood flow improved diaphragmatic function, thereby retarding the development of diaphragmatic fatigue. However, these results also indicate that postponing diaphragmatic fatigue via increased blood flow are through mechanisms independent of 0 2 delivery, such as alterations in perfusion pressure, extracellular fluid composition, or capillary surface available for substrate and metabolite exchange. Supinski and colleagues (1987) also support Ward and her co-workers as they reported that increasing blood flow partially reversed the loss of force generating capacity induced by repetitive high-intensity isometric contractions in an isolated diaphragm strip preparation. It is clear from the numerous studies performed that the precise cause of respiratory muscle fatigue is unknown; rather, it is probably a combination of different causes and may vary between conditions such as exercise intensity, type and duration as well as disease. Future studies and investigations are required to fill the gaps in the literature. 4.0 Methods of Inducing Respiratory Muscle Fatigue The question of whether or not the respiratory muscles become fatigued during high-intensity exercise and therefore may possibly be a limiting factor in exercise 56 performance has become a major interest to exercise physiologists. In order to answer these questions techniques to measure and induce respiratory muscle fatigue have been developed and practiced in a laboratory setting. Measurement of respiratory muscle fatigue involves assessment of respiratory muscle strength and endurance as was previously discussed. Techniques or methods used to induce respiratory muscle fatigue may include inspiration against a resistive load, voluntary hyperpnea, or exercising at a percent of maximal work capacity (VC^max) to exhaustion. Induction of respiratory muscle fatigue via loaded breathing involves inspiring against high resistance, or loaded inspiration and unloaded expiration, at a constant duty cycle. The amount of resistance is usually a predetermined percentage of maximal inspiratory pressure (P i m a x ) , or maximal diaphragmatic pressure ( P ^ max), measured on the same day as the fatigue induction. The subject is normally asked to breath against the resistance until task failure occurs, which is defined as failure to maintain the target pressure for at least 3 to 5 consecutive attempts. A duty cycle will be chosen and the subject will achieve this cycle usually with the aid of a metronome or auditory cue. Yan et al, ( 1 9 9 3 ) induced diaphragmatic fatigue in their subjects by having them breath against an inspiratory resistance requiring 6 0 % maximal transdiaphragmatic pressure with each breath until exhaustion (duty cycle of .60) . Similarly Laghi and colleagues ( 1 9 9 5 ) induced diaphragmatic fatigue in their subjects by instructing them to breath against a resistance equal to that of 6 0 % of predetermined P d i m a x with the target pressure visually displayed on an oscilloscope at a duty cycle equal to .50 . Mador et al, ( 1 9 9 1 ) and Sliwiriski et al, ( 1 9 9 6 ) achieved inspiratory muscle fatigue in their subjects by having them breath against an inspiratory threshold load while generating 8 0 % of their 5 7 predetermined maximal mouth pressure until they could no longer reach the target pressure. One of the most readily observed physiological responses to exercise is increased ventilation, although, it is uncertain how severely this hyperpnea stresses the ventilatory muscles. As an approach to answer this question authors have attempted to mimic the hyperpnea experienced during exercise in a laboratory setting. Martin et al, (1982) compared short-term maximal running performance with and without prior ventilatory work designed to reduce ventilatory muscle endurance. The work consisted of 150-minutes of sustained maximum ventilation performed isocapnically while the subjects were seated. The subjects, on average were able to maintain two thirds (68%) of their 12s-MVV. Martin and his colleagues (1982) concluded that reduced ventilatory muscle endurance alone is sufficient to decrease short-term maximal running performance. Bai et al, (1984) demonstrated that ventilatory muscle fatigue may limit endurance at high levels of ventilation. They studied the ventilatory muscle function before, during, and after short-term near-maximal voluntary normocapnic hyperpnea. Mador and associates (1996) had ten male subjects voluntarily breath at minute ventilation equal to or slightly greater than 60% of their 12s-MVV in order to determine whether diaphragmatic fatigue occurred after voluntary hyperpnea to task failure. Prior studies suggest that diaphragmatic fatigue can occur after voluntary hyperpnea at very high ventilatory levels (greater than 70% of M V V ) (Bai et al, 1984). With the aid of electromyography diaphragmatic fatigue has been shown in normal subjects hyperventilating above 70% of M V V , a ventilatory level often seen during peak exercise (Fitting, 1991). Mador and his associates (1996) concluded that long-lasting contractile fatigue of the diaphragm reliably 58 occurs after voluntary hyperpnea at levels sufficient to induce task failure. Hamnegard et al, (1996) investigated the effect of maximal isocapnic ventilation (MIV) on Pdi.-rw elicited by cervical magnetic stimulation and concluded that diaphragmatic fatigue may be a limiting factor in maximal ventilation in man. Many authors have shown that diaphragm fatigue can occur following intense exercise. Johnson and coworkers (1993) found significant diaphragmatic fatigue in subjects measuring P dj t w using BPNS before and after intense exercise at 85 and 95% of V 0 2 max- Mador and Dahuja (1996) also measured P d i during BPNS before and after subjects exercised at 70 and 75% of their maximal work capacity until volitional exhaustion and reported that diaphragmatic fatigue can be induced by high-intensity constant load exercise. Ker and Schultz (1996) have shown that inspiratory muscles do fatigue with intensive exercise. Loke et al, (1982) measured spirometry and respiratory muscle strength and endurance in runners before and after completion of a marathon race. The results showed no change in forced vital capacity (FVC), inspiratory capacity (IC), or flow rates from pre-race values, whereas, decreases in Pi m a x , P E max, Pdi ic, and M V V were demonstrated. They concluded that decrements in respiratory muscle strength and endurance suggest development of respiratory muscle fatigue after marathon running. 5.0 Effects of Respiratory Muscle Fatigue on Exercise Performance Respiratory muscle fatigue has been documented following loaded breathing, high-intensity exercise to exhaustion, sustained endurance exercise, voluntary hyperpnea to task failure, and of course during acute respiratory failure. Several different approaches have been made to investigate whether or not respiratory muscle fatigue limits exercise performance in healthy, normal individuals at various levels of fitness. 59 Past studies attempting to answer this question have included respiratory muscle unloading, respiratory muscle loading, exercise-induced respiratory muscle fatigue measures, and respiratory muscle training. In the past maximal exercise capacity was not usually considered to be limited by ventilation in normal subjects. This theory was supported by the observation that maximal exercise ventilation does not normally exceed 70% of M V V (Olafsson and Hyatt, 1969). This is slightly inaccurate because M V V is usually measured over a 12 to 15s time period and cannot be maintained for much longer. Various other authors have found that the maximal sustainable ventilation decreases with time and that the level that can exceed a 15-minute time period corresponds to 55 to 80% of M V V . Respiratory muscle fatigue most likely explains this inability to sustain M V V for more than 12 tol5 seconds (Fitting, 1991). 5.1 Respiratory Muscle Unloading According to Johnson and his colleagues (1996), the best technique to determine if respiratory muscle affects exercise performance is to first unload the respiratory muscles and second to observe whether or not performance is improved. If performance is in fact improved it may suggest that respiratory muscle fatigue had an effect on exercise performance, on the other hand if no effect is observed, it would be concluded that the degree of fatigue observed was not enough to alter human performance. Methods most commonly used to unload the respiratory muscles involve the use of reduced viscosity gases (helium) or pressure-assist ventilators. The result of unloading the respiratory muscles would be a decrease in whole-body V 0 2 secondary to the drop in respiratory V O 2 and an increase in endurance time (Johnson et al., 1996). These results 60 are based on three theoretical potential effects of unloading the respiratory muscles: (1) decrease in the work of breathing (2) decrease in blood flow demands and competition with locomotor muscles, and (3) decrease in the sensation of dyspnea (Johnson et al, 1996). A previous study performed by Aaron et al, (1985) examined the influence of helium/oxygen breathing on human performance (79% He, 2\%Oi) on a group of rowers at 80 and 90 to 95% V O 2 max to exhaustion. At the lower work intensity a significant difference in exercise time and whole-body V O 2 were not observed; however, at the higher work intensity, exercise time increased by 40% while breathing helium. Aaron and colleagues (1985) concluded from the results of this study that respiratory muscle fatigue and/or respiratory load may play a role in limiting human performance at exercise intensities greater than 90 to 95% of V O 2 max- Another method of unloading the respiratory muscles is pressure-assist; this method has been investigated by various authors (Gallagher and Younes (1989); and Marciniuk et al, 1994). The device acts as a demand regulator, sensing changes in mouth pressure and responding by partially unloading the respiratory muscles. In the studies mentioned no significant differences were observed in exercise time, whole-body V 0 2 , ventilation, or perception of effort at work intensities up to 85% of V 0 2 max. These results imply that respiratory muscle fatigue or load plays no role in overall performance at exercise intensities less than 85% of V 0 2 m a x . Harms and coworkers (2000) also unloaded the respiratory muscles using a feedback controlled proportional-assist ventilator (PAV) to reduce the work of the inspiratory muscles during exercise. In their study, respiratory muscle unloading during exercise reduced V O 2 , caused hyperventilation, and reduced the rate of change in perceptions of respiratory and limb discomfort throughout the duration of exercise. 61 Harms and his colleagues concluded that exercise performance at work intensities equal to or greater than 90% V O 2 is influenced by the work of breathing normally incurred at these levels. 5.2 Effects of Ventilatory Work on Respiratory Function Increased ventilation is a readily observed physiological response to exercise, although it is unclear how much this hyperpnea stresses the respiratory muscles. In order to answer this question many investigators have attempted to mimic this exercise hyperpnea in a laboratory setting and to observe the effects of prior ventilatory work or even respiratory muscle fatigue on subsequent exercise performance. Martin, Heinzelman, and Chen (1982), approached the previously mentioned question by comparing short-term maximal running performance in nine subjects with and without prior ventilatory work intended to decrease respiratory muscle endurance. This ventilatory work was accomplished with the subjects in a seated position and consisted of 150-minutes of sustained maximal isocapnic breathing. On average the subjects were able to maintain 68% of their 12-s M V V during this sustained long-term breathing test. Short-term maximal running performance following the ventilatory work was reduced compared to the control group (6.5 vs. 7.6 min; P< 0.01). Exercise stopped at significantly lower ventilation, and the subjects reached a significantly lower peak O2 uptake. The results of this study indicate that reduced respiratory muscle endurance by itself is a detriment to short-term exercise performance. Bai and his colleagues (1984) evaluated respiratory muscle function in five normal male subjects prior to, during and following short-term near-maximal voluntary (eucapnic) hyperpnea. Pleural and abdominal pressure measurements and diaphragm E M G during hyperpnea were taken at 62 76%, 79%, 86% of M V V , and at M V V . Decreases in P i m a x and P d i m a x were observed post-hyperpnea at 76% and 79% M V V . The decrease in P i m a x indicates that fatigue of other inspiratory muscles in addition to the diaphragm occurred. A decrease in the pressure-frequency curves of the diaphragm and the ratio of high-to-low frequency power of the diaphragm occurred in association with decreases in Pdj m a x , providing further evidence that diaphragm fatigued occurred. In order to attain higher levels of ventilation there was an increasing contribution of the expiratory muscles, as demonstrated by the analysis of the pressure-time product for the inspiratory and expiratory muscles. Bai and his coworkers concluded that respiratory muscle fatigue may limit endurance at high levels of ventilation. A study by Dodd et al., (1989) examined the effects of short-duration, high-intensity ventilatory work on subsequent exercise performance. They tested the hypothesis that 10 minutes of volitional isocapnic (85% of peak exercise ventilation) hyperpnea at a controlled frequency and tidal volume would cause a detriment to subsequent exercise performance because of respiratory muscle fatigue. The study involved 10 healthy, normal male subjects whose pulmonary function values (FVC, FEV, , FEVi /FVC) were not significantly altered by the volitional hyperpnea. Ventilation and gas exchange variables ( V 0 2 , V E , f, end-tidal P 0 2 and P C 0 2 , V E / V 0 2 , V _ / V C 0 2 , %Sa0 2) were also insignificantly altered during exercise following the volitional hyperpnea. Exercise time to exhaustion during this study did not change between treatments; therefore these observations indicate that short-term ventilatory work does not affect pulmonary function or subsequent exercise performance. Aaron et al., (1992) addressed two questions in their study (1) does exercise hyperpnea even reach a "critical useful level"? and (2) is the work of breathing at V 0 2 m a x fatiguing to the respiratory 63 muscles? In attempt to answer these two questions the subjects were required to exercise progressively to a maximal level for as long as they could and the Oncost of ventilation was determined. Tidal expiratory flow-volume and transpulmonary pressure-volume loops (Ptp) were also measured. At rest, the participant was then asked to mimic their maximum and moderate exercise Ptp-volume loops, and 0 2 cost of hyperpnea and the length of time the subjects could maintain reproduction of their maximum exercise loop was measured. At the maximum level of exercise the C^cost of ventilation was found to be 10 ± 1% of the V O 2 max, and the O2 cost of hyperpnea was measured at 9 ± 1%. The length of time the subjects could voluntarily mimic maximum exercise was, on average for all subjects, 3 to 10 times longer than the duration of maximal exercise. Aaron and his coworkers concluded that the work of breathing and O2 cost of ventilation during maximum exercise are non-fatiguing and sustainable. Hamnegard and colleagues (1996) investigated the effect of maximal isocapnic ventilation (MTV) on P d i , t w elicited by cervical magnetic stimulation. P d i , t w was measured in nine normal subjects before and after 2 minutes of MIV. Ventilation decreased by 35% for the nine subjects at 1 minute, Pdi, iw was also reduced (-24%) 10-minutes following MIV. Based on the results of this study it has been demonstrated that diaphragm contractility is reduced following MIV. Hamnegard and coworkers agree that diaphragmatic fatigue may be a limiting factor in maximal ventilation in man. Mador, Rodis and Diaz (1996) attempted to answer whether or not diaphragmatic fatigue occurs after voluntary hyperpnea to task failure. Ten healthy male subjects volunteered for this study, they were asked to breath at minute ventilation equal to or greater than 60% of their 12-s M V V until task failure. Transdiaphragmatic pressure was measured during and 10, 30, 60, and 120-minutes after 64 hyperpnea during bilateral supramaximal stimulation of the phrenic nerves. During transcutaneous stimulation, 7 of the 10 subjects displayed at least a 10% reduction in P d i following the hyperpnea task and a 10% or greater reduction in P d i was demonstrated during cervical stimulation in all 10 subjects following hyperpnea. Mador and coworkers concluded from the results of their study that voluntary hypernea to task failure can reliably produce long-lasting contractile fatigue of the diaphragm. 5.3 Respiratory Muscle Loading Another method used to examine the effects of respiratory muscle fatigue on exercise performance is to load the respiratory muscles. The most common way to load the respiratory (inspiratory) muscle is to have the subject inspire against a threshold load at a certain percentage of maximal inspiratory, as mentioned previously. Mador and Acevedo (1991) induced inspiratory muscle fatigue in ten healthy subjects by having them breath against an inspiratory load while generating 80% of their predetermined maximal mouth pressure until they could no longer reach the target pressure (subjects were able to chose own duty cycle and breathing pattern). On three separate occasions the subjects cycled to volitional exhaustion at 90% of their maximal capacity, once following inspiratory muscle fatigue, the other two occasions served as control trials without prior induction of respiratory muscle fatigue. Oxygen consumption, exercise time, heart rate, breathing pattern, and respiratory effort (using visual analogue scale [VAS]) were measured. Following the induction of fatigue exercise time was reduced compared to the control group (238±69 vs. 311±96s; P<0.001). Heart rate and oxygen consumption during the last minute of exercise were also reduced after the induction of fatigue compared to the control group. Effort of breathing reported by the subjects with 65 the use of VAS was higher after the induction of fatigue compared to the control group. The authors concluded that high-intensity exercise performance is impaired following the induction of inspiratory muscle fatigue. In another study performed by Sliwinski et al, (1996) the effect of induced global inspiratory muscle fatigue on respiratory muscle control during exercise at 30, 60, and 90% of maximal power output (W m a x ) was examined on a cycle ergometer. Inspiratory muscle fatigue was induced in a similar fashion as the previously mentioned study. Six healthy recreationally active males were asked to breath at 80% of a predetermined level of Pi m a x until task failure (duty cycle 0.6). When the subject could not reach the target pressure for five consecutive efforts inspiratory muscle fatigue was assumed. The subjects were tested on three separate occasions; the first test was used to determine maximal work capacity, which was accomplished on a cycle ergometer. The second two experimental test days required the subjects to exercise on the same cycle ergometer at the three workloads as a control run, after the induction of global inspiratory muscle fatigue. These tests were performed in random order on two separate days. Perceived breathlessness, breathing pattern, anteroposterior displacement of ribcage and abdomen, and esophageal and gastric pressures were measured. During the mild and moderate exercise bouts (30 and 60% W m a x ) no changes in ventilatory parameters were recorded, however, ventilatory response was altered during heavy exercise; both breathing frequency and minute ventilation were increased with minimal changes in tidal volume. P i m a x and Pdi were reduced by 23% and 58%, respectively. The authors concluded that global inspiratory muscle fatigue may impair exercise performance in some healthy subjects, for reasons unrelated to extreme breathlessness or other ventilatory factors. The authors concluded that the respiratory 66 system is remarkably adjustable in maintaining ventilation during exercise in the presence of contractile ventilatory impairment, even though half of the subjects in the study were unable to complete 4-minutes of exercise at 90% of V O 2 max following the induction of global inspiratory muscle fatigue. 5.4 Respiratory Muscle Training Training the respiratory muscles through resistive training or hyperpnea results in an increase in their strength and endurance and represents another approach to the question of whether or not respiratory muscle fatigue impairs exercise performance. It is well known that during whole-body exercise, the respiratory muscles are required to produce a significant amount of metabolic work, and there is also evidence to suggest the respiratory muscles adapt to exercise training in a similar fashion to the limb (skeletal) muscles. Boutellier et al, (1991) performed a study to examine the respiratory system as a limiting factor to exercise performance. Four healthy, sedentary subjects participated in the study; breathing and cycling endurance as well as physical working capacity were determined before and after a respiratory muscle training protocol. The subjects trained their respiratory system for a four-week period by breathing voluntarily 76-102.5 l/min, 30-minutes daily for five times a week. The subjects were asked to continue with their usual sedentary lifestyle. Both breathing endurance and cycle endurance increased by 268% and 50% respectively. Vital capacity, peak flow, F E V i , specific airway conductance and M V V did not change significantly following the training regime. Boutellier et al, (1992) performed another similar study with 8 normal, trained subjects. The subjects continued their habitual endurance training, with an additional 30-minutes daily breathing exercise at 85-160 L-min"1 for four weeks. The respiratory training 67 improved breathing endurance, and cycling endurance at the anaerobic threshold. After RMT, minute ventilation for a given exercise intensity was reduced and cycle performance at anaerobic threshold was prolonged. The authors concluded that the results of both studies indicate the respiratory system as a limiting factor in normal trained as well as untrained subjects. Stuessi et al, (2001) investigated the effects of a respiratory training program on exercise performance. The experimental group (E) underwent 15-weeks of 40-sessions breathing at 65-70% of their M V V for 30-minutes each session, whereas a control group (C) performed no respiratory muscle training at all. The thirteen subjects in the experimental group significantly increased their breathing endurance (+632%) whereas the 15 subjects in the control group had a nonsignificant (NS) reduction in their breathing endurance (-2%). The experimental group also significantly increased their cycling time to exhaustion at 70% of maximal work capacity (+24%), whereas the control group had a -4% reduction in exercise performance. The results of this study indicate that R M T does indeed have a positive effect on exercise performance and supports the conclusions of the previous studies mentioned. Other studies performed to investigate the effects of respiratory muscle training on exercise performance have shown contradicting results. Many of these studies consisted of small sample sizes, different respiratory training regimes and different laboratory tests of performance. The training-status of the subjects have been inconsistent so it is hard to compare the results of these different studies (Fairbarn et al, 1991; Voliantis et al, 2001). A study performed by Morgan et al, (1987) demonstrated a nonsignificant reduction in cycling performance following respiratory muscle training at 85% M V V 5 days per week for 3-weeks. Although breathing endurance appeared to be improved 68 significantly (+1575%) cycling performance at 95% VC>2max to exhaustion displayed 6% reduction. This is an interesting find as respiratory muscle fatigue as been found to occur at this intense level of exercise, and warrants further investigation of respiratory muscle fatigue as a limiting factor in exercise performance. 6.0 Recovery of Respiratory Muscle Fatigue The rate of recovery of muscle fatigue differs depending on the nature of the fatigue. Skeletal muscle fatigue can develop as a result of high (50-100-Hz) or low (10-30-Hz) rates of nerve activation. It appears that low frequency respiratory muscle fatigue has a slower recovery process compared to that of muscle fatigue occurring as a result of high frequency muscle activation. Previous studies conducted by Aubier and coworkers (1981) investigating diaphragmatic fatigue in healthy subjects, complete recovery of high frequency fatigue occurred within 25-minutes, whereas low-frequency fatigue persisted for at least 30-minutes. Yan and colleagues (1992) showed that low-frequency fatigued persisted one hour following its induction. Laghi et al., (1995) investigated the recovery pattern of diaphragmatic fatigue over 24-hours following IRL at 80% of Poi m a x until task failure. Fatigue was confirmed through the measurement of Poi using BPNS. Diaphragmatic fatigue induced in this experimental protocol resulted in large decreases in diaphragmatic contractility that persisted for at least 24-hours. 7.0 Conclusion Respiratory muscle fatigue has been shown to be a limiting factor in exercise performance. While controversy still exists in the literature, most authors agree that respiratory muscle fatigue can occur following high-intensity exercise as well as prolonged submaximal exercise, and therefore may be a limiting factor in exercise 69 performance. Although, due to incomplete and contrasting literature is necessary for further investigation of the respiratory system as a limiting factor in exercise performance. It is still uncertain whether or not diaphragm fatigue impairs exercise performance. Further studies investigating this topic will also provide a clearer picture of the mechanisms behind fatigue as well as any other ventilatory limitations to exercise in both healthy and diseased individuals. If diaphragm fatigue is indeed found to be a limiting factor in exercise performance implications for respiratory muscle training will be of importance for both athletes as well as in a clinical setting for rehabilitation in patients. 70 Table 6: Summary of the reported effects of respiratory muscle fatigue (RMF) on exercise performance and/or R M strength and endurance. Study Subjects Method of Inducing RMF Reported changes in RM function Exercise Load % change in performance Harms et al., (2000) 7 male competitive cyclists E]: unloaded R M (PAV) E 2 : loaded R M (IRL) C: unchanged R M E , : Dyspnea and Leg RPE 1 E 2 : Dyspnea and Leg RPE t when compared to controls Cycle @ 90% V0 2 max E , : t (EPT) 14 ± 5%, I V 0 2 E 2:1 EPT 15 ± 3% (both compared to control) Sliwiriski et al., (1996) 6 untrained males High IRL to exhaustion (80%P I m a x; D C @ 0.6) Pi max, Pdi ^ from baseline (sig) E: PIraax,(-23%) P d i (-58%) from baseline and C (sig), f V E , f ( s ig ) @ rest C: 30%,60%, 90% V0 2 max (4-min stages) E: 30%,60%, 90% V0 2 max following R M F cycle ergometer No diff in V 0 2 , C 0 2 output or HR b/w groups Hamnegard et al., (1996) 9 males untrained 2-min MIV PdiiTw(-23%) 10-min post; (-13%) 60-min post MIV (sig) During C M S Exercise not performed Not applicable Mador et al., (1996) 7 males 60% M V V to exhaustion Pdi B P N S (-10%) in 7/10 subjects (sig) C M S all subjects(-10%) (sig) 60-min post P^ sig reduced Exercise not performed Not applicable McConnell et al., (1996) 24 mod-trained males See exercise Load Pi peak (-10%) Paverage(-8%) Multi-stage incremental shuttle run to volitional fatigue (10-15-min) Not applicable; Showed severity of fatigue is related to baseline strength of R M Ker & Schultz (1996) 10 trained runners (7 males; 3 females) See exercise load Pi max 3 days post-race (NS) Turn I R M ( -26.5%) 3 days post-race (sig) Ultra-marathon (87km) Not Applicable Mador et al., (1993) 10 untrained (sedentary) males See exercise load Pdi ,xw (-17.5%) @ 10-min post (sig); (-7%) @ 60-min post Ex 80% W m a x to volitional exhaustion on bicycle erg. Not Applicable 71 Johnson et al., (1992) 12 males (range of fitness levels) See exercise load E l : Pdi.Tw (-8 to -32%); P d i Tetanic (-21% @ 1 0 - H z & - 1 3 % @ 20-Hz) @ all lung voumes (sig) Pdi, Tw (-15%) @ F R C (sig) E , : 9 5 % V 0 2 m a x ; & E 2 : 8 5 % V 0 2 m a x to exhaustion Short term run on treadmill Not Applicable Mador & Acevedo, (1991) 10 (7males; 3 females) Inspiratory threshold load @ 8 0 % P I m a x Not Applicable 90% V 0 2 m a x t o exhaustion on cycle ergometer E P T (-23.5%) (sig) @ last min of exercise V 0 2 , H R lower after induction of fatigue (sig) H i l l et al., (1991) 12 trained males See exercise load F V C (-7.1%) F E V , (-8.4%) FEF 2 5.75% (-15%) - a l l sig M V V no change Endurance triathlon Not Applicable Dodd et al., (1989) 10 aerobically trained males 10-min volitional isocapnia hyperpnea (85% exercise V E ) N S change in ventilation or gas exchange variables 85% peak exercise power output to exhaustion on cycle ergometer N S in time to exhaustion, P F measures Mart in et al., (1982) 9 (5 females; 4 males) 150-min sustained maximal ventilation (isocapnic) N S change in M V V , F E V , , F V C Treadmill run to exhaustion (self selected running speed; 1%T incline/min) E P T -14.5%) sig. exercise ceased @ lower V 0 2 , V E , & H R (sig) Loke et al., (1982) 4 males See exercise load Pdi (-20%) P I m a x ( - 1 6 . 5 % ) P E m a x ( - 2 8 % ) M V V ( - 1 0 % ) A l l sig N S D in IC, F V C , flow rates Marathon race (42.2-km) Not Applicable C , Control group; D C , Duty cycle (T^ T T o l ) ; E , Experimental group; E P T , Endurance performance time; R P E , Rating of perceived exertion; T L i m , respiratory endurance time. 72 Appendix C. Tables: Individual Subject Data Table 7. Participant Characteristics. Subject (n=10) Age (yrs) Height (cm) Mass (kg) 1 2 3 4 5 6 7 8 9 10 25 26 28 26 29 31 26 26 24 27 168.1 164.3 172.5 166.7 165.6 164.0 173.0 160.8 162.3 160.0 69.0 55.5 66.5 63.4 57.5 54.4 58.7 52.5 51.6 43.6 Mean SD 26.8 2.0 165.7 4.5 57.3 7.6 yrs, years; cm, centimeters; kg, kilograms. Table 8. Resting lung volumes of participants. Subject FVC (L) FEVi (L) FEVi/FVC (%) 25-75% F E F m a x (L-sec1) FEVi %Pred FVC %Pred 1 4.12 3.19 77.51 2.70 7.53 96.65 106.23 2 4.07 3.67 90.17 4.50 6.2 116.88 111.2 3 4.44 3.75 84.46 3.90 6.48 111.28 111.28 4 3.53 2.73 77.34 2.40 5.05 84.78 93.63 5 3.35 2.73 81.49 3.67 6.57 87.22 91.28 6 4.25 3.78 87.06 4.60 7.24 124.75 119.38 7 4.55 3.88 85.27 3.86 6.02 114.58 112.59 8 3.53 2.96 83.85 2.97 6.04 98.01 100.57 9 4.24 3.71 87.50 4.11 9.59 119.29 117.45 10 2.81 2.31 82.20 2.51 6.07 77.52 81.45 Mean SD 3.89 0.56 3.27 0.56 83.69 4.17 3.52 0.82 6.68 1.23 103.10 16.43 104.51 12.42 FVC, forced vital capacity; F E V ^ forced expiratory volume; F E V i / F V C , ratio of F E V i to F V C ; FEF 2 5 - 7 5 % , percent of forced expiratory volume occurring between 25 and 75% of the curve; F E F m a x , maximal forced expiratory flow in litres per second, F E V i pred, percent of predicted F E V i actually achieved; F V C % pred, percent of predicted F V C actually achieved. 73 Table 9. Ventilatory parameters at peak exercise. Individual subject data. Day 1. Subject VE(BTPS) V C 0 2 V E / V 0 2 V E / V C O _ R E R 1 119.07 32.43 34.28 32.08 1.13 2 124.40 45.18 54.84 47.35 1.24 3 92.86 37.40 36.59 40.66 1.04 4 94.18 37.76 33.26 33.98 1.05 5 95.00 31.43 36.92 34.20 1.11 6 118.80 37.16 38.51 34.25 1.19 7 104.84 36.67 35.80 34.13 1.10 8 91.14 36.71 39.03 36.10 1.11 9 106.65 36.18 50.29 46.35 1.17 10 73.73 37.82 43.48 41.84 1.14 Mean 102.07 36.87 40.30 38.09 1.13 SD 15.69 3.67 7.13 5.55 0.06 V E , minute ventilation in litres per minute; V 0 2 , 0 2 consumption in litres per minute; V C 0 2 , C 0 2 production in litres per minute; V _ / V 0 2 and V E / V C 0 2 , ventilatory equivalents for 0 2 and C 0 2 , respectively; RER, respiratory exchange ratio. Table 10. Ventilatory parameters at peak exercise. Individual subject data. Day 2. Subject V E (BTPS) v c o 2 V E / V 0 2 V E / V C 0 2 R E R 1 101.51 3.16 34.28 32.08 1.07 2 114.43 2.41 54.84 47.35 1.16 3 85.90 2.11 36.59 40.66 0.90 4 80.34 2.36 33.26 33.98 0.98 5 105.32 3.08 36.92 34.20 1.08 6 95.49 2.78 38.51 34.25 1.13 7 88.22 2.58 35.80 34.13 1.05 8 88.09 2.44 39.03 36.10 1.08 9 90.13 1.94 50.29 46.35 1.09 10 73.34 1.75 43.48 41.84 1.02 Mean 92.28 2.46 40.30 38.09 1.06 SD 12.19 0.46 7.13 5.55 0.07 V E > minute ventilation in litres per minute; V 0 2 , 0 2 consumption in litres per minute; V C 0 2 , C 0 2 production in litres per minute; V E / V 0 2 and V E / V C 0 2 , ventilatory equivalents for 0 2 and C 0 2 , respectively; RER, respiratory exchange ratio. 74 Table 11. Ventilatory parameters at peak exercise. Individual subject data. Day 3. Subject V E (BTPS) v c o 2 V E / V 0 2 V _ / V C 0 2 R E R 1 117.79 3.44 39.06 34.24 1.14 2 84.49 1.73 50.23 48.85 1.03 3 101.08 2.79 37.68 36.16 1.05 4 95.85 2.38 40.15 40.20 1.00 5 103.82 2.89 37.13 35.92 1.04 6 * * * 7 98.02 2.64 35.96 37.15 0.95 8 88.00 2.25 38.49 39.50 0.98 9 83.01 2.58 39.02 34.34 1.14 1 0 78.14 1.99 44.23 40.06 1.17 Mean 94 .47 2 .52 40 .22 38 .49 1.06 SD 12.39 0.51 4 .17 4 .51 0.08 * Denotes missing data V E , minute ventilation in litres per minute; V 0 2 , 0 2 consumption in litres per minute; V C 0 2 , C 0 2 production in litres per minute; V E / V 0 2 and V E / V C 0 2 , ventilatory equivalents for 0 2 and C 0 2 , respectively; RER, respiratory exchange ratio. Table 12. Ventilatory parameters at peak exercise. Individual subject data. Day 4. Subject V E (BTPS) v c o 2 V E / V 0 2 V E / V C O . R E R 1 102.13 3.24 33.90 31.57 1.08 2 120.32 2.22 55.01 54.25 1.00 3 100.28 2.54 39.51 41.36 . 0.96 4 101.35 2.67 37.76 37.91 1.00 5 109.52 2.88 37.01 38.09 0.97 6 103.30 2.57 41.83 40.16 1.04 7 100.50 2.53 39.58 39.58 1.06 8 90.84 2.29 39.45 39.70 1.00 9 95.45 2.76 41.46 34.60 1.20 10 71.92 1.78 42.77 40.74 1.06 Mean 99 .56 2 .55 40 .83 39 .80 1.04 SD 12.53 0.40 5 .32 5.90 0.07 V E , minute ventilation in litres per minute; V 0 2 , 0 2 consumption in litres per minute; V C 0 2 , C 0 2 production in litres per minute; V E / V 0 2 and V E / V C 0 2 , ventilatory equivalents for 0 2 and C 0 2 , respectively; RER, respiratory exchange ratio. 75 Table 13. Ventilatory parameters at peak exercise. Individual subject data. Day 5. Subject V E (BTPS) v c o 2 V E / V 0 2 V E / V C 0 2 RER 1 116.48 3.38 36.58 34.44 1.06 2 102.50 2.18 45.99 46.99 1.02 3 108.18 2.58 41.21 41.99 0.98 4 95.21 1.70 42.33 55.95 0.76 5 94.45 2.74 34.15 35.20 0.90 6 104.27 2.67 45.14 39.10 1.02 7 86.46 2.50 35.18 34.59 1.02 8 93.54 2.49 39.59 37.54 1.06 9 101.15 2.40 42.29 42.26 1.00 10 86.80 1.75 48.24 50.53 0.98 Mean 98.90 2.44 41.07 41.86 0.98 SD 9.46 0.49 4.47 7.29 0.09 V E i minute ventilation in litres per minute; V 0 2 , 0 2 consumption in litres per minute; V C 0 2 , C 0 2 production in litres per minute; V E / V 0 2 and V E / V C 0 2 , ventilatory equivalents for 0 2 and C 0 2 , respectively; R E R , respiratory exchange ratio. Table 14. Ventilatory parameters at peak exercise. Individual subject data. Day 6. Subject V E (BTPS) v c o 2 V E / V 0 2 V E / V C 0 2 RER 1 98.65 3.12 33.33 31.66 1.05 2 114.85 2.28 53.27 50.42 1.06 3 100.09 2.26 38.00 44.39 0.88 4 95.51 2.64 36.01 36.22 0.99 5 98.81 2.86 36.00 34.62 1.04 6 94.50 2.54 37.00 37.50 1.00 7 100.23 2.50 36.60 40.07 0.91 8 91.41 2.37 39.66 38.67 1.03 9 93.49 3.05 27.13 30.72 0.89 10 72.25 1.85 42.69 40.77 1.04 Mean 95.98 2.55 37.97 38.50 0.99 SD 10.53 0.39 6.39 5.90 0.07 V E , minute ventilation in litres per minute; V 0 2 , 0 2 consumption in litres per minute; V C 0 2 , C 0 2 production in litres per minute; V E / V 0 2 and V E / V C 0 2 , ventilatory equivalents for 0 2 and C 0 2 , respectively; R E R , respiratory exchange ratio. 76 Table 15. Performance at peak exercise. Individual subject data. Day 1. Subject HR (bpm) Dyspnea Borg 10-point Scale Leg discomfort Breathlessness VC*2 max (mLkg^min1) VO2 max (Lmin1) 1 193 maximal (10) very, very strong (9) 47.28 3.26 2 187 very, very strong (9) very strong (7) 38.73 2.14 3 186 strong (5) strong (5) 35.83 2.31 4 184 strong (5) strong (5) 39.53 2.51 5 187 maximal (10) very, very strong (9) 46.63 2.69 6 175 very strong (7) strong (5) 49.48 2.69 7 187 very, very strong (9) very strong (8) 44.38 2.60 8 182 maximal (10) strong (5) 42.65 2.25 9 183 very strong (8) strong (6) 48.65 2.52 10 186 very strong (8) strong (6) 39.48 1.72 Mean SD 185.00 4.62 43.26 4.72 2.47 0.41 HR, heart rate in beats per minute; Dyspnea, amount of leg discomfort and breathlessness at point volitional fatigue; V 0 2 m a x , maximum oxygen consumption in litres per minute and milliliters per kilogram of body mass per minute. Table 16. Performance at peak exercise. Individual data. Day 2. _ . . t HR Dyspnea Borg 10-point Scale V 0 2 m a x V0 2 m ax Subject . / T 1 -1 -K /¥ • - i \ (bpm) , ,. „ J _ A l , (mL-kg mm ) (Lmin ) Lee discomfort Breathlessness 1 183 maximal (10) maximal (10) 42.95 2.96 2 174 maximal (10) very, very strong (9) 37.70 2.09 3 179 maximal (10) very, very strong (9) 35.28 2.35 4 178 very, very strong (9) very, very strong (9) 38.03 2.42 5 190 maximal (10) maximal (10) 49.53 2.85 6 174 maximal (10) very, very strong (9) 45.40 2.47 7 180 very strong (8) very strong (7) 42.08 2.47 8 179 maximal (10) very strong (7) 42.88 2.25 9 177 maximal (10) very, very strong (9) 34.65 1.79 10 177 very, very strong (9) very strong (7) 38.63 1.68 Mean 179.10 40.71 2.33 SD 4.68 4.69 0.41 HR, heart rate in beats per minute; Dyspnea, amount of leg discomfort and breathlessness at point volitional fatigue; V O 2 max, maximum oxygen consumption in litres per minute and milliliters per kilogram of body mass per minute. 77 Table 17. Performance at peak exercise. Individual data. Day 3. Subject HR Dyspnea Borg 10-point Scale VO2 max VO2 max (bpm) Leg discomfort Breathlessness (mL-kg -^min *) (L-min"1) 1 176 very strong (9) very strong (8) 43.78 3.02 2 177 maximal (10) very, very strong (9) 30.40 1.68 3 177 maximal (10) maximal (10) 40.23 2.68 4 177 very, very strong (9) very, very strong (9) 37.63 2.39 5 184 very, very strong (9) very strong (8) 48.53 2.80 6 * maximal (10) very, very strong (9) * * 7 186 maximal (10) maximal (10) 46.60 2.73 8 181 maximal (10) very, very strong (9) 43.93 2.31 9 175 maximal (10) very, very strong (9) 41.90 2.17 10 181 very strong (7) very, very strong (9) 40.58 1.77 Mean 179.33 41.51 2.25 SD 3.84 5.33 0.47 * Denotes missing data. HR, heart rate in beats per minute; Dyspnea, amount of leg discomfort and breathlessness at point volitional fatigue; V 0 2 max, maximum oxygen consumption in litres per minute and milliliters per kilogram of body mass per minute. Table 18. Performance at peak exercise. Individual data. Day 4. Subject HR Dyspnea Borg 10-point Scale V 0 2 max VO2 max (bpm) Leg discomfort Breathlessness (mL-kg'-min *) (L-min1) 1 169 very strong (7) strong (5) 43.70 3.01 2 178 very, very strong (9) maximal (10) 40.13 2.22 3 172 maximal (10) maximal (10) 38.08 2.54 4 182 very strong (7) very strong (7) 42.78 2.69 5 186 maximal (10) very, very strong (9) 51.38 2.96 6 171 very, very strong (9) very strong (8) 45.35 2.47 7 175 maximal (10) very, very strong (9) 42.30 2.53 8 183 maximal (10) maximal (10) 43.78 2.30 9 175 maximal (10) maximal (10) 44.50 2.30 10 177 very strong (8) very strong (8) 38.70 1.68 Mean 176.80 43.07 2.20 SD 5.53 3.81 0.28 HR, heart rate in beats per minute; Dyspnea, amount of leg discomfort and breathlessness at point volitional fatigue; V 0 2 max, maximum oxygen consumption in litres per minute and milliliters per kilogram of body mass per minute. 78 Table 19. Performance at peak exercise. Individual data. Day 5. Subject HR Dyspnea Borg 10-point Scale VO2 max VO2 max (bpm) Leg discomfort Breathlessness (mLkg'min *) (L-min'1) 1 180 maximal (10) very strong (8) 46.03 3.17 2 180 maximal (10) very strong (8) 40.35 2.23 3 179 very strong (7) very strong (7) 39.38 2.63 4 187 very, very strong (9) very strong (8) 35.43 2.25 5 181 very, very strong (9) maximal (10) 49.05 2.82 6 177 maximal (10) very strong (8) 47.08 2.56 7 183 very, very strong (9) very, very strong (9) 41.98 2.50 8 184 maximal (10) very, very strong (9) 44.93 2.36 9 185 maximal (10) maximal (10) 46.25 2.39 10 184 very strong (7) very strong (7) 41.35 1.80 Mean 182 43.2 2.26 SD 3.09 4.18 0.33 HR, heart rate in beats per minute; Dyspnea, amount of leg discomfort and breathlessness at point volitional fatigue; V O 2 max, maximum oxygen consumption in litres per minute and milliliters per kilogram of body mass per minute. Table 20. Performance at peak exercise. Individual data. Day 6. Subject HR Dyspnea V 0 2 max V 0 2 max (bpm) Leg discomfort Breathlessness (mLkg^-min !) (L min'1) 1 173 very strong (8) very strong (8) 42.93 2.96 2 173 maximal (10) very, very strong (9) 38.98 2.16 3 182 very, very strong (9) very, very strong (9) 39.55 2.64 4 183 very strong (8) very, very strong (9) 41.78 2.65 5 188 very, very strong (9) very, very strong (9) 47.65 2.75 6 173 maximal (10) very strong (8) 46.95 2.55 7 183 maximal (10) very, very strong (9) 46.80 2.74 8 185 maximal (10) very, very strong (9) 43.80 2.31 9 177 maximal (10) very strong (7) 66.60 3.44 10 181 very strong (7) very strong (8) 40.45 1.37 Mean 180 45.55 2.47 SD 5.45 8.03 0.25 HR, heart rate in beats per minute; Dyspnea, amount of leg discomfort and breathlessness at point volitional fatigue; V O 2 max, maximum oxygen consumption in litres per minute and milliliters per kilogram of body mass per minute. 79 Table 21. Ventilation in Litres per minute during the 15-minute voluntary hyperpnea task. Individual subject data. Day 2 Day 3 Day 4 RM fatigue R M fatigue R M fatigue V Q 2 max test T T E test T T E test Percent of Percent of Percent of Subject V E (BTPS) baseline V E (BTPS) baseline V E (BTPS) baseline MVV (%) M W ( % ) MVV (%) 1 110.0 75.7 98.3 78.1 69.6 48.3 2 115.5 72.2 109.8 77.3 130.9 81.3 3 74.0 67.3 95.3 80.8 78.4 69.4 4 81.8 73.0 79.8 70.0 65.7 58.7 5 100.9 78.8 94.9 75.9 101.4 83.1 6 114.8 70.4 139.8 83.7 122.6 78.1 7 105.0 86.1 100.6 74.0 109.3 85.3 8 97.5 73.3 83.6 74.0 88.1 78.0 9 103.7 61.2 106.8 64.0 107.2 64.5 10 63.1 70.1 57.5 67.6 63.3 70.3 Mean 96.63 72.81 96.64 74.53 93.65 71.70 SD 17.82 6.67 21.46 6.01 24.17 11.84 V E , average minute ventilation throughout hyperpnea task, in litres per minute. Percent of baseline M V V , average percentage of baseline M V V achieved throughout hyperpnea task. 80 Table 22. M V V at rest, following hyperpnea task and exercise of all participants. Test Day 2 (VO-> m a x : R M fatigue) Baseline M V V M V V M V V M V V M V V Post-Exercise (5-min) Subject Post-RMF (l-min) Post-RMF Post-Exercise (2-min) (3-min) 1 126 99 103 120 124 2 160 146 144 151 160 3 110 99 104 107 108 4 112 71 92 99 99 5 128 106 109 120 118 6 163 140 146 146 151 7 133 126 124 125 116 8 133 126 124 125 116 9 170 155 157 165 165 10 85 68 .77 95 89 Test Day 3 (EPT: R M fatigue) 1 126 106 104 117 113 2 161 142 136 152 148 3 118 104 103 101 106 4 114 92 99 112 111 5 125 118 119 135 131 6 167 153 151 161 159 7 136 128 120 133 130 8 113 114 106 104 103 9 168 157 157 172 170 10 85 62 66 87 76 Test Day 4 (EPT: R M fatigue) 1 144 113 109 129 125 2 161 136 130 145 140 3 113 107 101 114 110 4 112 93 94 96 89 5 122 108 110 122 119 6 157 150 147 150 151 7 128 122 120 116 123 8 113 103 88 107 97 9 168 157 157 172 170 10 90 77 82 92 92 M V V , litres per minute; EPT, endurance performance test. 81 Table 23. Individual subject data, menstrual cycles (day). Subject Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 1 3 23 19 10 28 6 2 3 9 24 4 23 18 3 20 16 4 13 13 22 4 23 8 26 25 12 11 5 14 9 20 23 8 5 6 4 8 3 14 3 11 7 12 13 9 27 5 16 8 2 6 27 20 9 12 9 28 1 22 7 17 1 10 14 7 3 20 5 26 Number represents menstrual day within 28-day cycle for each testing day. Table 24. Individual subject data, handgrip strength before and after the induction of R M fatigue. H G strength (kg) Subject Day2:V02max Day 3: E P T Day 4: E P T RM Fatigue R M Fatigue R M Fatigue Pre Post Pre Post Pre Post 1 32.0 33.5 30.5 30.5 35.0 36.0 2 31.5 31.0 30.0 31.0 31.5 28.0 3 32.0 33.0 31.0 33.0 33.0 32.0 4 32.0 31.0 28.0 28.5 29.0 29.0 5 30.0 29.0 31.0 33.0 30.5 29.0 6 35.0 35.0 35.0 37.0 34.0 33.0 7 35.0 37.0 37.0 39.0 36.0 38.0 8 30.0 33.0 34.0 33.0 33.0 33.0 9 32.0 31.0 33.0 34.0 31.5 32.0 10 31.0 30.0 30.0 29.5 27.0 29.0 Mean 32.1 32.4 32.0 32.9 32.1 31.9 SD 1.7 2.4 2.7 3.3 2.7 3.3 HG, hand grip strength in kilograms. 82 Appendix D: Pilot Data Summary Seven healthy female subjects with various fitness levels were tested in order to assess M V V as an indicator of respiratory muscle fatigue. The study took place in the exercise physiology lab at Allan McGavin Sports Medicine Center. Briefly, the subjects were required to come into the lab and perform testing to ensure normal pulmonary function. Spirometry measures were performed with the same device mentioned previously, FEV) FVC, and F E F 2 5 . 7 5 % were measured along with M V V . M V V was measured until 3 consecutive measures were obtained within 5% of each other. The largest of these 3 values was used in order to calculate 70% M V V . Each subject was then asked to breathe at 70% M V V (hyperpnea R M fatiguing-task) for 15 minutes (See Figure 1 for setup). FEV] F V C , FEF25-75% were measured immediately following the R M fatiguing task to ensure bronchoconstriction was not the cause for post-RM fatigue drop in M V V . M V V was measured following the R M fatiguing task at 0, 2, 3, 5, 10 and 15-minutes post R M fatigue. The percent drop in post-fatigue M V V was calculated. The subjects were tested on two different days separated by at least 48 hours to ensure reliability of the measures. Subjects were asked to refrain from exhaustive exercise, caffeine consumption for 12 hours prior to testing, and food and liquid consumption (excluding water) for 2 hours prior to testing. Results Al l subjects showed a reduction in M V V immediately (0-min) following the 15-minute R M fatiguing task except one subject who showed an increase in M V V from measured baseline values. The mean percent fall in M V V (SD) at 0-minutes post-RM fatigue was 12.3% (6.6), -16.1% (6.2) at 2-min, - 16% (5.2) at 3-min, -17.1% (6.8) at 5-83 min, -13.5% (6.3) at 10-min, and -12.5% (6.8) at 15-minutes post R M fatigue (See Table 3). Statistical analysis using one-way A N O V A , with repeated measures, demonstrated a significant F-ratio (a < 0.01) at all times measured post-fatigue. The results indicate that M V V was still significantly reduced from baseline values at 15-minutes post-fatigue. A Tukey's HSD was applied post-hoc and the greatest difference in M V V was observed at 5-minutes post-fatigue. The subjects were required to visit the lab on two separate occasions with a minimum of 42-hours rest in order to test the reliability of the tests. Reliability was determined between days for M V V at 5-minutes post fatigue with a con-elation coefficient of r = 0.962. Conclusion The results of this experiment indicate that the 15-minute hyperpnea task at >70% M V V can consistently result in respiratory muscle fatigue in healthy female subjects, when using percent drop in M V V as an indicator of fatigue. As a group the percent mean fall in F E V i was 4.4%, indicating that bronchoconstriction was not a factor in causing the reduction seen in M V V post-hyperpnea. The results indicate that this type of fatiguing task produces a longer-lasting low-frequency type of respiratory muscle fatigue as M V V was still significantly reduced 15-minutes post-hyperpnea. In a study performed by Mador et al., (1996) the subjects were required to breathe at minute ventilation equal to or greater than 60% of their M V V until task failure. Twitch transdiaphragmatic pressure (Pdi, T w ) was measured before and after the breathing task. At 10-minutes post hyperpnea Pdi.Tw was significantly reduced from baseline values in all subjects and remained significantly reduced for 1-hour post hyperpnea. Mador and his associates (1996) 84 concluded that long-lasting fatigue of the diaphragm reliably occurs after voluntary hyperpnea at levels sufficient to induce task failure. Pilot Data: Raw Data Maximal Voluntary Ventilation as an Indicator of Respiratory Muscle Fatigue Following 15-minutes of Voluntary Hyperpnea. Table 25. Age, height, mass, individual subject data. Subject Age (yrs) Weight (kg) Height (cm) 1 26 62.6 174.3 2 29 57.0 167.0 3 31 53.0 165.0 4 26 45.0 156.0 5 25 69.0 169.7 6 26 57.7 164.9 7 28 64.5 165.5 Mean 27.3 58.4 166.1 SD 2.0 7.4 5.2 yrs, years; cm, centimeters; kg, kilograms. 85 Table 26. Resting lung volumes before and after 15-minute the hyperpnea task, individual subject data. Pre- Post- Pre- Post-Subject Test Day hyperpnea hyperpnea hyperpnea hyperpnea F E V , F E V i F V C F V C 1 Day 1 3.62 3.54 4.55 4.53 1 Day 2 3.55 3.46 4.51 4.48 2 Day 1 2.43 2.43 3.05 3.04 2 . Day 2 2.93 2.84 3.67 3.56 3 Day 1 3.00 2.96 3.76 3.69 3 Day 2 2.98 3.16 3.74 3.96 4 Day 1 3.23 3.42 4.02 4.25 4 Day 2 3.45 3.36 4.37 4.02 5 Day 1 2.39 2.40 2.80 2.83 5 Day 2 2.89 2.29 3.40 2.65 6 Day 1 3.18 3.00 4.36 4.17 6 Day 2 3.21 3.23 4.14 4.23 7 Day 1 3.79 3.67 4.25 3.83 7. Day 2 3.84 3.84 4.33 4.36 Mean 3.18 3.11 3.93 3.83 SD 0.45 0.49 0.55 0.61 F V C , forced vital capacity, litres per minute; F E V i , forced expiratory volume, litres per minute. 86 Table 27. Maximal voluntary ventilation before and after the 15-minute hyperpnea task, individual subject data. Subject Test Pre Pre Pre Day MVV MVV MVV V E @ Average Post Post Post Post Post Post 70% V E M V V M V V M V V M V V M V V M V V M V V (% M V V ) 0-min 2-min 3-min 5-min 10-min 15-min 1 1 128 134 131 94.0 63.0 • 114 114 118 119 122 123 1 2 135 138 133 96.6 73.0 116 113 116 110 122 120 2 1 129 123 122 86.1 66.7 115 109 105 106 104 109 2 2 121 114 114 79.8 78.5 110 104 104 101 109 108 3 1 145 146 148 103.6 69.8 152 137 134 139 142 145 3 2 159 150 150 111.3 71.0 145 140 140 138 144 153 4 1 131 127 135 94.5 87.3 123 118 109 102 107 117 4 2 114 106 102 79.8 118.0 102 81 81 80 100 84 5 1 83 86 89 62.3 78.4 84 78 80 82 90 91 5 2 94 86 86 65.8 90.0 65 67 78 70 70 82 6 1 126 124 131 91.7 73.6 115 112 108 108 110 114 6 2 134 135 137 95.9 86.2 123 118 117 110 119 112 7 1 156 163 162 114.0 81.3 141 136 133 136 137 145 7 2 164 168 163 117.6 93.6 145 138 135 140 144 151 Mean 129.9 128.6 128.8 92.4 70.0 117.9 111.8 111.3 110.1 115.7 118.1 SD 22.9 24.9 24.2 16.6 5.3 24.0 23.1 20.7 22.8 21.7 23.6 M V V , maximal voluntary ventilation, in litres per minute; V E , average minute ventilation LI II W U Z j l I V J U l t l ^ p ^ i p i l ^ l l I U J 1 V , i l l 1 1 11 WO L_/V^l I I U 1 1 U L W . X V 1 V V 1 U V / A L / U J V 1 1 I percentage of baseline M V V achieved throughout hyperpnea task. 87 Table 28. Percent drop in MVV, FEV t , and FVC following 15-minute hyperpnea task, individual subject data. Post Post Post Post Post Post Subject Test FEVi FVC MVV MVV MVV MVV MVV MVV Day (%) (%) 0-min 2-min 3-min 5-min 10-min 15-min (%) (%) (%) (%) (%) (%) 1 1 2 1 15 15 12 11 9 8 1 2 (+) (+) 16 18 16 20 12 13 2 1 0 0 11 16 19 18 20 15 2 2 3 3 4 9 9 12 4 5 3 1 1 2 (+) 8 10 6 4 2 3 2 (+) (+) 9 12 12 13 10 4 4 1 (+) (+) 9 13 19 25 21 13 4 2 3 8 11 29 29 30 12 26 5 1 (+) (+) 6 12 11 8 (+) (+) 5 2 21 22 31 29 17 26 26 19 6 1 6 4 12 15 18 18 16 13 6 2 (+) (+) 10 14 15 20 13 18 7 1 3 10 13 17 18 17 16 11 7 2 0 (+) 14 18 20 17 14 10 Mean 4 6 12 16 16 17 14 12 SD 6 7 7 6 5 7 6 7 (+) Represents an increase 88 Figure 15. Absolute change in M V V following 15-minute hyperpnea task, individual subject data. Day 1. Note: Each line represents individual subject data. 89 Figure 16. Absolute change in M V V following 15-minute hyperpnea task, individual subject data. Day 2. Post M V V @ 0- Post M V V @2min Post M V V @ 3min Post M V V @ 5min Post M V V @ Post M V V @ min lOmin 15min Time Post Hyperpnea Note: Each line represents individual subject data. 90 Figure 17. Comparison of change in M V V following 15-minute hyperpnea task between Test Days 1 and 2. 140 135 130 125 120 115 110 105 100 95 90 85 80 75 70 65 60 55 50 45 40 35 30 25 20 15 10 5 0 i l l l • Baseline Immediate-post Hyperpnea 2-min post @ 3-min post @ 5-min post @ 10-min post @ 15-rnin post 91 Appendix E: Borg 10-point Scale for ratings of perceived exertion. 0 Nothing at all 0.5 Very, very easy 1 Very easy 2 Easy 3 Moderately hard 4 Somewhat hard 5 Hard 6 7 Very hard 8 9 10 Very, very hard 92 

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