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Effects of previous dynamic arm exercise on poweroutput during repeated maximal sprint cyclingG.C. Bogdanis a , M.E. Nevill a & H.K.A. Lakomy aa Department of Physical Education, Sports Science and Recreation Management ,Loughborough University of Technology , Loughborough, LE11 3TU, UKPublished online: 01 Feb 2008.

To cite this article: G.C. Bogdanis , M.E. Nevill & H.K.A. Lakomy (1994) Effects of previous dynamic arm exercise on poweroutput during repeated maximal sprint cycling, Journal of Sports Sciences, 12:4, 363-370, DOI: 10.1080/02640419408732182

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Journal of Sports Sciences, 1994, 12, 363-370

Effects of previous dynamic arm exercise on poweroutput during repeated maximal sprint cycling

G.C. BOGDANIS,* M.E. NEVILL and H.K.A. LAKOMYDepartment of Physical Education, Sports Science and Recreation Management, Loughborough University ofTechnology, Loughborough LE11 3TU, UK

Accepted 3 February 1993

This study examined the effects of elevating blood lactate concentration by arm exercise on subsequentperformance during repeated 30 s sprints with the legs. Eight malestudents performed two 30 s cycle ergometersprints separated by 6 min of recovery, on two occasions. On one occasion the subjects performed only the two30 s cycle ergometer sprints ('legs')> while on the other occasion 5 min of heavy arm cranking preceded the twosprints ('arms and legs'). Blood lactate concentration was determined from capillary samples at rest, after astandardized warm-up and 3 and 5 min following each exercise bout. In the 'legs' condition, the peak poweroutput (PPO) and mean power output (MPO) in the second sprint were 92% (P < 0.05) and 85% (P < 0.01) of thevalues attained during the first sprint, respectively. Prior arm exercise, which increased blood lactate to 11.0 ± 0.6mM, had no effect on PPO and MPO during the first cycle ergometer sprint ( 4% drop, N.S.). However, in thesecond sprint after prior arm exercise, PPO was 10% lower than the PPO attained during the correspondingsprint in the 'legs' condition (sprint 2 'arms and legs' 963 ± 42 W, sprint 2 'legs' 1074 ± 60 W, P<0.05), whileMPO was better maintained (sprint 2 'arms and legs' 517 ± 17 W, sprint 2 "legs' 549±24 W, N.s.). The rate ofblood lactate accumulation after both cycle ergometer sprints was considerably decreased (by 50%) whenblood lactate levels were pre-elevated by arm crank exercise. It is suggested that the elevation of blood lactatelevels by prior arm exercise can cause a significant drop in PPO of the second sprint by decreasing musclebuffering capacity and lactate/H+ efflux from the muscle. The less pronounced drop in MPO during the secondsprint in the 'arms and legs' condition was assumed to be due to an increased aerobic contribution to energysupply.

Keywords : Blood lactate, prior arm exercise, fatigue, recovery, sprint cycling.

Introduction

The role of inactive muscle as an effective site for bloodlactate clearance has long been recognized (Ahlborg etal., 1975). Although the mechanisms for the trans-location of lactate (La~) and the corresponding H + (dueto lactic acid dissociation) from and to the muscle are notclear, the involvement of a carrier mechanism forLa~/H+ co-transport plays a significant role in humanmuscle Quel, 1988, 1991).

During lactate infusion or an elevation of blood lactateconcentration due to exercise, inactive skeletal muscletakes up La~ and H+ , acting as both a passive 'sink' andutilizer (Gladden et al, 1980; Gladden, 1989; Kowal-chuk et al., 1988). Despite H + uptake, the pH of inactivemuscles remains almost unchanged, at the expense of a

* To whom all correspondence should be addressed.

0264-0414/94 © 1994 E. & F.N. Spon

decreased ability of the muscle to buffer further changesin intracellular [H+] (Hultman et al., 1985). This resultsin a decreased endurance capacity of the previouslyinactive muscles (Karlsson et al., 1975; Yates et al.,1983) caused by a higher degree of muscle acidificationduring contraction. Furthermore, the decreasedLa~/H+ efflux from the muscle, due to a decreasedLa~/H+ gradient between muscle and blood and/or asaturation of a La~/H+ carrier mechanism Quel, 1988),also contributes to the decrease in muscle pH duringsubsequent exercise. However, the maximal isometricforce remains unaffected (Yates et al., 1983). The limitednumber of studies in this area has been confined to eitherisometric or submaximal dynamic exercise.

The purpose of the present investigation was toexamine the effects of elevating blood lactate concentra-tion by arm crank exercise, on dynamic performanceduring two 30 s maximal sprints on a cycle ergometer.

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Methods

Subjects

Eight male university students volunteered to particip-ate in this study. Their mean (+S.D.) age, height andbody mass were 26+4 years, 176 + 6 cm and 80.7 + 11kg, respectively. Although all the subjects were physic-ally active, none was involved in regular training. Thesubjects were informed in writing about the purpose ofthe study, any known risks and the right to terminateparticipation at will. Each expressed his understandingby signing a statement of informed consent.

Equipment

A modified friction-loaded cycle ergometer (Monark,model 864), interfaced with a microcomputer, was usedin order to attain high-frequency logging of the flywheelangular velocity. The instantaneous power generatedduring the sprints was corrected for the changes inkinetic energy of the flywheel (Lakomy, 1986). Arestraining harness, passed around the subject's waist,was used during the cycle ergometer sprints so as to limitthe exercise to the lower limbs. The two side-straps ofthe belt were fixed to a metal rail, bolted to the floorbehind the bicycle frame. Pilot studies showed thatpower generation was not affected by the use of therestraining harness. The optimal seat height wasadjusted for each subject so that the knee was slightlyflexed when the pedal was at the bottom of its travel.Toe-clips were used to secure the subject's feet on thepedals.

Arm cranking tests were carried out using a modified,wall-mounted, arm crank ergometer (Monark Rehab

Trainer, model 881). The principles for power calcula-tions during arm cranking were the same as thosedescribed above for cycle ergometer sprinting. A digitalspeedometer was placed in front of the subject so as toprovide feedback about the crank rate. The subjectplacement in relation to the pedal cranks was precise andrepeatable. The axis of the pedal cranks was adjusted tocorrespond to the subject's shoulder height (Sawka etal., 1983). A head support was used to standardize forbody position and limit the excessive extraneous move-ments, while the feet were placed under the chair toensure minimal leg involvement during arm cranking.

Experimental procedures and protocol

Prior to any experimental testing, each subject com-pleted at least two practice sessions on both ergometers.The subjects were requested to follow their normal diet(for 48 h) and refrain from any form of intense physicalexercise (for 24 h) before each test. Each subjectperformed all tests at the same time of the day, whichwas at least 4 h after any meal. Two experimental testswere carried out in a random order, at least 4 days apart.

During one test, the subjects were required toperform two 30 s maximal cycle ergometer sprintsagainst a resistance of 75 g kg" ' body mass (BM), from arolling start of approximately 70 rev min"1. The sprintswere separated by 6 min of passive recovery on thebicycle seat (see Fig. 1).

In the other session, the subjects completed 5 min ofarm crank exercise (4.5 min at 80 rev min"1 and 30 sall-out cranking at the end), against a resistancedetermined for each individual from a 30 s maximal armcranking sprint performed on a separate day. The loadrepresented 30% of mean power output of the arm

ONLY IN THE "ARMS AND LEGS" CONDITION RECOVERY

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Figure 1 Schematic representation of the experimental design. B.S., capillary blood samples.

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Prior arm exercise and power output during sprint cycling 365

sprint, as this was found to be the maximal sustainablework rate for 5 min of arm cranking (unpublishedobservations). Six minutes after the arm crank exercise,two 30 s maximal cycle ergometer sprints were per-formed, with a 6 min passive recovery in between. Astandardized warm-up on both ergometers precededeach session (Fig. 1). Strong verbal encouragement wasgiven throughout the test. The peak power output(PPO), mean power output (MPO) and the percentagedecline from peak to end power output (fatigue index:F.I.) were calculated for each 30 s sprint.

Blood sampling and analysis

Duplicate samples (20 ^1 each) of arterialized capillaryblood were taken from a pre-warmed thumb for lactatedetermination at rest, after the standardized warm-upand 3 and 5 min following each exercise bout (see Fig. 1).Capillary samples were immediately deproteinized in2.5% perchloric acid, stored at — 20°C and analysed at alater date using a fluorometric method described byMaughan (1982).

. Statistical analysisA two-way analysis of variance (ANOVA) for repeatedmeasures on both factors was used for statisticalevaluation. Where significant F-ratios (P<0.05) werefound, the means were compared using a Tukey post-hoctest. The relationships between the variables wereexamined by calculating the product-moment correla-tion coefficient (r). The results are presented as themean + standard error.

Results

Power output

The peak power output (PPO) and mean power output(MPO) of each cycle ergometer sprint, in both experi-mental conditions, are shown in Fig. 2. The poweroutput and pedal rate profiles of these sprints areillustrated in Fig. 3.

Prior arm exercise had only a small, non-significanteffect on PPO and MPO during the first cycle ergometersprint. During the second sprint in the 'arms and legs'condition, MPO was similar to that attained in thecontrol 'legs' condition. However, PPO during thesecond sprint after arm exercise was 10% lower(P<0.05) than the PPO attained during the secondsprint in the 'legs' condition (Fig. 2). It is noteworthythat the difference in pedal speed between the secondsprints of the two conditions was more pronouncedduring the first few seconds (Fig. 3). In the 'legs'condition, PPO and MPO in the second sprint were

1400 i

legs

arms and legs

ac

SPRINT1

I legs

arms and legs

SPRINT 2

SPRINT 1 SPRINT 2

Figure 2 Peak power output (top) and mean power output(bottom) during sprints 1 and 2, with ('arms and legs') andwithout ('legs') preceding arm exercise (x ± S.E.). a, P<0.01from sprint 1 ; b, P < 0.05 from sprint 1 ; c, P < 0.05 from 'legs'.

92 % (P < 0.05) and 85 % (P < 0.01 ) of the values attainedduring the first sprint, respectively.

There was no difference in the fatigue index (F.I.) forthe first and second sprint in the 'arms and legs'condition (63 + 2 and 65 ± 3 % ; N.S.). However, thefatigue index was higher during the second sprint, whencompared with the first sprint, in the 'legs' condition(62 + 2 vs 67 + 3%, P<0.01).

Strong negative relationships (r= —0.75; P<0.05)were found between PPO per kg body mass (PPO/BM)attained in the first sprint ('legs' condition), and the PPOand MPO recovery in the second sprint in bothexperimental conditions (MPO or PPO recovery =MPO or PPO during sprint 2 expressed as a percentageof sprint 1). These relationships suggest that the morepowerful subjects had the slower rate of recovery ofpower output. Similar relationships were also found forthe absolute PPO values. The subjects with higher PPOduring the first sprint ('legs' condition) also had a higherF.I. for that sprint (r = 0.72; P<0.05). In addition, highnegative correlations were found between F.I. in thefirst sprint and MPO recovery in the second sprint, in

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5"

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Figure 3 Power output (top) and pedal speed profiles(bottom) during sprints 1 and 2, with (ARMS/LEGS) andwithout (LEGS) previous arm exercise (mean for eightsubjects; s.E. omitted for clarity).

both experimental conditions (r=— 0.93 to —0.96;P<0.01;seeFig. 4).

Blood lactate and heart rate

The blood lactate responses to the preceding armexercise and the 30 s cycle ergometer sprints, in bothexperimental conditions, are illustrated in Fig. 5 (top).The highest blood lactate concentration ([La]) wasobserved 5 min after each bout, with the exception of thesecond sprint in the 'arms and legs' condition, where thehighest [La] was observed 3 min post-recovery. Bloodlactate after the first cycle ergometer sprint was signific-antly different between the 'legs' and the 'arms and legs'conditions (P<0.01), but similar values were reachedafter the second sprint (Fig. 5).

The increase in [La] after each sprint is shown in Fig.5 (bottom). For the 'legs' condition, the 'delta lactate'

CM

y - 146.47 - 0.98940X RA2 - 0.871

r = - 0 . 9 3

50 60 70

F.I legs 1 (%)

Figure 4 The relationship between the fatigue index (F.I.)of the first sprint in the 'legs' condition and mean power outputrecovery for the second sprint. The regression equation,correlation coefficient and coefficient of determination are alsoshown (P < 0.01 ; n=8).

value for the first sprint was obtained by subtracting the[La] post-warm-up from that following sprint 1,whereas for the 'arms and legs' condition, the corres-ponding 'delta' value was the difference between [La]after the arm crank exercise and that attained after sprint1. For sprint 2, 'delta lactate' was calculated bysubtracting the [La] 5 min following sprint 1 from thehighest [La] after sprint 2.

It is evident that the rate of blood lactate accumulationwas considerably descreased (by »50%) when bloodlactate levels were pre-elevated by arm crank exercise.More pronounced decreases in the rate of blood lactateaccumulation were observed after the second sprint,where delta lactate values were »30% of those foundfollowing sprint 1.

The [La] after the first sprint was found to benegatively correlated with power output recovery dur-ing the second sprint, especially during the 'arms andlegs' condition. The highest correlation was obtained forMPO recovery at the second sprint during the 'arms andlegs' condition (r= -0.79; P<0.05; Fig. 6). It wouldseem, therefore, that high blood lactate levels are relatedto a decreased recovery of mean power output in thesecond sprint.

The peak heart rate (HR) attained during the 'legs'condition was similar for the first and second sprints(184+10 vs 180 + 8 beats min"1). There was atendencyfor HR to decrease with each successive exercise bout inthe 'arms and legs' condition (arms only =184 + 8,sprint 1 = 181 + 10 and sprint 2 = 176 + 9 beats min"1;N.S.). In both experimental conditions, the percentdecrease in HR at sprint 2 was correlated with thepercent drop in PPO and MPO during the sprint(r=0.82-0.88;P<0.01).

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p<0.01 100

20-

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rest W.U. 3 5 3 5TIME (min)

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Figure 5 Blood lactate concentration at rest, post-warm-up,and 3 and 5 min after each exercise bout, for the twoexperimental conditions (top), and increases in blood lactateconcentration (delta values) after sprints 1 and 2, in bothconditions (bottom). Values are x ± s.E. a, P<0.01 from'legs'; b, P<0.01 from arms; c, /><0.01 from sprint 1.

Discussion

The results of this study demonstrated that prior armexercise had a different effect on power output duringthe two subsequent 30 s sprints. While all power outputindices dropped by « 4 % during the first sprintfollowing arm exercise, PPO was affected more thanMPO by prior arm exercise during the second sprint. AsPPO and MPO during the first sprint were equallyaffected by preceding arm exercise, this would suggestthat a common factor, or factors, were operating incausing fatigue during sprint 1.

In the present study, it was assumed that an elevationin H+ and blood lactate levels due to intense armexercise, would result in an uptake of La~ and H + by theleg muscles, which in turn could decrease their perform-ance. Since the La~ is not known to have any adverseeffect on energy metabolism or the contraction process(Sahlin, 1986), the changes in intracellular [H+] will

CM

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y = 130.78 - 2.6474x RA2 - 0.621

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Peak [La] post sprint 1 arms and legs (mM)

Figure 6 The relationship between the highest blood lactateconcentration after the first sprint in the 'arms and legs'condition and the mean power output recovery at the secondsprint. The regression equation, correlation coefficient andcoefficient of determination are also shown (P<0.05; n = 8).

determine the degree of performance impairment.Karlsson et al. (1975) reponed that concomitant withLa~ and H + uptake by non-exercising muscles, there is adecrease in muscle phosphocreatine (PCr) due to theeffects of H+ on creatine kinase equilibrium. However,no muscle pH measurements were made in their study,and therefore the extent and consequent implications ofthe decrease in pH are not known.

Evidence for the nature of the changes in restingmuscle homoeostasis following acidification of the bloodwas furnished by Hultman et al. (1985). They found thatammonium chloride (NH4C1) ingestion results in adecreased muscle and blood buffering capacity, withouta significant decrease in resting muscle pH. However, apronounced decrease in muscle pH was seen afterelectrical stimulation at «70% of maximum voluntarycontraction after NH4C1 ingestion. This was accom-panied by a decreased force production, which wassignificant only after 75 s of contraction. Studies thathave investigated the effects of NH4Cl-induced acidosison sprint performance, have found that a decrease inblood pH has little influence on short-term (30 s) poweroutput, but results in a significantly decreased bloodlactate concentration (McCartney et al., 1983a). Thesefindings are in agreement with the results of the presentstudy, where despite a maintained power output duringthe first sprint following arm exercise, the increase in[La] after that sprint was only half of that induced by thefirst sprint during the 'legs' condition. Both a reducedLa~/H+ efflux from the muscle, and an inhibition ofglycolysis by H+ , can be put forward as possibleexplanations for the decreased rate of lactate accumu-lation. A possibility exists that towards the last secondsof the first sprint, the pre-elevated blood lactate and H+

caused a saturation of a carrier mechanism and/or a

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decrease in the H+ gradient between muscle and bloodQuel, 1988; Gladden, 1989), thereby resulting in adecreased La~/H+ efflux and consequently higherintracellular [H+]. However, this did not significantlyaffect power output during the first sprint. On the otherhand, results from studies examining the effects ofsimilar, exercise-induced changes in blood acid-basestatus, on exercise of longer duration with previouslyresting muscle groups, have shown decreases of 21-31 %in endurance capacity (Karlsson et al., 1975; Yates et al.,1983). It would seem, therefore, that the decrease inperformance due to prior acidification of the blood is afunction of exercise time. Consequently, due to the shortduration of the sprints in the present study (30 s), theeffects of a pre-elevated [La] on power output wereminimal during the first sprint.

The situation is nevertheless different when short-term exercise is repeated following blood acidification.During the 6 min of recovery between the two sprints,one would expect an almost complete resynthesis of PCr(Harris et al., 1976), and a corresponding recovery of thepeak force/power output (Hitchcock, 1989; Sahlin andRen, 1989; Sargeant and Dolan, 1987). However, thePPO during the second sprint after arm exercise in thepresent study was significantly depressed. If leg musclepH was indeed lower in the recovery period after thefirst sprint, then a decreased rate of PCr resynthesis dueto the effect of H+ on creatine kinase equilibriumprobably occurred (Sahlin et al., 1979). Since PCr isconsidered to be linked to a high power output over thefirst few seconds of high-intensity exercise, a low initialcontent might affect PPO. A reduced PCr resynthesiswas also observed by Spriet et al. (1989), during thesecond and third bouts of three 30 s sprints which wereseparated by 4 min of recovery. This decrease in PCrresynthesis was attributed to 'pooling of the blood' inthe legs, because no pedalling was allowed during theresting period between sprints.

Alternatively, a slowing of the relaxation rate of themuscle is considered to be related to a decreased musclepH. Hydrogen ions will affect the activity of the enzymesCa2+ re-uptake ATPase and myosin ATPase (Cady etah, 1989) and sarcoplasmic reticulum function (Naka-maru and Schwartz, 1972; Allen et al., 1992). Animpaired relaxation rate during the second sprint willaffect the ability of the subject to accelerate the flywheeland hence generate a high PPO, since quick movementsare the result of the time-dependent contraction andrelaxation of different muscles (Sahlin, 1986). It isinteresting to note that during the first few seconds ofthat sprint, the subjects were pedalling much moreslowly, whereas the major part of the sprint wasperformed at a similar velocity to the correspondingsprint during the 'legs' condition (see Fig. 3).

On the other hand, the fact that MPO was better

maintained seems paradoxical, considering the possi-bility of a decreased anaerobic ATP turnover rate due tolower [PCr] and an impaired glycolysis through an H+

inhibition of the key enzymes PFK and phosphorylase(Trivedi and Danforth, 1966; Spriet et al, 1989). Themaintenance of power output at reasonably high levels,despite a possibly decreased anaerobic energy provision,may be explained by an increased contribution byaerobic metabolism.

Careful inspection of the pedal speed profiles (Fig. 3)shows that during the last half of the second sprint, inboth conditions, the legs were cycling very slowly. Thedrop in pedal speed and power to levels lower than 70 revmin"1 and 400 W, respectively, during the last 10 s ofsprint 2, probably indicates fatigue of the fast-twitch(FT) fibres and therefore an increasing reliance on slow-twitch (ST) fibres in order to maintain power generationvia aerobic pathways. These suggestions are supportedby the findings of other studies employing repeated 30 ssprints designs. In the study by Spriet et al. (1989), thetotal work done during the third 30 s sprint was 82% ofthe work in sprint 2, whereas glycolysis was only 32% ofthat in sprint 2, with similar ATP and PCr changes.These authors concluded that total work in bout 3 wasmaintained by a greater reliance on slow-twitch fibresand oxidative metabolism. Similar conclusions werereached by McCartney et al. (1986), who found evidenceof an increased intramuscular fat metabolism support-ing power generation at the later stages of a repeated 30 ssprints protocol. Furthermore, it has been shown thatfaster cardiovascular adjustments resulting in fasterI^O2 kinetics occur after prior exercise with the same orother muscle groups (Pendergast et al., 1983). Thus,prior exercise would facilitate a shift to a greater aerobiccontribution to energy supply. Even though &O2 duringthe sprints was not measured in the present study, anincrease in PO2 during the last sprint after arm exerciseprobably occurred. It is interesting to note that I^O2maxhas been found to be negatively correlated with thefatigue index during all-out cycling (30 s) at slowpedalling velocities (60 rev min"1; McCartney et al.,1983b), implying a substantial reliance on aerobicmetabolism and slow-twitch fibres.

The increase in [La] after the second sprint in the'arms and legs' condition (Fig. 5) was only 2.1 mM,showing both a decreased lactate (and probably H+)efflux and a reduced glycolytic contribution. Addition-ally, blood lactate peaked earlier (3 min) after that sprint.Therefore, it seems reasonable to suggest that the higherblood lactate is related to a lower rate of blood lactateaccumulation. Experiments in vitro using frog sartor-ious muscle have shown that extracellular pH andbicarbonate concentration can influence lactate and H+

efflux from the muscle, and are also related to tensionrecovery (Mainwood and Worsley-Brown, 1975;

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Prior arm exercise and power output during sprint cycling 369

Renaud 1989). Furthermore, Rieu et al. (1988) alsoobserved a decrease in 'delta' lactate values when bloodlactate concentration was increased by repeated 45 streadmill runs at 175% VO2 max. Similar findings werereported by McCartney et al. (1986) and Spriet et al.(1989).

Another finding of the present study is that both PPOand MPO during the second sprint in the 'legs'condition were significantly depressed, even after 6 minof recovery (Fig. 2). This observation shows thatrecovery of muscle metabolites and power output after ashort-term all-out sprint (30 s) takes longer, in compari-son with prior exercise of lower intensity (e.g. Harris etal, 1976; Hitchcock, 1989; Sargeant and Dolan, 1987).

In the present study, the subjects with the higherPPO/BM during the first sprint (i.e. the more powerfulsubjects), had the higher fatigue index and also the lowerMPO and PPO recovery rates for the second sprint. Thedifferent recovery rates between individuals might berelated to differences in muscle fibre composition.Results from studies in which the 30 s Wingate test wasperformed, showed a positive correlation between thepercentage of fast-twitch fibres of the quadriceps muscleand the fatigue index (Karlsson et al., 1981). Further-more, it has been shown that individuals with mainly FTfibres have a limited ability to maintain force productionduring, and to recover between, repeated bouts ofmaximal isokinetic knee extensions (Colliander et al.,1988). These findings imply that the function of FTfibres is impaired far more in comparison with ST fibresby repeated sprint exercise. Several in vitro studies haveshown that FT fibres are more sensitive to changes in theintracellular environment (Donaldson, 1983). AlthoughFT fibres have a higher basal PCr content, the rate ofPCr utilization is faster compared with that of ST fibres(Tesch et al., 1989). Recent evidence by Greenhaff et al.(1992) showed that during a 30 s sprint on a non-motorized treadmill, the glycogenolytic rate in FTfibres is almost twice as high as that in ST fibres. Thiswill probably result in a more pronounced accumulationof H+ in FT fibres. It would appear, therefore, that FTfibres will 'fatigue' more, due to (1) a H+ effect onglycolysis and the contractile apparatus and (2) adecrease in PCr.

In summary, this study has shown that previous armexercise has an effect on power output during the secondof two 30 s cycle ergometer sprints. The most probablemechanism for the reduction in power output underconditions where blood lactate is previously elevated, isa reduced lactate and H+ gradient between muscle andblood, together with a decreased blood and inactivemuscle buffering capacity. Slowing of relaxation due toH+ and availability of PCr may be the reasons for alarger drop in PPO during the second sprint in the 'armsand legs' condition, while MPO was affected less

probably because of a higher aerobic contribution to theenergy supply.

Acknowledgements

G.C.B. was a recipient of a postgraduate scholarship from theGreek State Scholarships Foundation.

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