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A metabolic comparison of isokinetic and free sprinting Roberts, Gregory Alan 1993-08-20

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A METABOLIC COMPARISON OF ISOKINETIC AND FREESPRINTINGByGregory Alan RobertsB.P.E., University of British Columbia, 1990A THESIS SUBMITTED IN PARTIAL FULFILLMENT OFTHE REQUIREMENTS FOR THE DEGREE OFMASTER OF SCIENCEinTHE FACULTY OF GRADUATE STUDIESSCHOOL OF HUMAN KINETICSWe accept this thesis as conformingto the required standardTHE UNIVERSITY OF BRITISH COLUMBIAOCTOBER 1993© GREGORY ALAN ROBERTS, 1993In presenting this thesis in partial fulfilment of the requirements for an advanceddegree at the University of British Columbia, I agree that the Library shall make itfreely available for reference and study. I further agree that permission for extensivecopying of this thesis for scholarly purposes may be granted by the head of mydepartment or by his or her representatives. It is understood that copying orpublication of this thesis for financial gain shall not be allowed without my writtenpermission.(Signature) Department of  kiA/VP K^SASThe University of British ColumbiaVancouver, CanadaDate  CCTOlk--)Q (q/93DE-6 (2/88)ABSTRACTThe purpose of this study was to examine the Excess Post-Exercise Oxygen Consumption(EPOC) and peak blood lactate responses of sprinters following exhaustive treadmillrunning, maximal isokinetic and free sprinting. Eight university sprinters (mean: age =24.8 yrs., ht. = 178.9 cm., wt. = 74.9 kg.) performed a 2 minute anaerobic speed test(AST) and tethered isokinetic and free sprinting protocols consisting of five secondmaximal repetitions separated by ten second active recoveries. A five repetition isokineticset was compared to five and ten repetition free sprint sets.A correlation (r = +0.87) was calculated between the EPOC and peak blood lactate valuesover the four experimental protocols. Tukey's post hoc comparisons determinedsignificantly different corrected EPOC (HSD = 2.04, x < 0.05) and peak blood lactate(HSD = 1.72, 0( < 0.05) cell means between the 2 minute AST (15.16 ± 2.59 Litres;14.83 ± 1.21 mmol/L) and the other three protocols: the 5 repetition anaerobic powermaster (APM) (11.38 ± 2.72 Litres; 12.77 ± 1.97 mmol/L), the 10 repetition free sprint(9.88 ± 2.80 Litres; 11.25± 2.15 mmol/L) and the 5 repetition free sprint (9.09 ± 2.51Litres; 9.83 ± 3.09 mmol/L). Additionally, significance was between the 5 repetitionAPM condition and the 5 repetition free sprint condition. These findings suggest that five,5 second isokinetic sprinting repetitions require more work in less time and therebyproduce a metabolic demand similar to ten, 5 second free sprinting repetitions.IITABLE OF CONTENTSABSTRACT ^ IITABLE OF CONTENTS^ IIILIST OF TABLES VLIST OF FIGURES VIACKNOWLEDGEMENTS ^ VIIINTRODUCTION ^ 11.1 Statement of the Problem^ 31.2 Hypotheses  31.3 Significance of the Study 41.4 Definition of Terms 41.5 Delimitations ^  51.6 Limitations 5LITERATURE REVIEW 62.1 Anaerobiosis^  62.2 Anaerobic Muscular Fatigue^  82.3 Effect of Exercise Intensity and Duration on EPOC ^ 92.4 Mechanisms and Metabolic Components of EPOC 102.5 Lactate ^  122.5.1 Blood Lactate Kinetics ^  132.5.2 Supramaximal Exercise  142.5.3 Blood Flow ^  162.5.4 Role of 02 in Lactic Acid Production ^ 172.6 VO2 Baselines  182.7 Methodologically Induced Individual Variation  192.8 Isokinetic Dynamometry^ 202.8.1 Research Value of Isokinetics^ 202.8.2 Effect of Gravity and Inertia 212.9 Modalities ^ 22PROCEDURES 253.1 Subjects 253.2 Pre-Experimental Protocol^ 253.3 Research design ^ 253.4 Experimental Protocol and Procedures ^ 253.4.1 Overview of Procedures 253.4.2 Anaerobic Speed Tests 263.4.3 Isokinetic Sprints ^ 273.4.4 Free Sprints 283.5 Data Collection^ 283.5.1 Oxygen Consumption 283.5.2 Resting Metabolic Rate ^ 283.5.3 Excess Post-exercise Oxygen Consumption ^ 293.5.4 Maximum EPOC 293.5.5 Power Outputs ^ 303.5.6 Blood Lactate 303.5.7 Free Sprint Distances 303.6 Statistical Analysis  31IIITABLE OF CONTENTS^ IVRESULTS ^ 324.1 Subjects Descriptive Data ^ 324.2 Performance Data ^ 324.3 Results of Hypotheses 414.3.1 EPOC Means 414.3.2 Peak Blood Lactate Means ^ 41DISCUSSION ^ 425.1 Subjects 425.2 EPOC 425.3 Blood Lactate ^ 455.4 EPOC and Blood Lactate Relationship^ 475.5 Anaerobic Power Master ^ 485.6 Work ^ 495.7 Conclusions 49RECOMENDATIONS 51APPENDIX ^ 52REFERENCES 58BIOGRAPHICAL INFORMATION^ 64LIST OF TABLES Table 1:^Subjects Mean Descriptive Data ^ 32Table 2:^2 Min AST Means ^ 34Table 3:^5 Repetition APM Sprint Means ^ 34Table 4:^10 Repetition Free Sprint Means 34Table 5:^5 Repetition Free Sprint Means ^ 35Table 6:^Proportion of AST Peak La and EPOC30min Means^ 35Table 7:^Repeated Measures 1 X 4 Anova ^ 39Table 8:^Tukey's Post Hoc Comparison of Corrected EPOC^ 39Table 9:^Tukey's Post Hoc Comparison of Peak Blood Lactate ^ 40Table 10:^Individual Subject Descriptive Data ^ 52Table 11:^Individual 2 Minute AST Data 53Table 12:^Individual 5 Repetition APM Data ^ 54Table 13:^Individual 10 Repetition Free Sprint Data 55Table 14:^Individual 5 Repetition Free Sprint Data ^ 56Table 15:^Individual Proportion of AST Peak La and EPOC30min Means ^ 57VLIST OF FIGURESFigure 1:^Line Graph of Mean Post-Exercise Oxygen Consumption ^ 36Figure 2:^Bar Graph of Mean Excess Post-Exercise Oxygen Consumption ^ 37Figure 3:^Bar Graph of Mean Post-Exercise Peak Blood Lactate ^ 38VIACKNOWLEDGEMENTSThe author wishes to extend sincere appreciation to his committee members Dr. E.C.Rhodes, Dr. K.D. Coutts and Dr. D.C. McKenzie. Special thanks is given to his advisorDr. E.C. Rhodes for showing trust, patience and understanding in teaching the graduateropes to an extremely unpolished academic. Further appreciation is extended to DianaJespersen and Dusan Benicky for their time and effort in lending technical assistance. Theauthor would like to sincerely thank the ten subjects; Martin Pardoe, Simon Caruth, TroyIvie, Todd Kennelly, Bob Dalton, Larry Downey, Duane Amphlett, Ryan Hall, James Lucand Shaun Lux for their kind cooperation, efforts and patience. The author further wishesto extend his admiration for the subjects who must have questioned their judgement toparticipate in such grueling bouts of exercise despite their highly trained condition. Lastlythe author wishes to thank his parents Alan and Bernice Roberts for their direction,influence and support which made a university education possible.VIIINTRODUCTIONTo date anaerobic performance has primarily been researched and quantified using singleexhausting bouts of exercise. With the development of portable oxygen analyzers and inthe field ergometry, research into interval performance and training is now a viableprospect. Research into intermittent supramaximal exercise may further the understandingof the bio energetic and recovery processes functioning during intervals of anaerobicexertion.Shortcomings exist in the literature concerning the recovery of the adenosine triphosphate-creatine phosphate (ATP-CP) cycle and the role glycolysis plays in short bursts of highintensity intermittent anaerobic work. Medbo et al (1988) contend that creatine phosphateis broken down very rapidly and contributes little to the accumulated 02 deficit with anincreased exercise duration beyond 15 seconds. Subsequently, the main process thataccounts for further anaerobic formation of ATP is glycolysis. However, the glycolysisdominance may not apply to the same degree to interval work which has a five secondexercise duration and ten second recovery interval thereby, allowing partial restoration ofthe CP concentrations. Harris et al (1976) found that CP resynthesized biphasicallydemonstrating a fast and a slow component. The components were found to have half-times of 21 - 22 seconds and over 170 seconds respectively after 6 minutes of exhaustiveexercise. However, it has been contended that the conditions of the preceeding exercisemay affect the replenishment rate of CP. The scene is further complicated by the findingsof Medbo and Tabata (1989) which claim that oxygen consumption can attain 85% ofmaximum 15 seconds from the commencement of exercise. Therefore, the contribution ofaerobic metabolism to supramaximal exercises may be greater than previously thought.1INTRODUCTION^ 2Further probing raises the question of, what limits anaerobic performance and causesfatigue? Medbo et al (1988) suggest that the maximal rate of glycogen degradation maybe a limiting factor for the rate of anaerobic ATP formation. This is supported by theobservation that, independent of the absolute magnitude of the anaerobic capacity, aleveling off of the accumulated 02 deficit occurs after 2 minutes of exhaustive exercise.Similarly, Weyland et al (1993) found that the 02 deficit plateaued after only 70 secondsof exhaustive stationary bicycle exercise. Hence subjects with a large anaerobic capacityare able to produce ATP at a much higher rate than subjects with a low anaerobiccapacity. Accordingly, it has been shown that sprint-trained subjects have a higheraccumulated 02 deficit and accumulate more lactate in the blood than endurance-trainedsubjects during 1 min of exhausting exercise (Medbo et al 1988).However, despite the maximal rate of glycogen degradation it is interesting that fatigue isexperienced during short exercise bouts, even though the blood and muscle lactateaccumulations are far from maximal. Therefore, factors other than acidosis, producedfrom glycogen metabolism, may inhibit high intensity exercise (Medbo et al 1988).The development of two new modalities, the APM, an isokinetic sprint ergometer and theCosmed K2, a telemetered portable self-contained oxygen consumption analyzer, make ittechnically possible to analyze the performance of interval sprinting. The combination ofthese two instruments facilitates the comparison of resisted (isokinetic) sprinting andunresisted (free) sprinting via measurement of Excess Post-exercise Oxygen Consumption.^INTRODUCTION^ 3Elevated oxygen consumption after exercise recently termed "Excess Post-exerciseOyxgen Consumption" (EPOC) is a well established phenomenon (Bahr et al 1992, Goreand Withers 1990; Maehlum et al 1986; Stainsby and Barclay 1970). The volume ofEPOC has been applied to quantify the homeostatic disturbance produced by exercise(Sedlock et al 1989). Thereby, the volume of EPOC, unlike the accumulated 02 deficit, isviewed, not as an indication of anaerobic capacity, but as an indicator of recovery andadaptive energy employed by the entire body.1.1 Statement of the ProblemThis study was designed to compare EPOC and peak lactate responses to performances onthe isokinetic APM and free sprinting; as well as, a comparison relative to the performanceof a 2 minute AST.1.2 HypothesesIt was hypothesized that the EPOC and peak blood lactate responses to 5 and 10 freerepetitions and 5 APM repetitions would produce relationships of the following:A) 5 Rep APMEPOC > 10 Rep FreeSprintEpoc > 5 Rep FreeSprintEpOCB) 5 Rep APMBLa > 10 Rep FreeSprintBLa > 5 Rep FreeSprintBLaC) 5 Rep APMEPOC—= ASTEPOCINTRODUCTION^ 41.3 Significance of the StudyThis study serves to validate isokinetic sprinting as a valuable sprint training supplement.This form of sprinting demonstrates the ability to perform more work in less time. Thisstudy is also significant in that it applies EPOC as an indicator of homeostatic disturbancerather than analyzing the processes which produce EPOC. Using the power of a repeatedmeasures design both EPOC and peak blood lactate are able to metabolically comparedifferent forms of supramaximal exercise.1.4 Definition of TermsANAEROBIC SPEED TEST (AST): A graded treadmill run to exhaustion.EXCESS POST-EXERCISE OXYGEN CONSUMPTION (EPOC): The summedvolume of all 02 derived processes in excess of resting VO2 values that restore metabolichomeostasis in response to exercise. These processes include not only disturbances in theworking muscles but all organs and tissues of the body (Roth et al 1988). Consequently,EPOC is more than mere repayment of the Ct, deficit (Gore and Withers 1989).FREE SPRINTING: Unihibited sprinting performed on a horizontal surface.ISOKINETIC SPRINTING: Sprinting performed on a horizontal surface with resistanceprovided by an isokinetic tethering device.02 DEFICIT: The difference between the total oxygen consumed during exercise and theamount of oxygen required to produce the ATP to perform the exercise.SUPRAMAXIMAL EXERCISE: An intensity of exercise requiring a rate of ATPproduction that exceeds the maximal power of the aerobic system.INTRODUCTION^ 51.5 DelimitationsThis study was delimited by the following:A) a sample of male university varsity sprinters between the ages of 19 and 30 years.B) the methodology and work bouts performed to determine and produce the EPOC'sand peak blood lactate concentrations.C) a respiratory gas sampling rate set at 15 second intervals.1.6 LimitationsThis study was limited by the following:A) the individuals metabolic response to the exercise protocols.B) the data collection capabilities of the Cosmed K2, the APM and the KontronMedical lactate analyzer 640.C) the assumption of a maximal effort by each subject for each test.D) the present understanding of EPOC.E) the sensitivity each subjects' oxygen consumption to the discomfort of conditionsimposed on them other than the intended experimental exercise.LITERATURE REVIEWPost-exercise oxygen consumption was first examined by Hill and associates in the 1920's.The "oxygen debt" hypothesis stated that lactate metabolism was linked to post-exerciseoxygen consumption. They concluded that the excess oxygen metabolized 1/5 of thelactate produced to provide energy for the conversion of the remaining 4/5 of the lactateto glycogen. In the 1930's Margaria et al elaborated the hypothesis by discriminating afast ("alactacid") and a slow ("lactacid") recovery oxygen curve components. Thishypothesis states that the fast phase represents the restoration of ATP and CP stores,while the slow phase reflects the oxidation of lactate. Since Margaria et al numerousstudies have demonstrated a discrepancy between the post-exercise lactate concentrationsand VO2 (Gaesser and Brooks 1984).It is apparent that the hypotheses of Hill et al and Margaria et al are overly simplistic. Asno complete account of the post-exercise metabolism exists, the term EPOC has beendeemed to describe the set of phenomena that occur during recovery from exercise. It isan appropriate term as it avoids implication of causality in describing the elevation ofmetabolic rate above resting levels after exercise (Gaesser and Brooks 1984, Stainsby andBarclay 1970).2.1 AnaerobiosisEnergy requirements for supramaximal efforts are met by phosphagen-splitting (hydrolysisof ATP and CP), glycolysis (hydrolysis of glycogen to lactic acid) and oxidativemechanisms (changes in blood and muscle oxygen saturations) respectively in asequentially contributing and overlapping fashion (Davies 1971; Evans 1981, Wenger and6LITERATURE REVIEW^ 7Reed 1976). Due to the delayed increase of oxygen uptake at the onset of exercise theproportional contribution of aerobic metabolism to total energy turnover increases withtime (Medbo and Tabata 1989). The dependence on anaerobic versus aerobic metabolismis associated with the intensity and duration of the exercise (Gollnick et al 1986).However, the energy requirements for 4-5 seconds for all-out efforts of short duration aremainly met by phosphagen-splitting (Kaczkowski et al 1982; Maehlum et al 1986) whichproceeds at a rate independent of 02 supply and is limited only by the amount of ATP andCP in the muscle (Davies 1971) and the magnitude of CNS recruitment (Radford 1984).In activities that demand high tension and/or velocity of movement fast twitch units mustbe recruited to supplement the aerobically produced energy. Accordingly, the leg musclesof successful athletes involved in muscle strength and power activities possess apredominance of fast twitch muscle fibre area (Kaczkowski 1982; Radford 1984).Decreases in ATP and CP concentrations in skeletal muscle during exercise vary with therelative work rate. Training results in a lower decline of these muscle high energyphosphate concentrations in the same exercising individual. Two factors that may accountfor a lower decrease in high energy phosphate concentrations, a smaller increase in lactateconcentration and a smaller EPOC are the following: 1) a more rapid rise in 02 delivery,resulting in the development of less muscle hypoxia at the onset of exercise 2) animprovement in oxygen availability to the contractile fibres made possible by the exercisetraining-induced adaptations in the muscle resulting in the increased extraction of 02 fromthe blood (Hagberg et al 1980) and 3) an increase in the magnitude of the recoveryenzyme profile (Astrand et al 1986).^LITERATURE REVIEW^ 8Hagberg et al (1980) further reported that under submaximal conditions trained individualswere capable of increasing their V02 more rapidly than untrained individuals. Moreimportantly, it was found that V02 adjusted to energy need more rapidly after trainingeven at the same relative work rate. It seems clear that in addition to the relative workrate, the individual's level of training plays an important role in determining the timecourse of the adjustment to exercise and the time course of recovery. Such adaptationsare magnified under supramaximal conditions and explain the ability of aerobic metabolismto supply upwards of 40% of the total ATP required for 30 seconds of exhaustive exercise(Medbo and Tabata 1989). The major weakness of Kreb's cycle lies in itscompartmentalization in the mitochondria, thus limiting the rate of transportation of theATP to the cross bridges. Conceptually, the intramitochondrially produced ATP are beingtransported to the cytosol more rapidly and in greater magnitude (Wenger and Reed1976). Functionally, the adaptation of the aerobic energy system to supramaximalexercise increases the duration that the ATP-CP and glycolytic systems can function at agiven intensity before anaerobic arrest.2.2 Anaerobic Muscular FatigueAnaerobic muscular fatigue primarily occurs as a consequence of lactate accumulationwhich lowers muscle and blood pH and in turn inhibits (PFK). These effects serve toreduce the glycolytic flux of ATP. The increased acidity has been suggested to affect thepermeability of membranes to Na + and K+ effectively hyperpolarizing the cell anddecreasing contractility. This effect is even more pronounced in type IIB (-85mv) overtype I (-70mv) fibres as their inherent resting potential is lower. Additional inhibitoryeffects have been implicated by the accumulation of H+ which compete with Ca+ forbinding sites on actomyosin effectively rendering these cross bridges disfunctional(Wenger and Reed 1976).LITERATURE REVIEW^ 92.3 Effect of Exercise Intensity and Duration on EPOCWhen exercise ceases abruptly, oxygen uptake does not return immediately to the pre-exercise level. Oxygen uptake decreases exponentially, approaching the pre-exercise levelalmost asymptotically. During the period of time in which the oxygen deficit isaccumulating, the metabolizing tissues are using stored oxygen and energy sources such asfree ATP, CP and glycogen for energy production. These sources of energy are"borrowed" and presumably must be restored via 02 uptake, hence the term "EPOC".The existence of EPOC is well established but the magnitude, duration and physiologicalbasis after various intensities and durations of exercise is still debated (A. Gore andWithers 1990; Maehlum et al 1986; Stainsby and Barclay 1970).Exercise intensity affects both the magnitude and duration of EPOC, whereas the exerciseduration affects only the duration of EPOC (Bahr and Sejersted 1991). The duration ofEPOC is not necessarily related to the amount of postexercise energy expenditure asrecovery metabolism is affected by the magnitude of the homeostatic disturbance such thatexercise intensities exceeding approximately 50% VO2max will have an increasinglygreater impact on EPOC. It seems that when exercise intensity is greater, the caloricexpenditure at the onset of recovery is greater due to the elevated metabolic rate duringexercise which is carried over into the EPOC. The magnitude and duration of EPOC arenot necessarily related and both should be assessed when examining the postexerciseresponse (Sedlock et al 1989).Consensus has been achieved that 02 deficit reaches a maximum magnitude for exhaustivebouts of running lasting 2 min or more which is consistent with peak blood lactateconcentrations achieved after 2 minutes of exhaustive exercise. Estimations of EPOCvolumes, which are closely associated with 02 deficit, vary from 30 minutes to 72 hours inLITERATURE REVIEW^ 10duration (Maehlum et al 1986; Medbo 1988). It is likely that the varied reports of EPOCduration are due to the lack of standardized methods for, determining 02 consumptionbaselines and producing exercise protocols.Gore and Withers (1990) reported that the magnitude of EPOC increases with exerciseintensity linearly for exercise bouts between 20% and 80% VO2max whereas it has beenshown to increase exponentially once exercise intensity approaches 100% VO2max. In arepeated measures factorial design exercise intensity was the major determinant of EPOCsince it explained five times more of the EPOC variance than either exercise duration orthe intensity duration interaction (Gore and Withers 1990).2.4 Mechanisms and Metabolic Components of EPOCBecause the mitochondrion is the site of 02 consumption in the cell, the explanation of theelevated post-exercise VO2 may be found at the level of this cellular organelle. Directcontrol of mitochondrial respiration may be exerted by concentrations of primarily ADP inaddition to ATP, Pi and CP. Mahler and Homsher (1982) proposed that the rate-limitingstep is the intramitochondrial production of ADP by creatine kinase. Indirect control ofmitochondrial respiration may include a variety of factors, including catecholamines,thyroxine, glucocorticoids, fatty acids, calcium ions and temperature (Gaesser and Brooks1984; Roth et al 1988).It may be stated that metabolic rate will return to control levels when all the factors thatinfluence mitochondrial respiration have returned to control levels. Without carefulconsideration of all the factors influencing mitochondrial respiration, measurements of theelevated post-exercise VO2 may be of limited value (Gaesser and Brooks 1984).LITERATURE REVIEW^ 11Numerous factors have been associated with the elevated postexercise metabolic rate.However, the relative contribution of each factor remains unknown (Sedlock et al 1989).Exercise triggers a multitude of processes that must return to a basal turnover rate duringthe recovery period (Bahr and Sejersted 1991). Therefore, other tissues as well as musclemust be involved since whole body EPOC is much greater than can be accounted for bylocal muscle events (Bahr et al 1992; Bahr and Sejersted 1991; Bangsbo et al 1990;Stainsby 1970). The components of the EPOC are believed to include the following:1)replenishment of 02 stores in blood and muscle 2) resynthesis of ATP and CP in theexercising muscles 3) metabolism of lactic acid 4) repletion of glycogen 5) response tocatecholamine release 6) oxidation of fat 7) turnover of substrate cycles 8) elevation ofbody temperature 9) compensatory increased protein synthesis 10) restoration of ionichomeostasis 11) thermic effect of food and 12) elevated physiological functioning (Bahr etal 1987; B. Bahr and Sejersted 1991; Bangsbo et al 1990; Bangsbo et al 1991; Bielinski etal 1985; Medbo et al 1988; Roth et al 1988; Stainsby and Barclay 1970).Bangsbo et al (1991) concluded the metabolism of lactate, ADP, inorganic phosphate andcreatine could account for only 47% of recovery 02 from 0 to 10 min Consequently theclassical lactate theory of EPOC has been strongly refuted and a large body of literaturenow contends that EPOC may be explained in terms of the numerous factors listed above(Gore and Withers 1990).LITERATURE REVIEW^ 122.5 LactateLactic acid, the endproduct of glycolysis, increases in concentration in the bloodexponentially with increasing exercise intensity (Gollnick et al 1986). Lactic acid is astrong organic acid (pK=3.8). At physiological pH values it will dissociate to a proton(HI) and an anion (C3H603 -). Isolated mitochondria oxidize exogenous lactate at thesame or greater rate than pyruvate. Thereby, it is impossible to estimate lactic acidproduction rates during exercise from measurements of blood lactate levels or to interpretthe blood lactate inflection point solely as a sudden increase in production. Lactic acidosisoccurs to some degree at all exercise intensities and is due to the difference between its netrelease to and clearance from the blood. Therefore, measurement of blood lactateconcentration only allows speculation on its underlying mechanisms (Gollnick et al 1986,Stainsby and Brooks 1990).Any ATP produced from glycolysis leading to lactate formation will not have required theuse of oxygen. Lactate production appears to be large under some circumstances andapparently contributes a savings in oxygen uptake which is measureable but lactateproduction is transient, being large only early in activity (Stainsby and Barclay 1970).Another beneficial aspect of lactate production concerns the extrememly high rate ofenergy derivation associated with glycolysis or glycogenolysis. The degradation of 1 g ofcarbohydrate to lactate does not yield as much energy as the combustion of 1 g ofcarbohydrate or fat combusted to water and carbon dioxide; however, the rate at whichthe energy is produced surpasses by far the speed with which energy can be derivedaerobically (Jacobs 1986).LITERATURE REVIEW^ 13Traditionally, lactate has been considered to be a metabolic end product whose appearancein muscle and blood during exercise was thought to indicate anaerobic metabolism(Brooks and Gaesser 1980). In fact, non-oxidative metabolism must supplement aerobicmetabolism in order to meet ATP requirements of working muscle but lactate production,in contracting muscle, can occur even when the muscle is well oxygenated. Therefore,lactate levels in the blood can certainly be influenced by factors other than the degree ofoxygenation (Gaesser and Brooks 1984).2.5.1 Blood Lactate KineticsThe activity of lactate dehydrogenase in skeletal muscle is far greater than the combinedactivities of enzymes providing alternate pathways for pyruvate metabolism and the ratelimiting enzyme for the Kreb's cycle. In fact, lactate is produced at rest at approximately100 mg • kg-1 h-1 . Therefore, lactate production in muscle is an inevitable consequenceof glycolytic carbon flux (Brooks 1986, Gaesser and Brooks 1984).A small fraction of lactate moves across cell membranes via simple diffusion. However,most lactate appears to move across cell membranes in conjunction with a cation (Na+ orH+) via facilitated transport. Consequently, the blood lactate increases and peaksapproximately 5 minutes after exercise because the active muscle intracellular lactateconcentration is not in equilibrium with the extracellar space and the blood. Additionally,decreasing pH inhibits key glycolytic enzymes and only a minor fraction of the lactic acidformed may diffuse to the cell membrane for transport to the extracellular space near thecell membrane. Thus the exchange of lactate between cells and blood is affected by lactateconcentration, proton gradients, intracellular pH and intracellular metabolism; thereby, notsolely reflecting the rate of glycolysis. It appears transport is restricted, equilibrium is notLITERATURE REVIEW^ 14achieved and significant cell-to-blood gradients do exist and the net output may be delayedsignificantly relative to net production (Gollnick et al 1986, Stainsby and Brooks 1990).Training produces effects on the hormonal response to exercise which could effect thelactate production. Untrained compared to trained individuals demonstrate a strongeradrenergic response to exercise, which has been linked to an excessive rate ofglycogenolysis. The elevated glycogenolysis produces an excess of pyruvate which isconverted to lactate via lactate dehydrogenase resulting in a functionally falsely elevatedblood lactate (Brooks 1986, Gollnick et al 1986). Meanwhile, interval sprint trainingproduces enzymatic adaptations of increased capacity to derive ATP from both glycolyticand oxidative processes (Jacobs et al 1987).The reasoning for the production and distribution of lactate is explained by the lactateshuttle theory. It hypothesizes that lactate serves as: 1) a substrate to maintain bloodglucose via hepatic gluconeogenesis and more importantly as 2) an oxidizable substratefrom active muscle (areas of production) to many diverse tissues (areas of net removal),thereby functionally distributing substrate and removing metabolic "waste". Fittingly, therate of these two fates of lactate are linearly related to arterial lactate concentration andexponentially related to VO2 (Brooks 1986, Stainsby and Brooks 1990).2.5.2 Supramaximal ExerciseMuscle lactate production and accumulation will occur almost immediately with the onsetof exercise which demands more energy than can be provided aerobically. Adaptiveresponses to training with this type of exercise include an enhanced ability to 'pump out'lactate quickly from the muscle to the circulation (Jacobs 1986).LITERATURE REVIEW^ 15Consequently, the main difference between trained and untrained individuals during heavyexercise is the greater metabolic clearance rate (MCR) imparted by training. Thisdifference may be partly attributable to a lesser autonomic response in the trained. Higherblood glucose levels in the trained during heavy exercise are consistent with themaintenance of splanchnic blood flow. In untrained individuals the stress of heavyexercise may trigger an autonomic response that shunts blood away from thegluconeogenic organs and toward contracting muscle, thus limiting the capacity for releaseof glucose from the liver (Donovan and Brooks 1983).The lactate response to supramaximal exercise is a sensitive indicator of adaptation to"sprint training" and is correlated with supramaximal exercise performance Although thelactate response to exercise is reproducible under standardized conditions blood lactateconcentration can be influenced by the site of blood sampling, ambient temperature,changes in the body's acid-base balance prior to exercise, prior exercise and dietarymanipulation (Jacobs 1986).The highest lactate concentrations after single bouts of maximal exercise are induced byexercise corresponding in duration to a 400m or 800m run. Such lactate levels can reach25 mmolfL or 15 to 20 times normal resting concentrations. These peak blood lactatevalues after exhaustive exercise are reliable if activity following exercise is standardized.The rate at which lactate leaves the muscle cell will influence the rate of recovery fromlocal muscular fatigue when supramaximal exercise is subsequently resumed (Jacobs1986).Interestingly, anaerobic capacity according to Schnabel and Kindermann (1983) can bereliably estimated by the increase in arterial lactate concentration over the pre-exerciseLITERATURE REVIEW^ 16value of a 40 second submaximal test ("L40) and the maximal arterial lactate level in themaximal test (Lmax) which explains 30.8% and 57.2% of the variability in maximum timerespectively. Additionally, if the run is performed at the same speed in all subjects, time toexhaustion is a measure for inter-subject comparisons of anaerobic capacity.(Schnabel andKindermann 1983)2.5.3 Blood FlowOther compounding factors include the competition for blood flow. As exercise intensityand the mass of active muscle increases, central commmand in concert with assortedperipheral chemoreceptor and mechanoreceptor afferent inputs increases sympatheticvasoconstrictor activity to muscle and other tissues. In the active muscles this constrictoractivity is opposed by local vasodilator mechanisms, which are linked by unestablishedmechanisms to the metabolic rate of the muscle. As would be expected for proportionalcontrol systems, the system does not fully compensate. As a result, flow does not rise asmuch as VO2 and extration of 02 increases to aid in the elevation of VO2 (Stainsby andBrooks 1990).Immediately after a sudden modest (20-30%) reduction in flow the force of contractiondecreases with little increase in extraction. As a result, VO2 decreases almost as much asthe flow. Indications are that contracting muscle performance and VO2 are very sensitiveto changes in blood flow and suggest that the effect is not mediated via 02 limitation inthe mitochondria. Whatever the mechanism, flow is a significant effector of VO2 andwhen it is changed VO2 may be changed. Because of competition for flow, the maximalVO2 of a given muscle is reduced, compared to that when working alone, when a largeLITERATURE REVIEW^ 17mass of muscle is active at the same time. But at no time is the muscle so hypoxic that 02transport limits oxidative phosphorylation in the muscles (Stainsby and Brooks 1990).2.5.4 Role of 02 in Lactic Acid ProductionThe rate of lactate production may not always be a suitable indicator of oxygen lack evenwhen hypoxia is severe. Stainsby and Brooks (1990) demonstrated that raising arterialPo2 by breathing 100% 02 had no effect on V02, contraction performance or lactateproduction during repetitive twitches. Therefore, during severe hypoxia oxygen lack maybe present but metabolic arrest may reduce substrate availability and preclude productionof lactic acid. Measurements of muscle myoglobin saturation during repetitive twitchcontractions have shown 02 to be low but adequate in muscle mitochondria and directlyunrelated to lactate production under free flow, normoxic conditions at any level (Stainsbyand Brooks 1990).Breathing hypoxic gas causes muscle blood flow to increase and (a-v)02 to decreaseduring submaximal exercise so that muscle VO2 is maintained during hypoxemia. Musclenet efficiency remains at 23% during hypoxic exercise as during normoxic exercise. Incontrast to the constancy of VO2 and muscular efficiency, net lactate release increasesdramatically during hypoxia. A 3-4 fold increase in arterial epinephrine levels areobserved during hypoxic exercise. Accordingly, it is possible to suggest that the increasedmuscle lactate outflow is, in part, due to a Beta adrenergic stimulation of muscleglycogenolysis (Stainsby and Brooks 1990).LITERATURE REVIEW^ 182.6 VO2 BaselinesRecovery oxygen volumes would be expected to be different when different recoverybaselines are used. Traditionally, three baselines have been used in studies of recoveryoxygen. These are 1) basal metabolic rate (BMR) 2) resting metabolic rate (RMR) and 3)light work metabolic rate (Stainsby and Barclay 1970).BMR is probably the proper baseline for measurement of recovery oxygen but because ofthe tedium necessary to achieve BMR it is impractical and almost never used. The mostcommonly used baseline which seems to yield reproducable results is RMR. Use of RMRassumes that whatever created the RMR continues unchanged through the exercise periodand throughout recovery. However, this assumption ignores the anticipatory response toexercise which is present pre-exercise but non-existent post-exercise. Consequently, onemust raise the issue as to what recovery includes and what parts of it one wishes to study(Stainsby and Barclay 1970).Often pre-exercise resting baseline volumes are significantly greater than recovery baselinevolumes. This disparity may be largely explained by the anticipatory responses toexercise. As a result, by convention, metabolic adjustments made before and afterexercise are evaluated by means of pre- and post-exercise baseline substractions (Roth etal 1988). Additionally, resting oxygen consumption may vary diurnally; therefore, controlvalues should be taken at the same time of day as the postexercise values (Maehlum et al1986).LITERATURE REVIEW^ 192. 7 Methodologically Induced Individual VariationDetermination of an individuals performed work may be obscured solely by the measure ofexternal work. Since energy is expended and oxidizable substrate formed whethermuscular contractions perform external work or not, due to imperfect biomechanics ormaintainence of posture, the metabolic cost of the work is the proper measure ofperformed work. With the exception of limited blood flow, isometric work andpathological conditions, internal work (oxygen metabolism) occurs at a set efficiency.Alternately, external work occurs at a variable efficiency because of variation in suchfactors as neuromuscular coordination, biomechanics and anatomical anamolies.Consequently, external work ultimately impacts internal work creating metabolicindividual variations (Henry 1951).Additionally, subjects with greater maximal aerobic power have a more rapid time courseof early recovery but similar total EPOC possibly reflecting the influence of increasedmetabolic heat load produced by performing greater absolute, albeit equal relativeworkload. As a result, variability in the degree of aerobic training will influence the EPOCprofile but not the total volume (Kaminsky et al 1987).Above all, the experience of fatigue is the single most important source of methodologicalerror. Fatigue is a subjective experience that is influenced by motivation and is thereforedifficult to assess objectively. Surprisingly Medbo et al (1988) found the values for theacccumulated 02 deficit to be highly reproducible for all durations. For exhausting boutslasting 2 min the precision (standard deviation) was 3 mUkg, corresponding to a relativeerror of 4% of the maximal accumulated 02 deficit. Apparently, motivated subjects wellaccustomed to strictly standardized procedures produce small methodological errors(Medbo et al 1988).LITERATURE REVIEW^ 202.8 Isokinetic DynamometryIsokinetic contraction is the muscular contraction that involves constant velocity limbmovements around a joint. The velocity of movement is maintained constant by a specialdynamometer such that the resistance produced is equal to the muscular forces appliedthroughout the range of movement (Baltzopoulos and Brodie 1989). In this manner, thecontrolled variable is the velocity of muscular shortening and not the resistance as isnormally the case in muscle strength testing where the velocity becomes a consequence ofthe load applied on the muscle (Thorstensson et al 1976). This method provides theopportunity to manipulate the speed so as to establish conditions specific to exercise withregard to contraction speed. Once an isokinetic device is set at a specific operating speed,it permits and demands muscular contractions at that speed (Baltzopoulos and Brodie1989; Hislop and Perrine 1967).The load acting in isokinetic exercise is the result of the mechanical process of energyabsorption which an isokinetic device performs in order to keep the exercise speedconstant. Energy cannot be dissipated by acceleration because this is mechanicallyprevented by the device. Because the energy is not dissipated anywhere in the process, itcompletely converts to a resisting force which is always proportional to the magnitude ofthe input (muscular force). Thus it varies in relation to the efficiency of the skeletalleverage (Hislop and Perrine 1967).2.8.1 Research Value of IsokineticsIsokinetic dynamometry is popular because it avoids invasive technique, is simple toadminister and short in duration. Statistically it is repeatable, reliable, valid and sensitiveto changes in anaerobic fitness. Isokinetic endurance tests represent valid laboratory testsLITERATURE REVIEW^ 21for evaluating high-intensity, short-term exercise in which the muscle is primarilydependent upon anaerobic processes for energy release (Patton and Duggan 1987). Peakpower is assumed to reflect maximal power generation by the breakdown of phosphagensduring the initial repetition; whereas, mean power represents energy production fromcombined phosphagen utilization and glycogenolysis over the entire duration of the test(Smith 1987).2.8.2 Effect of Gravity and InertiaIsokinetic dynamometers like the cybex measure the muscle moment, which is the muscleforce application times the length of the radius of the lever arm from the axis to the line ofmuscle pull, which is usually labelled the "muscle torque." The primary limitations of theCybex dynamometer include torque overshoot during acceleration of the limb to theregulated speed (inertial effects) and a lack of gravity compensation (Alexander 1990;Baltzopoulos and Brodie 1989). This has been demonstrated by Osternig (1975) whofound the maximum isokinetic torque values tended to shift to more extended jointpositions as the speed of knee extension increased. This shift may have been due to themomentum of the leg during the faster isokinetic speeds overcoming some of the inertia ofthe weight of the leg as it was extended (Osternig 1975).The underlying weakness in the cybex mechanism lies in its analysis of vertical planemovements; therefore, the limbs are not only working against the dynamometer but arealternately aided and opposed by gravity throughout the range of motion. Often thesegravitational forces have not been taken into account, and the error involved can be quitelarge (Winter 1981). A key feature of the APM is the fact that it analyzes movements inthe horizontal plane which involves no gravitational forces (Rhodes and Roberts 1992).LITERATURE REVIEW^ 22Although the Kin/Com has largely overcome the limitations plaguing the Cybex(Alexander 1989) it is still a laboratory test and is not feasible as an in the field testingmodality.2.9 ModalitiesUntil recently, direct metabolic and ergometric analyses were not possible on intervalsprinting. Previous technology permitted the analysis of sprinting exercise solely by singleexhausting exercise bouts such as the AST. The development of a new modality, the APMand a telemetered portable self-contained 02 consumption analyzer (Cosmed K2) nowmake it technologically possible to ergometrically and metabolically analyze theperformance of interval sprinting.The APM is a new isokinetic tool that has been engineered to calculate the linear meanand peak power output for up to a twenty-four metre distance. This unit consists of arecoiling drum with 24 metres of cord wrapped around it. The unit allows cord to bereeled off the drum at a preprogrammed rate, of up to 5 m/s, which is regulated through amicroprocessor that controls an electromagnetic brake installed on the drum. Thefunctioning module and its accompanying supportive frame is extremely portable, easy toassemble and simple to use. The athlete fitted with a waist belt, that is harnessed to thecord of the APM with a hand clasp, sprints away from the device. Once the athlete hasaccelerated to a pre-set velocity, the unit adaptively controls the athlete for a preselectedtime and then stops the forward motion (Rhodes et al 1991).The power output is calculated every 1/100th of a second by measuring the cord tensionand unwound length. The LCD displayed output is the average power generated duringall completed strides during the designated time. The power and length of each completeLITERATURE REVIEW^ 23stride is also calculated and can be diplayed on a PC optionally attached to the ergometer.Reliability coefficients ranged from .81 to .88 using human subjects while coefficientsreached .99 dropping known weights from a suspended APM (Rhodes et al 1991).Similar to ergometry the field of metabolic physiology has been broadened with thedevelopment of, the Cosmed K2, a telemetered portable self-contained 02 consumptionanalyzer. The K2 consists of a portable analyzer unit and a receiver unit. The analyzerunit is firmly but not restrictively straped to the subject's chest and consists of a face mask,an expiratory gas sampling pump, a dynamic micro chamber, an 02 analyzer, a cardiacfrequency transmitter and a radio transmitter. The unit processes and displays the data onthe receiver unit with an option of 15, 30, and 60 second interval printouts. Mostimportantly the Cosmed K2 allows the absolute freedom of movement during performanceof exercise. The Cosmed K2 and the 2001 exercise system demonstrate strong correlationco-efficients for VO2 (r=0.95), VE (r=0.96) and HR (r=0.97) using stationary bicycleexercise . However, a significant difference was found in VE at higher workloads (Iennaet al 1992).Lothian et al (1993) found that the variability between trials with the Cosmed K2 and theQuinton on-line oxygen analysing system were 3.0 - 11.4% and 1.1 -3.9% respectively.Findings also demonstrated that at workloads in excess of 1.10 L/min the Cosmed K2underestimated the V02. Similarly, Peel and Utsey (1993) found the Cosmed K2produced VO2's 2 - 3 ml min-1 kg-1 lower than a Gould 9000PC metabolic system.However, these results were based on treadmill exercise which produces slippage of theface mask with the motion of the head and subsequent air leakage leading to the findingsof lower VO2's compared to conventional metabolic systems. Alternately Dal Monte et al(1989) found no significant difference between the Cosmed K2 and the Jaeger on-lineLITERATURE REVIEW^ 24system for different workloads using stationary bicycling. Lothian et al (1993) attributesthe latter finding to the type of exercise used in which head movement is minimal thusreducing the air leakage to a minimum.The combination of these two instruments facilitates a novel comparison of the energyrequirements between resisted (isokinetic) sprinting and unresisted free sprinting. Rhodesand Roberts (1992) yielded APM power outputs of up to 1428 watts. The APMdemonstrates the capacity to generate unparalleled exercise intensities under accuratelysimulated performance conditions with the exception of speed.PROCEDURES3.1 SubjectsTen male U.B.C. varsity sprinter and middle distance track athletes served as the subjectpool. The experimentation was conducted during the Canadian Interuniversity AthleticUnion (C.I.A.U.) competitive season to ensure all subjects would be in a highly trainedcondition. Subjects were requested to be 2 hours postabsorptive before each test.3.2 Pre-Experimental ProtocolPrior to granting written consent subjects were fully informed and familarized with theequipment, the tests to be performed and the degree of exhaustion which would beexperienced during the experimentation. Interested individuals completed a writteninformed consent form and a physical activity readiness questionnaire (PAR Q).3.3 Research designThe study employed a four condition (2 Min AST, 5 Rep APM, 5 Free, 10 Free) repeatedmeasures design.3.4 Experimental Protocol and Procedures3.4.1 Overview ofProceduresSubjects were required to perform eight tests in all, each on separate days. The eight testsconsisted of three sets. Set one involved lying supine for 10 minutes fitted with a K2oxygen analyzer to measure fasting RMR. Tests in the second and third sets were25PROCEDURES^ 26performed randomly and not necessarily in the order described. The second set, tests twoto four, consisted of three 8 mph AST's: one at 15% grade, one at 20% grade and one at25% grade. The purpose of the three AST's was to establish an intensity vs. durationperformance curve for each individual and to extrapolate a treadmill angle which wouldexhaust that subject after two minutes of running at 8 mph.The third set of tests was the experimental trials. The fifth test was a 2 minute AST,performed at the angle extrapolated from the set two data, which additionally entailedmeasuring peak blood lactate and fitting the athlete with a Cosmed K2 system prior to thetest to measure EPOC. The two minute AST was designed to assess maximum attainableEPOC. The remaining three tests contrasted in that they were not exhaustive but stillrequired maximal efforts and like test five necessitated fitting of the Cosmed K2 systemprior to the test. Two sprinting conditions, an isokinetic protocol and an unresisted (free)protocol, were also employed. Test number six, the isokinetic condition, required subjectsto perform one set of five, five second, three metres per second repetitions, each separatedby a 10 second fifteen metre return jog. Tests seven and eight, the free sprintingconditions, entailed the performance of one set of 10 repetitions and one set of 5repetitions respectively. Each repetition, in both tests, was five seconds in duration andwas separated by a ten second, fifteen metre jogging recovery.3.4.2 Anaerobic Speed TestsAll four AST's were performed in the J.M. Buchanan Exercise Science Laboratory at theU.B.C. Aquatic Centre. The treadmill was elevated to a specified angle and set at 8 mph.Subjects were instructed to hold on to the hand rails and by their own volition to step onto the moving treadmill. Subjects ran until exhaustion, at which time they straddled thePROCEDURES^ 27treadmill and grabbed the handrails. Performance was measured by duration in secondsmaintained on the treadmill Timing of the run commenced once the subject had hoppedon to the treadmill and released his grip from the handrails and stopped once the subjecthad departed the treadmill or had grasped the handrails once again.3.4.3 Isokinetic SprintsIsokinetic sprints (test six) were conducted on an APM in the U.B.C. Thunderbird stadiumconcourse. Subjects were fitted with a waist belt which was clasped on to a cord whichwas wound on to the recoiling drum of the APM. The APM protocol involved 5repetitions of 5 seconds at 3 metres per second with a 10 second recovery. The subjectwas harnessed to the APM and the test was started as the subject initiated the firstrepetition. The APM allowed the sprinter to accelerate up to the programmed velocity (3m/s) after which time the uncoiling drum was isokinetically braked, making accelerationimpossible. The five second timer was automatically activated once the isokinetic brakehad engaged. Once the five second interval was over the machine braked the sprinter to arapid stop and activated the 10 second recovery timer. The subject was cued of the end ofthe ten second recovery and the simultaneous start of the next repetition by an electronicbeeper. During the recovery subjects were required to jog back to the APM to allow it torecoil the cord for the next interval. At the end of the fifth repetition the subject wasdetached from the APM and lead into the training room, which was directly adjacent fromthe finishing position, and made to lie supine on a plinthe for collection of blood andEPOC.PROCEDURES^ 283.4.4 Free SprintsThe two free sprinting conditions were also performed in the U.B.C. Thunderbird stadiumconcourse. The free sprint protocols mimicked the isokinetic condition to facilitate validcomparisons of the free and isokinetic conditions. The 5 repetition and 10 repetition freesprint protocols (tests seven and eight) required subjects to perform maximal sprintingrepetitions of 5 seconds separated by 10 second, 15 metre jogging recoveries. Signallingwas performed manually using a whistle in response to a continously running stopwatchand each test was designed so that the subject would complete the last repetition adjacentto the training room to minimize any further activity post-experimental. Upon completionof the fifth and tenth repetitions in their respective tests, blood lactate and EPOC weremeasured.3.5 Data Collection 3.5.1 Oxygen ConsumptionAll oxygen consumption analysis was performed with a portable K2 oxygen analyzer,which was set to sample every 15 seconds. Oxygen consumption analysis was performedfor RMR determination (test one), the 2 minute AST (test five), the 5 repetition isokineticsprint protocol (test six), the 5 repetition free sprint protocol (test seven) and the 10repetition free sprint protocol (test eight).3.5.2 Resting Metabolic RateEach subject's fasting resting oxygen consumption was measured for 10 minutes in thesupine position to assess RMR. The assessment took place at the subject's residence justPROCEDURES^ 29after waking up but prior to eating breakfast. RMR was calculated as the mean rate(L/min) of oxygen consumption for the last five minutes of the ten minute session.3.5.3 Excess Post-exercise Oxygen ConsumptionSubject's were layed to rest supine on a plinthe and thirty minute EPOC volumes (litres)were measured immediately after each test in set three. The Cosmed K2 oxygenconsumption analyzer was activated and continuously run from three minutes prior to thetest to thirty minutes post-exercise. Oxygen consumption was averaged for each minutefrom the four 15 second sampling intervals; consequently, absolute EPOC was calculatedas the sum of the thirty one minute averages and corrected EPOC was calculated asabsolute EPOC minus 30 minutes of RMR conditions extrapolated from the 5 minuteRMR measurement.3.5.4 Maximum EPOCMaximum EPOC was determined for each subject in response to, test five, an eight mphAST at an angle designed to last 2 minutes for each subject. The 2 minute value wasbased on the findings of Medbo et al (1988) who documented a plateauing of theattainable 02 deficit after 2 minutes of exhaustive treadmill running. This recognizedvalue circumvents the assignment of an arbitrary AST duration to elicit a maximumEPOC.PROCEDURES^ 303.5.5 Power OutputsPower outputs for each isokinetic repetition were measured in watts directly by the APMstrain gauges. The power output is the average for all the strides in the five secondinterval. Alternately, AST power outputs had to be calculated using trigonometry. Directpower measures were not obtainable for the free sprinting protocol.3.5.6 Blood LactateCutaneous finger tip 20 microlitre blood samples were collected one, three and fiveminutes post-exercise after each set three test while the subject lay on a plinthe. Thesamples were immediately haemolyzed and analyzed with a Kontron Medical lactateanalyzer 640 to determine the blood lactate concentration in millimoles per litre.3.5. 7 Free Sprint DistancesThe free sprint repetition and total distances were assessed using a marker droppingsystem. Ten sets of two markers were made. Marker sets 1 to 5 were used for the 5repetition protocol while all ten marker sets, 1 to 10, were used for the 10 repetitionprotocol. Each set of two markers were numbered 1 to 10 to indicate the respectiverepetition. One set of markers were handed to the subject prior to the start of eachrepetition. One marker was dropped at the starting postition while the other marker wasdropped when the five second interval whistle was heard. After the test was over alldistances between matching markers were measured in metres using a tape measure.PROCEDURES^ 313.6 Statistical AnalysisAn analysis of variance was used to compare the dependent variables EPOC (litres), andpeak blood lactate (mmol/L) over the four experimental conditions (tests 5 to 8). Astatistical significance level of (p< 0.001) was used in the analyses. Significant differencesbetween EPOC and peak blood lactate cell means were elucidated using Tukey's post hoccomparisons. Statistical significance level of (0( = 0.05) was used in the analyses. Acorrelation was then performed to measure the relationship of EPOC to peak bloodlactate.RESULTS4.1 Subjects Descriptive DataTen anaerobically trained university track athletes participated in this study. Two subjectswere not included in the data analysis because they did not perform their greatest EPOCafter the 2 min AST protocol. All subjects were in good health and injury free for eachtest. Descriptive data (age, height, weight, RMR. and RMR 30 minute volume) for theeight subjects are presented in Table 1.IITable 1: Subjects Mean Descriptive Data Age Height Weight RMR RMR(years) (cm) (kg) (litres/min) 30 MinuteVolume(litres)Mean 24.8 178.9 74.9 0.25 7.39St.Dev. 3.7 6.0 6.6 0.02 0.604.2 Performance DataThe variables of EPOC30min (litres) and peak blood lactate (mmol/L) were repeatedlymeasured over the four experimental protocols (tests 5 to 8) and correlated (r = +0.87).An ANOVA for each variable, shown in Table 7, over the four protocols revealedsignificant differences (p<.001) between the cell means. Tukey's post hoc comparison of32RESULTS^ 33EPOC30min means, displayed by Table 8, demonstrates that the significant differences(HSD = 2.02; 0( = .05) were between the 2 minute AST and 5 free sprinting repetitions(6.07), the 2 minute AST and 10 free sprinting repetitions (5.28), the 2 minute AST and 5APM repetitions (3.78) and 5 APM repetitions and 5 free sprinting repetitions (2.29).Similarily, Tukey's post hoc comparison of peak blood lactate means shown by Table 9,demonstrates that the significant differences (HSD = 1.72; a = .05) were between the 2minute AST and 5 free sprinting repetitions (5.00), the 2 minute AST and 10 free sprintingrepetitions (3.58), the 2 minute AST and 5 APM repetitions (2.06) and 5 APM repetitionsand 5 free sprinting repetitions (2.94).Tables 2 thru 5 also display post-exercise oxygen consumption (POC) for 1 minute(POC1Min) and other means further relevant to each described test. Expanded tables ofindividual data are provided in the Appendix. Table 6 expresses the EPOC30min andpeak blood lactate means for 5 APM, 10 free and 5 free repetitions as a percentage of the2 Min AST EPOC30min and peak blood lactate means.Figures 1, 2 and 3 graphically represent the POC over time, the volume of EPOC and thepeak concentrations of blood lactate respectively for the four experimental protocols.RESULTS^ 34!Table 2: 2 Minute AST Means; Test 5°A^Duration Watts Watts/Kg 1 MIN 30 MIN 30 MIN Peak LaGrade (seconds)^ POC^POC^EPOC (mmol/L)(litres)^(litres)^(litres)Mean 15.4 122 398.8 5.3 3.28 22.55 15.16 14.83St.Dev. 1.9 5.24 52.8 0.65 0.29 2.37 2.59 1.21Table 3: 5 Repetition APM Sprint Means; Test 6^Total Watts/Kg 1 MIN^30 MIN^30 MIN Peak LaWatts^POC^POC^EPOC mmol/L(litres)^(litres)^(litres)Mean^4362.9^58.2^2.68^18.77^11.38^12.77St.Dev.^508.6^4.00^0.43^2.84^2.72^1.97'Table 4: 10 Repetition Free Sprint Means; Test 7Total^1 MIN^30 MIN 30 MIN Peak LaDistance^POC^POC^EPOC^mmol/L(metres)^(litres)^(litres)^(litres)Mean^347.85^2.52^17.27^9.88^11.25St.Dev.^18.28^0.32^2.96^2.80^2.15RESULTS^ 35Table 5: 5 Repetition Free Sprint Means; Test 8Total^1 MIN^30 MIN 30 MIN Peak LaDistance^POC POC^EPOC^mmol/L(metres)^(litres)^(litres)^(litres)Mean 183.87 2.55 16.48 9.09 9.83St.Dev. 14.11 0.38 2.48 2.51 3.09'Table 6: Proportion of AST Peak La and EPOC30mi n Means5 Rep APM^10 Rep Free^5 Rep FreeEPOC 75.1%± 11.9 65.2%± 15.2 60.0%± 11.030 MinPeak La 86.1%±9.3 75.9%±9.8 66.3%± 15.7RESULTS^ 36Figure 1: Line Graph of Mean Post-Exercise Oxygen Consumption3.5tr 2.5e20f1.50xgen 0.52 Minute AST5 Repetition APM10 Repetition Free5 Repetition FreeRMR Baseline1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30Time (Minutres)RESULTS^ 37IIFigure 2: Bar Graph of Mean Excess Post-Exercise Oxygen Consumption^IJL 161t^14re 1215.1611.38S10 9.889.09O 8f6042en 2MinAST 5 APM 10 Free 5 FreeRESULTS^ 38IIFigure 3: Bar Graph of Mean Post-Exercise Peak Blood Lactate16mm 1414.831 12.7712 11.25L10 9.830f^8L^6a4ta^2te 0 2 Min AST 5 Rep APM 10 Free 5 Free-  ■■RESULTS^ 391Table 7: Repeated Measures 1 x 4 AnovaVariable^Sprinting Protocol^Significance(df, p)^(Yes/No)Peak Lactate^(18, .000)*^YesEPOC^(21, .000)^Yes30 Min* Note degrees of freedom are lower for peak lactate due to the inability to extract bloodfrom subject 2.Table 8: Tukey's Post Hoc Comparison of EPOC DataHSD= 2.02; 0(= .055FREE 10FREE 5 Rep APM 2 Min AST9.09 9.88 11.38 15.165FREE 9.09 0 0.79 2.29* 6.07*10FREE 9.88 0 1.5 5.28*5 Rep APM 11.38 0 3.78*2 Min AST 15.16 0* = Significant difference (0( = .05)RESULTS^ 40Table 9: Tukey's Post Hoc Comparison of Peak Blood Lactate DataHSD= 1.72; a= .055FREE 10FREE 5 Rep APM 2 Min AST9.83 11.25 12.77 14.835FREE 9.83 0 1.42 2.94* 5.00*10FREE 11.25 0 1.52 3.58*5 RepAPM 12.77 0 2.06*2 Min AST 14.83 0* = Significant difference (a =.05)RESULTS^ 414.3 Results of Hypotheses4.3.1 EPOC MeansA) 5 Rep APMEPOC---EPOC – 2 Min ASTEpOC^ RejectB) 5 Rep APM— -EPOC 10 Rep FreeSprintEpoc^ RejectC) 5 Rep APMEPOC 5 Rep FreeSprintEpOC^ Accept4.3.2 Peak Blood Lactate MeansA) 5 Rep APMBLa = 2 Min ASTBLa^ RejectB) 5 Rep APMBLa 10 Rep FreeSprintna^ RejectC) 5 Rep APMBLA 5 Rep FreeSprintna^ AcceptDISCUSSIONThe uniqueness of the exercise protocols, modalities and methodologies used in this study,make it difficult to compare previous findings with those presented in this paper. Thevariables analyzed have complicated underlying mechanisms and have not yet beendecisively quantified during exercise; therefore, the discussion will be somewhat general.Ten subjects participated in this study to investigate if EPOC30miN and peak bloodlactate responses are significantly different between maximal isokinetic and free sprintinginterval workbouts.5.1 SubjectsThe subject pool used in this study appears to be descriptively typical of other studieswhich used trained athletes. The fasting RMIZ. (0.25 L ± 0.02) falls well within the rangeof other findings (Bahr et al 1987, Bahr et al 1991). Similarly, the other descriptivecharacteristics of height, weight and age are undistinguished from one other supramaximalEPOC study (Bahr et al 1992).5.2 EPOCConsiderable debate surrounds the accounting of the processes which produce EPOC;however, there is little dispute over the existence of EPOC (Bahr et al 1992, Gore andWithers 1990; Maehlum et al 1986; Stainsby and Barclay 1970) and its validity as aquantifier of homeostatic disturbance (Sedlock et al 1989). However, until all theprocesses which influence EPOC are traceable and measureable, EPOC research will betechnologically limited to interpreting the volume of EPOC simply as an index of overall42DISCUSSION^ 43post-exercise recovery metabolism (Gaesser and Brooks 1984). Most EPOC research hasbeen confined to submaximal exercise and some low level supramaximal exercise.EPOC is a multifactorial process which is accounted for by more than just the eventsoccuring in the active muscle bed and other required cellular metabolism (Bahr et al1992). Processess reported to contribute to EPOC are the following: 1) replenishment of02 stores in blood and muscle 2) resynthesis of ATP and CP in the exercising muscles 3)conversion of lactate to glycogen 4) repletion of glycogen 5) response to catecholaminerelease 6) oxidation of fat 7) turnover of substrate cycles 8) elevation of body temperature9) compensatory increased protein synthesis 10) restoration of ionic homeostasis 11)thermic effect of food and 12) elevated physiological functioning (Bahr et al 1987; B. Bahrand Sejersted 1991; Bangsbo et al 1990; Bangsbo et al 1991; Bielinski et al 1985; Medboet al 1988; Roth et al 1988; Stainsby and Barclay 1970). EPOC estimates the total energyrequired to restore homeostasis. Even when controlling for catecholamines andtemperature, less than one third of the first three minutes of EPOC can be traced andaccounted for by the major oxygen requiring processes, which are the following 1) ATPand CP resynthesis 2) reloading of haemoglobin and myoglobin and 3) glycogenresynthesis (Bangsbo et al 1989). Therefore, EPOC is technologically limited toestimating the magnitude of homeostatic disturbance (Sedlock et al 1989).Non-steady workrate supramaximal exercises do not allow a linear extrapolation of 02demand and subsequent calculation of 02 deficit. Therefore, EPOC must be used as ameasure of recovery from metabolic stress. Although EPOC reflects more than anaerobiccatabolism (Bangsbo et al 1989; Gaesser and Brooks 1984; Medbo et al 1988; Stainsbyand Barclay 1970) it is a sensitive measure of performance improvements and of thecapacity to perform exhaustive exercise of short duration (Hermansen 1969). HermansenDISCUSSION^ 44was able, using 02 debt, to distinguish a highly trained athlete's 100M, 200M and 400Mperformances and was able to rank highly trained, trained, and untrained subjectsaccording to a standardized short duration performance Since Hermansen's study, theterm 02 debt has been replaced with the term EPOC to avoid any implication of causalitywhen explaining the elevated oxygen consumption. The change is purely in nomenclatureand not in method of analysis (Gaesser and Brooks 1984). Thus, the value of the EPOCmeasurement lies in its ability to metabolically compare non-steady state exercises such asisokinetic and free sprinting.The metabolic rate during the terminal stage of exercise carries over into recovery.Sedlock et al (1989) who used aerobic exercise, suggests that the initial metabolic rate inrecovery is an index of the intensity of the exercise. However, the metabolic rate asmeasured by 02 consumption reaches a ceiling at the VO2Max. As a result,supramaximal efforts of differing intensities will produce similar initial recovery VO2's.EPOCimiN after isokinetic and both free sprints were the same, demonstrating only thatthe three conditions maximally taxed the aerobic system for the given intermittentprotocol. Therefore, the three forms of sprinting used in this experiment can not bemetabolically classified by EPOCimiN.Gore and Withers (1990) using a repeated measures 3 X 3 factorial (30%, 50%, 70%V02mAx * 20, 50, 80 minutes), intensity by duration, design found that intensityexplained five times the variance in EPOC volume that duration or the intensity durationinteraction did. The EPOC30mm volume in this study predominantly reflects theintensity of each condition given the small duration range (25 and 50 seconds). TheEPOC differences found between 5 and 10 free sprints are surprisingly small, 9.09 and9.88 litres respectively; however, closer inspection reveals strikingly similar intensitiesDISCUSSION^ 45demonstrated by the average distance of each repetition, 36.77 and 34.79 metresrespectively. These results support the findings of Gore and Withers that exerciseintensity has an overwhelming influence over duration.The total distances attained by the free sprint protocols most closely reflect a 200 and 400metre sprint, not taking the recovery periods into account. Hermansen (1969) in arepeated 02 debt comparison of a 200 (22.2 seconds) and 400 metre (48.1 seconds) sprintfound an EPOC8mIN differential of 1 litre. The EPOC8mIN differential of the 5 and 10free sprints of this study was 0.20 litres. The slightly higher intensity of 5 repetitionsreduces the effect of the exercise duration of 10 repetitions.5.3 Blood LactateBlood lactate is the product of one process, albeit a net resultant of many factors.Generally, the net release of lactate to the blood is a function of the mass of musclerecruited, its fiber type composition and its intensity of activation (Stainsby and Brooks1990). Long duration submaximal exercise bouts eventually produce an equilibriumbetween lactate production and removal, resulting in a large total flux of lactate which isnot accurately reflected by the blood lactate concentration. Alternately, short durationsupramaximal exercise bouts produce increased blood lactate concentrations due to thetype IIB muscle fiber recruitment but also due to the cessation of exercise and subsequentrestriction of lactate clearance mechanisms by the reduction in blood flow and VO2(Jacobs 1986; Stainsby and Brooks 1990).The supramaximal blood lactate concentration reflects the production of lactate whereasthe submaximal blood lactate concentration reflects the capacity of the blood lactateclearance mechanisms (Astrand et al 1986; Gollnick et al 1986; Jacobs 1986; Stainsby andDISCUSSION^ 46Brooks 1990). Under the protocols used in this study, the factors which usually obscurethe findings based on peak blood lactates have largely been removed using a repeatedmeasures supramaximal protocol. Subsequently, the supramaximal peak blood lactateswill predominantly indicate the degree of glycolysis that occured in the active musculature.The larger lactate response of isokinetic sprinting over free sprinting as indicated by thepeak blood lactate values (Table 6) illustrates that the greater intensity demanded byisokinetic sprinting stimulates a greater turnover of glycolysis.Similar to EPOC, peak blood lactate data limits researchers to speculate on its underlyingmechanisms. Lactate appearance in the blood is the net result of its production,metabolism and transport from the cells and removal from the blood. Consequently theconcentration of lactate in the blood does not necessarily accurately reflect theintracellular glycolytic activity (Stainsby and Brooks 1990) However, the volume oflactate has been estimated from its concentration in the blood. This requires estimatingthe distribution volume for lactate and the exercising muscle mass which invokesconsiderable controversy (Astrand et al 1986).Despite the reported limitations of using blood lactate concentrations it has been shownthat, the repeated measures design, the exclusive use of sprinting, and the short durationand range of exercise (25 - 50 seconds) used in this study, minimizes the fluxing of lactate.Thus the concentration of blood lactate is indicative of the actual volume of lactatereleased to the blood. It is assumed from the similarity of all the exercise protocols thatthe same accumulation and clearance mechanisms are at work; thereby, facilitating a directcomparison of conditions using the peak blood lactate concentrations. In a literaturereview Jacobs (1986) concluded that the lactate response to supramaximal exercise was asensitive indicator of adaptation to sprint training and went on to state that it correlated toDISCUSSION^ 47supramaximal performance. Consequently, peak lactate concentration after supramaximalexercise of 1 minute duration is often used as a reliable index of glycolytic capacity. Thisis provided that the conditions following the exercise are standardized (Jacobs 1986).5.4 EPOC and Blood Lactate RelationshipSince Hermansen's study in 1969, there has been a paucity of research literature pertainingto the measurement of EPOC and peak blood lactate after short duration, maximal andexhaustive exercises. Bahr et al (1992) studied intensities at 108% of VO2mAx whichelicited an EPOC ih of 7.8 0.7 1 and a peak blood lactate value of 9.98 ± 1.10 mmo1.1 -1 after 3 x 2min bouts of stationary cycling. Comparatively, the present studydemonstrates the overwhelming influence of intensity over duration on EPOC and peakblood lactate. The 2 Min AST produced an EPOC30miN of 15.16 2.59 1 and a peakblood lactate of 14.83 ± 1.21 mmol .1 -1 . The least taxing (5 Free) condition evoked anEPOC30mIN of 9.09 2.5 1 and a peak blood lactate of 9.83 3.09 mmol•The correlation (r = +0.87) between EPOC30EN and peak blood lactate parallels thefinding of Bahr et al (1992). Bahr found a significant relationship (r = +0.86) between themean increase in blood lactate concentration over the first hour post-exercise andEPOCih. The correlations by no means imply that the amount of lactate produceddirectly dictates the EPOC volume, rather these variables are spuriously related by theeffect of intensity. Both EPOC and peak blood lactate concentration are products of theeffect of intensity of exercise. Correspondingly, induced lactacidemia via circulatoryocclusion, which does not reflect the intensity of exercise, does not result in an elevationof EPOC. The predominant removal of lactate during exercise recovery through oxidationdoes not allow lactate to critically contribute to EPOC (Roth et al 1988). Despite theDISCUSSION^ 48close relationship, lactate contributes to only a small part of EPOC (Bangsbo et al 1989;Bangsbo et al 1990).Five free sprint repetitions demand a larger proportion of ATP from the ATP-CP cyclethan 10 free sprints. The supply of CP gets progressively more depleted with theperformance of each repetition (Kaczkowski 1982). Subsequently, glycolytically derivedATP will be relied on. This helps to explain the larger lactate concentration produced by10 free sprints, while the findings of Bangsbo et al (1989, 1990) serve to explain the non-compensatory increase in EPOC.Maintainenance of the same free sprinting intensity of exercise requires a compensatoryincrease in the cycling of the glycolytic and Kreb's cycles. The increased glycolyticactivity results in a greater but not significantly different peak blood lactate response to 10free repetitions over 5 free repetitions. The predominantly oxidative fate of lactate resultsin an insignificantly larger 10 free repetition EPOC. Alternately, 5 isokinetic repetitionsare more intense and produce a greater homeostatic disturbance, resulting in both a largerpeak lactate and EPOC response.5.5 Anaerobic Power MasterMedbo and Tabata (1989) found that anaerobic ATP generation is highest during theinitial 5 - 10 seconds of a Wingate test; therefore, tests of peak power should last for 10seconds or less. These findings present the first repetition of the APM test as an idealindex of peak power generation. Particularly appealing is the fact that the test isperformed by sprinting and not cycling like the Wingate test. This form of peak powerassessment could be applicable to a wider range of sports. The APM can be easilyadapted to the environment of any linear motion sports performance. Besides sprinting,Rhodes et al (1991) used the APM in the analysis of power output for ice skating. TheDISCUSSION^ 49mean power output found by Rhodes and Roberts (1992) on the APM agrees with themean power (1001.3 ± 128.6 watts) produced in the first repetition of the present study.5.6 WorkThe comparison of the 5 and 10 free sprinting protocols via distance sprinted is a valid oneby virtue of the similarity of the two conditions. However, they do not compare toisokinetic or treadmill sprinting by similar performance variables. Also the isokinetic andtreadmill tests do not compare to each other by wattage. The wattage produced runningon a graded treadmill is a function of the subjects mass and the vertical displacement. Thewattage is based solely on the physical work performed; therefore, the metabolic cost isonly partially reflected. Alternately, the APM produces a strict horizontal resisting force,the wattage of which wholly reflects the energy output of the individual. Consequently,the wattage calculated by the 2 minute AST protocol (398.8 ± 52.8) is much smaller thanthat of the 5 repetition APM protocol (4362.9 ± 508.6). Therefore, to compare the non-steady state conditions, a common objective measure of metabolic demand (EPOC andpeak blood lactate) must be employed.5. 7 ConclusionsIn conclusion, this study demonstrates that there is a significant EPOC30mIN and peakblood lactate response between 5 isokinetic sprint repetitions and 5 free sprint repetitionsand no significant EPOC30mIN and peak blood lactate response between 5 isokineticsprint repetitions and 10 free sprint repetitions.Essentially the study shows the metabolic value of isokinetic tethered sprinting. Morephysical work is performed in less time compared to free sprinting. The isokinetic deviceDISCUSSION^ 50is specific to the acceleration of non-resisted performance; however, it is not applicable totraining maximal non-resisted velocities. Therefore, the value of the Anaerobic PowerMaster is as a supplement to sprint training acceleration and training the glycolyticpathways. However, to distinguish the true value of isokinetic sprinting a controlledlongitudinal training study using non-sprint trained individuals must be employed.Also the study has proven the value of employing a portable oxygen analyzer to measureEPOC and to compare non-steady state exercises. This improved technology facilitatesthe use of data collection from "field" performances. The applicability of research toactual sport performance is thereby enhanced.RECOMENDATIONSAn interesting hypothesis based on the rationale of this study is that the effect of intensity,duration, and the intensity duration interaction on EPOC may be maximal for exhaustiveexercise which elicits a peak 02 deficit as described by Medbo (1988). It would beinteresting to test the hypothesis that the percentage of maximal 02 deficit performed foran exhaustive exercise may correlate to the subsequent percentage of maximal EPOC.Much of the literature on EPOC focuses on acounting for the processes which producepost-exercise oxygen consumption in excess of RMR. The findings are consistentlyinconclusive and based on widely differing exercise protocols. The direction that EPOCresearch has taken, appears to have reached a deadlock with the state of technology.Further, attempts to account for the occurrence of EPOC do not appear to be advancingthe body of knowledge. Until further technological advances facilitate objective tracing ofpost-exercise oxygen consuming processes, EPOC research in the mean time would yieldgreater returns by applying the concept in its present state of understanding to establish itsvalue as a research variable. It has been demonstrated that significance of EPOC toweight loss is negligible (Bahr and Sejersted 1991); therefore, it may prove valuable inresearching the vastly untouched realm of non-steady workrate ultra-supramaximalexercise, which does not lend itself to 02 deficit determination.51APPENDIXTable 10: Individual Subject Descriptive Data Subject Age(years)Height(cm)Weight(kg)RMR(litres/min)RMR30 minutevolume(litres)1 26 180.80 83.30 0.22 6.602 27 186.70 82.10 0.22 6.603 20 180.30 81.40 0.25 7.504 22 178.70 70.60 0.28 8.405 26 183.90 74.80 0.24 7.206 30 171.50 66.00 0.25 7.507 27 168.90 69.10 0.25 7.508 20 180.70 71.70 0.26 7.8052APPENDIX^ 53II Table 11: Individual 2 Minute AST Data; Test 5Subject^%^Duration Total Watts 1 Min 30 Min 30 Min Peak LaGrade (seconds) Watts /Kg^POC^POC EPOC (mmol/L)(litres)^(litres)^(litres)1 16.00 119 459.88 5.54 2.94 22.72 16.12 14.562 13.00 130 369.68 4.51 3.61 26.16 19.56 N/A3 15.25 120 427.92 5.28 3.35 24.65 17.15 16.704 16.50 122 405.57 5.71 3.43 22.92 14.52 15.225 16.50 117 428.42 5.71 3.18 21.73 14.53 14.546 17.00 117 388.33 5.88 3.47 20.38 12.88 13.767 12.00 130 287.26 4.16 2.78 18.57 11.07 13.188 17.00 121 423.63 5.88 3.45 23.28 15.48 15.86APPENDIX^ 54II Table 12: Individual 5 Repetition APM Data; Test 6Subject TotalWattsWatts/Kg 1 MinPOC(litres)30 MinPOC(litres)30 MinEPOC(litres)Peak La(mmol/L)1 5152.00 62.07 2.71 18.28 11.68 12.662 4447.00 54.23 3.48 20.44 13.84 N/A3 4956.00 61.19 2.53 21.72 14.22 16.004 3755.00 52.89 2.79 22.46 14.06 12.565 4075.00 54.33 2.41 15.40 8.20 9.786 3799.00 57.56 2.53 16.96 9.46 12.687 4188.00 60.70 2.04 14.89 7.39 11.468 4531.00 62.93 2.98 19.97 12.17 14.27APPENDIX^ 55II Table13: Individual 10 Repetition Free Sprint Data; Test 7Subject Total 1 Min 30 Min 30 Min Peak LaDistance POC POC EPOC (mmol/L)(metres) (litres) (litres) (litres)1 361.20 2.64 14.33 7.73 9.282 340.15 2.60 17.06 10.46 N/A3 356.50 3.10 22.78 15.28 14.884 331.40 2.35 17.50 9.10 12.065 341.35 2.16 14.57 7.37 9.126 369.30 2.53 17.85 10.35 11.247 317.25 2.09 14.34 6.84 9.428 365.65 2.68 19.73 11.93 12.72APPENDIX^ 56Table 14: Individual 5 Repetition Free Sprint Data; Test 8 Subject Total 1 Min 30 Min 30 Min Peak LaDistance POC POC EPOC (mmol/L)(metres) (litres) (litres) (litres)1 200.65 2.95 15.47 8.87 8.002 164.75 3.04 18.49 11.89 N/A3 185.20 2.56 18.85 11.35 16.384 172.30 1.86 16.27 7.87 8.005 175.55 2.35 13.58 6.38 8.046 187.40 2.35 16.13 8.63 9.287 178.80 2.51 13.06 5.56 8.148 206.30 2.79 19.96 12.16 10.96APPENDIX^ 57Table 15: Individual Proportion of AST Peak La andEPOC30min MeansSubject 5 Rep APMEPOC30min^Peak La10 Rep FreeEPOC30min^Peak La5 Rep FreeEPOC30min^Peak La1 72.5% 87.0% 50.0% 63.7% 55.0% 54.9%2 70.8% N/A 53.5% N/A 60.8% N/A3 82.9% 95.8% 90.8% 89.1% 66.2% 98.1%4 96.8% 82.5% 62.7% 79.2% 54.2% 52.6%5 56.4% 67.3% 50.7% 62.7% 43.9% 55.3%6 73.4% 92.2% 80.4% 81.7% 67.0% 67.4%7 66.8% 86.9% 61.8% 71.5% 50.2% 61.8%8 78.6% 90.0% 77.1% 80.2% 78.6% 69.1%REFERENCESAlexander M.J.L. 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