Effects of prior exercise and recovery duration on oxygen uptake kinetics during heavy exercise in humans

Transcription

1 Effects of prior exercise and recovery duration on oxygen uptake kinetics during heavy exercise in humans Mark Burnley *, Jonathan H. Doust, Helen Carter and Andrew M. Jones *Chelsea School Research Centre, University of Brighton, Gaudick Road, Eastbourne, East Sussex BN20 7SP, School of Sport, Exercise and Leisure, University of Surrey Roehampton, West Hill, London SW15 3SN and Department of Exercise and Sport Science, Manchester Metropolitan University, Hassall Road, Alsager ST7 2HL, UK (Manuscript received 6 September 2000; accepted 1 March 2001) Prior heavy exercise (above the lactate threshold, LT) reduces the amplitude of the pulmonary oxygen uptake (V O2 ) slow component during heavy exercise, yet the precise effect of prior heavy exercise on the phase II V O2 response remains to be established. This study was designed to test the hypotheses that (1) prior heavy exercise increases the amplitude of the phase II V O2 response independently of changes in the baseline V O2 value and (2) the effect of prior exercise depends on the amount of external work done during prior exercise, irrespective of the intensity of the prior exercise. Nine subjects performed two 6 min bouts of heavy cycling exercise separated by 6 min baseline pedalling recovery (A), two 6 min heavy exercise bouts separated by 12 min recovery (6 min rest and 6 min baseline pedalling, B), and a bout of moderate exercise (below the LT) in which the same amount of external work was performed as during the prior heavy exercise, followed by 6 min heavy exercise (C). In both tests A and B, prior heavy exercise significantly increased the absolute V O2 amplitude at the end of phase II (by ~150 ml min _1 ), and reduced the amplitude of the V O2 slow component by a similar amount. Following 12 min of recovery (B), baseline V O2, but not blood [lactate], had returned to pre-exercise levels, indicating that these effects occurred independently of changes in baseline V O2. Prior moderate exercise (C) had no effect on either the V O2 or blood [lactate] responses to subsequent heavy exercise. The V O2 response to heavy exercise was therefore dependent on the intensity of prior exercise, and the effects on the amplitudes of the phase II and slow V O2 components persisted for at least 12 min following prior heavy exercise. Experimental Physiology (2001) 86.3, The pulmonary oxygen uptake (V O2 ) response to constant intensity exercise reflects the time course of the adjustment of muscle O 2 consumption towards a steady state, following a short delay reflecting the transit time of blood flow from the exercising muscle to the lung (Barstow et al. 1990; Grassi, 2000). It has been reported that a prior bout of heavy exercise (above the lactate threshold, LT) speeds the V O2 kinetics during subsequent heavy exercise (Gerbino et al. 1996; MacDonald et al. 1997). Both of these studies characterised the heavy exercise V O2 response using a single dynamic parameter ( effective time constant or mean response time). Although these monoexponential approximations may be reasonable for the interpretation of V O2 kinetics during moderate intensity exercise (below the LT), where a steady state V O2 is normally attained within 2 3 min, they may not be appropriate for the determination of the V O2 kinetics of heavy exercise (Whipp & Wasserman, 1972; Linnarsson, 1974). The delayed emergence of the V O2 slow component during heavy exercise (Barstow & Mole, 1991; Paterson & Whipp, 1991) significantly distorts the monoexponential description of the V O2 response (Linnarsson, 1974; Barstow et al. 1993; Burnley et al. 2000). In a recent study from our laboratory (Burnley et al. 2000), we used a model which characterised the three identifiable phases of the V O2 response with separate independent exponential functions (Fig. 1; Barstow et al. 1996). Using this modelling approach, we showed that the speeding of monoexponential V O2 kinetics noted previously was caused by a reduction in the amplitude of the V O2 slow component, and not by a speeding of phase II kinetics, because the associated time constant (r 1 ) was unaltered in the second exercise bout. These results indicate that if convective and/or diffusive oxygen delivery is increased by prior heavy exercise (Gerbino et al. 1996), then this has no discernible effect on the time course of the phase II V O2 response during subsequent heavy exercise. In our previous study (Burnley et al. 2000), in addition to the reduction in the amplitude of the V O2 slow component, we found that prior heavy exercise increased the absolute amplitude of the V O2 response at the end of phase II. Further, in all 10 of the subjects tested, baseline V O2 was elevated at the onset of the second bout of heavy exercise. However, because the parameter A 1 fi (the net amplitude of the phase II response, Fig. 1) is defined as the increase in V O2 above baseline during Publication of The Physiological Society Corresponding author: m.burnley@bton.ac.uk 2122

2 418 M. Burnley, J. H. Doust, H. Carter and A. M. Jones Exp. Physiol Table 1. Subjects physical characteristics Subject Age Sex Height Mass LT Peak V O2 Peak V O2 (years) (m) (kg) (l min _1 ) (l min _1 ) (ml kg _1 min _1 ) 122 M M M F M M M F M Mean S.D phase II, it was unclear whether the increase in the absolute V O2 amplitude at the end of phase II was dependent on the elevation in baseline V O2. If the elevation in absolute V O2 at the end of phase II reflected a true increase in the amplitude A 1 fi, that was not identified due to an elevation in baseline V O2, then it would be expected that A 1 fi would still be increased if the pre-exercise baseline V O2 was restored. To test the hypothesis that the elevation in the absolute V O2 amplitude at the end of phase II would persist if baseline V O2 was restored following prior heavy exercise, we extended the duration of recovery between two bouts of heavy exercise from 6 to 12 min. A second aim of the present study was to examine the influence of prior moderate exercise on the V O2 response to heavy exercise. In all previous studies, prior moderate exercise has not had any significant influence on the V O2 response to subsequent heavy exercise (Gerbino et al. 1996; MacDonald et al. 1997; Burnley et al. 2000). But all of these studies used prior moderate and heavy exercise of the same duration to examine the potential intensity-dependent effect of prior exercise. In the study of Burnley et al. (2000) approximately twice as much external work was accomplished during 6 min of heavy exercise (mean, 83 kj) compared to 6 min of moderate exercise (mean, 39 kj). Given the potentially important influence of elevated muscle temperature on the V O2 kinetic response to heavy exercise (Koga et al. 1997), equating the total work done may be of greater importance than equating the exercise duration when comparing prior moderate and heavy exercise. Therefore, we also tested the hypothesis that a prior bout of moderate exercise in which the same amount of external work was done as during a 6 min bout of heavy exercise would increase the absolute V O2 amplitude at the end of phase II and reduce the amplitude of the V O2 slow component. METHODS Subjects Nine healthy volunteers provided written informed consent to participate in this study, which was approved by the ethics committee of the University of Brighton, UK. The physical characteristics of the subjects are shown in Table 1. Experimental design The subjects reported to the laboratory in a rested, well hydrated state on seven occasions at the same time of day (±2 h) over a 2 week period. The first test was used to determine LT and peak V O2, whilst the other visits were used to complete the study. These six latter tests were performed in a random order. Only one test was performed on a given day, and tests were separated by at least 24 h. Figure 1 The three-phase response to constant intensity heavy exercise described with the three component exponential model of Barstow et al. (1996). Roman numerals at the top of the figure indicate each phase of the response. Adapted from Burnley et al. (2000).

3 Exp. Physiol Oxygen uptake kinetics during heavy exercise 419 Measurement of lactate threshold and peak V O2 All testing was performed on an electrically braked cycle ergometer (Jaeger ER 800, Germany), that has an accuracy of ±3 % for power outputs of up to 1000 W independent of pedal cadence. Each subject therefore self-selected a cadence of between 70 and 90 r.p.m., and maintained this throughout all tests (± 2 r.p.m.). Lactate threshold and peak V O2 were determined from an incremental cycle protocol. The tests began at a power output of W, and the power output was increased by 25 W every 4 min. At the end of each 4 min stage, a blood sample (~25 µl) was collected from the fingertip into a capillary tube for immediate analysis of blood lactate concentration ([lactate] blood ) using an automated lactate analyser (YSI Stat 2300, Yellow Springs, OH, USA). This analyser was calibrated hourly with a 5 mm lactate standard supplied by the manufacturer (YSI 2747). The 4 min stages were terminated when [lactate] blood increased by 1mM or more on two consecutive stages. The subjects completed between six and nine of these stages. When the 4 min stages were completed, the power output was increased in 25 W increments every minute until the subjects reached volitional exhaustion. Throughout the incremental test, pulmonary gas exchange was measured breath-by-breath, as described below. The steady-state V O2 for a given power output was taken as that measured over the last 30 s of each 4 min stage, while peak V O2 was determined as the highest value recorded in any 30 s period prior to the subject s volitional termination of the test. The LT was determined as a sudden and sustained increase in [lactate] blood above resting levels from visual inspection of individual plots of [lactate] blood vs. V O2 by two experienced, independent reviewers. Study 1: Effects of recovery duration Two exercise protocols were performed by the subjects, similar in design to those used previously (Gerbino et al. 1996; Burnley et al. 2000; see Fig. 2). The experimental tests consisted of two bouts of heavy exercise (at a power output half-way between LT and peak V O2 ) lasting 6 min, separated by a period of recovery. Before the onset of the first heavy intensity bout, 3 min of baseline cycling (at 20 W) was performed, followed by an immediate (square wave) increase in power output to the desired intensity. Constant intensity exercise was then sustained for 6 min. The first protocol involved two bouts of heavy intensity exercise separated by 6 min of recovery at 20 W. The second protocol required subjects to complete the first heavy intensity bout and then rest sitting upright on the cycle ergometer for 6 min. At the end of this period, subjects then resumed pedalling at 20 W for a further 6 min before completing a second heavy intensity bout. Therefore, the second protocol resulted in a doubling of recovery duration from 6 to 12 min without performing any additional external work to that of the standard 6 min recovery protocol used previously (see Fig. 2). To increase the signal-to-noise ratio, subjects performed each of these protocols twice. Immediately before and after each heavy intensity exercise bout, a capillary blood sample was taken from the fingertip for the determination of [lactate] blood, as described above. Study 2: Effects of prior moderate exercise The subjects performed another protocol which consisted of an initial 3 min period of cycling at 20 W, followed by of a bout of moderate intensity exercise (at a power output requiring 80 % of the LT), followed by a further 6 min of recovery at 20 W. The subjects then performed 6 min of heavy intensity exercise followed by a further 6 min of cycling at 20 W (Fig. 2). The duration of the prior moderate bout of exercise was calculated such that the subjects accomplished the same amount of external work during the moderate intensity exercise as was performed during the heavy exercise bouts (86 ± 3 kj, mean ± S.E.M.). The duration of the moderate intensity exercise bouts was min. As for the first study, the subjects performed this protocol twice on separate occasions. Figure 2 The three exercise protocols performed by each subject. In the 6 min recovery protocol, subjects pedalled for 3 min at 20 W, followed by an abrupt increase to a power output half-way between LT and peak (50 % ), which was sustained for 6 min. There then followed 6 min of recovery at 20 W, followed by the same increase in exercise intensity and a further 6 min recovery. The 12 min recovery and prior moderate exercise protocols followed a similar design, with an extra 6 min passive recovery and prolonged moderate exercise being performed, respectively, as shown.

4 420 M. Burnley, J. H. Doust, H. Carter and A. M. Jones Exp. Physiol Table 2. Oxygen uptake and blood [lactate] responses to heavy exercise Heavy exercise Heavy exercise Heavy exercise Initial bout of after after after prior heavy exercise 6 min recovery 12 min recovery moderate exercise V O2,b (l min _1 ) 0.80 ± ± 0.03 ac 0.80 ± 0.03 b 0.81± 0.02 Phase I A 0 fi (l min _1 ) 0.62 ± ± ± ± 0.07 r 0 (s) 12.7 ± ± ± ± 3.1 Phase II TD 1 (s) 21.3 ± ± 2.1 a 18.2 ± ± 3.1 A 1 fi (l min _1 ) 2.06 ± ± ± 0.09 abc 2.06 ± 0.08 r 1 (s) 24.6 ± ± ± ± 2.2 V O2,b + A 0 fi (l min _1 ) 2.86 ± ± 0.10 ac 3.00 ± 0.09 ac 2.87 ± 0.09 Slow component TD 2 (s) ± ± ± ± 5.7 A 2 fi (l min _1 ) 0.34 ± ± 0.03 ac 0.20 ± 0.03 ac 0.32 ± 0.04 Relative A 2 fi (%) 14.2 ± ± 1.5 ac 8.3 ± 1.2 ac 13.0 ± 1.7 r 2 (s) ± ± ± ± 13.1 Overall response Absolute EE V O2 (l min _1 ) 3.20 ± ± ± ± 0.09 Baseline blood [lactate] (mm) 0.8 ± ± 0.2 ac 2.4 ± 0.2 abc 0.7 ± 0.1 EE blood [lactate] (mm) 5.0 ± ± ± ± 0.2 All values are expressed as mean ± S.E.M. Parameters of the V O2 response are as detailed in the Methods section. a Significantly different from initial heavy exercise (P <0.05); b Significantly different from heavy exercise after 6 min recovery (P <0.05); c Significantly different from heavy exercise after prior moderate exercise (P <0.05). Measurement of pulmonary gas exchange Pulmonary gas exchange was measured breath-by-breath throughout all tests. Subjects wore a nose clip and breathed though a mouthpiece connected to a low resistance (0.65 cmh 2 Ol _1 s _1 at 8.5ls _1 ) turbine volume transducer for the measurement of inspiratory and expiratory volumes (Interface Associates, CA, USA). The turbine was calibrated using a 3 l calibration syringe (Hans Rudolph Inc., KS, USA). The dead space volume of the mouthpiece was 90 ml. A 2 m long capillary tube was used to continuously draw gas from the mouthpiece into a mass spectrometer (CaSE QP9000, Morgan Medical, Kent, UK) at a rate of 60 ml min _1. The mass spectrometer was tuned to measure O 2, CO 2 and N 2 concentrations at a rate of 50 Hz, and was calibrated before each test using a single-point calibration gas containing gases of known concentration (British Oxygen Company, London, UK). Volume and concentration signals underwent time alignment and analog digital conversion, and breath-by-breath values for V O2, carbon dioxide output (V CO2 ) and expired ventilation (V E ) were calculated and displayed on-line. Heart rate was continuously monitored using short-range telemetry (Polar Sports Tester, Kempele, Finland). Data analysis The breath-by-breath V O2 data were linearly interpolated to provided second-by-second values following the elimination of outlying breaths (defined as those that were ± 500 ml min _1 different from the average of the previous five breaths). For each subject, the two performances of each protocol were time aligned and averaged to provide one set of second-by-second data for each variation of the protocol. The V O2 responses were then modelled with iterative non-linear regression techniques in which minimising the sum of squared error was the criterion for convergence, using purpose-built fitting software. The time course of the V O2 response after the onset of exercise was described in terms of a three-component exponential function. Each exponential curve was used to describe one phase of the response. The first phase began at the onset of exercise, whereas the other terms began after independent time delays (Barstow et al. 1996): V O2 (t) = V O2,b +A 0 (1_ exp(_t/r 0 )) phase I (cardiodynamic component) + A 1 (1_ exp(_(t_td 1 )/r 1 )) phase II (primary component) + A 2 (1_ exp(_(t_td 2 )/r 2 )) phase III (slow component) (1) where V O2,b is the baseline V O2 measured in the 3 min preceding the onset of exercise; A 0, A 1 and A 2 are the amplitudes for the exponential curves; r 0, r 1 and r 2 are the time constants; and TD 1 and TD 2 are the time delays (Fig. 1). The phase I response was terminated at the onset of phase II (at TD 1 ), and given the value for that time (defined A 0 fi). The amplitude of the primary response (A 1 fi) was defined as the increase in V O2 from baseline to the end of phase II (i.e. A 0 fi + A 1 ). The absolute amplitude of the V O2 response at the end of phase II was calculated as the sum of baseline V O2 and A 1 fi. The amplitude of the V O2 slow component was determined as the increase in V O2 from TD 2 to the end of exercise (defined A 2 fi), rather than from the asymptotic value (A 2 ), which may project beyond the value at 6 min (end-exercise).

5 Exp. Physiol Oxygen uptake kinetics during heavy exercise 421 Statistical analysis The responses to the square-wave bouts of heavy exercise were compared using a one-way repeated measures ANOVA with post hoc Bonferroni-adjusted paired-samples confidence intervals. The relevant responses compared were the responses to initial heavy exercise, heavy exercise following 6 or 12 min of heavy exercise and heavy exercise performed following prior moderate exercise. The F ratios were interpreted as demonstrating a significant effect when P <0.05. RESULTS The incremental test data showed that the LT occurred at (mean ± S.D.) 63 ± 8% of peak V O2, and resulted in exercise power outputs of 120 ± 30 W for moderate exercise and 240 ± 30 W for heavy intensity exercise. Study 1: Effects of recovery duration The V O2 responses to heavy exercise as a function of recovery duration are shown in Table 2. In comparison to the initial bout of heavy exercise, the response to heavy exercise after 6 min of recovery was essentially the same as that observed previously (Burnley et al. 2000). Specifically, baseline V O2 was increased by ~120 ml min _1 prior to the onset of the second bout of heavy exercise (F 3,8 = 27.01, P<0.001, Table 2). In response to exercise, neither the amplitudes (A 0 fi and A 1 fi) nor the kinetics (r 0 and r 1 ) of the phase I and II responses were significantly altered by prior heavy exercise (Table 2), although the phase II response began earlier in the second heavy exercise bout (TD 1, F 3,8 = 4.69, P=0.01). Although prior heavy exercise did not significantly affect the V O2 response above baseline at the end of phase II (A 1 fi), the absolute V O2 response (baseline V O2 + A 1 fi) was increased by ~160 ml min _1 in the second heavy exercise bout (F 3,8 = 14.81, P<0.001, Table 2). The amplitude of the V O2 slow component was reduced by ~160 ml min _1 following prior heavy exercise (F 3,8 = 13.91, P<0.001, Table 2). Due to the elevation in the absolute V O2 response at the end of phase II and the reduced V O2 slow component, the V O2 values recorded at the end of exercise were similar between these two exercise bouts (F 3,8 = 0.75, P=0.54, Table 2). Table 2 shows that the 12 min recovery period allowed V O2 to return to pre-exercise baseline levels prior to the onset of the second heavy exercise bout. In contrast to the V O2 response following 6 min of recovery, A 1 fi was increased by ~130 ml min _1 following 12 min of recovery (F 3,8 = 11.16, P<0.001, Table 2). This increase in A 1 fi occurred without any change in the phase II time constant, and was followed by a reduction in the amplitude of the V O2 slow component that was similar in magnitude to that following 6 min of recovery (i.e. ~140 ml min _1, Table 2 and Fig. 3). As a consequence, the absolute end-exercise V O2 (V O2,EE) was again similar to that at the end of the initial bout of heavy intensity exercise. Indeed, there was a striking similarity in the absolute V O2,EE value between the three exercise conditions. Figure 4 provides the clearest demonstration of the effects of prior heavy exercise and recovery duration. The upper panel (Fig. 4A) shows the superimposed responses to heavy exercise in the 6 min recovery protocol. It is clear from this plot that prior heavy exercise resulted in an elevation in baseline (reflecting incomplete recovery from the prior heavy exercise) and an elevation in the absolute V O2 amplitude at the end of phase II (~2 min into exercise) in the second heavy exercise bout. The amplitude of the V O2 slow component was reduced by prior heavy exercise such that V O2 at the end of exercise was similar in both prior and subsequent exercise bouts. Figure 4B shows that following 12 min recovery the increase in V O2 at ~2 min persists in the second heavy exercise bout despite the equivalence of baseline V O2 between prior and subsequent heavy exercise. The increase in V O2 at 2 min in this plot therefore reflects a true increase in the net amplitude of the phase II response (A 1 fi). The subsequent reduction in the amplitude of the V O2 slow component, of similar absolute magnitude to the increase in A 1 fi, resulted in the attainment of a similar end exercise V O2. Table 2 shows that the baseline V O2 remains elevated following only 6 min (compared to 12 min) recovery. That the absolute V O2 amplitude at the end of phase II was also elevated during heavy exercise following only 6 min recovery therefore suggests that the inability to detect an elevation in A 1 fi was a consequence of baseline V O2 being Figure 3 Responses to the 6 min (A) and 12 min (B) recovery protocols in subject 1. Notice the similarity of responses in the first and second bouts of heavy exercise between protocols, the latter occurring despite the difference in recovery duration.

6 422 M. Burnley, J. H. Doust, H. Carter and A. M. Jones Exp. Physiol elevated by a similar magnitude (~120 ml min _1 ) to the increase in A 1 fi observed following 12 min of recovery. Neither the 6 min nor the 12 min recovery periods allowed capillary [lactate] blood to return to baseline levels. Although the baseline [lactate] blood was ~1.0 mm lower following 12 min recovery than after only 6 min, this value was still significantly elevated compared to the baseline [lactate] blood in the initial heavy exercise bout (F 3,8 = 82.10, P<0.001, Table 2). Despite these differences, the end-exercise [lactate] blood values were similar across conditions (F 3,8 = 1.78, P=0.18). Study 2: Effects of prior moderate exercise As shown in Table 2, prior moderate exercise had no significant effect on the V O2 or blood lactate responses to heavy exercise compared to the initial bout of heavy exercise. Thus, prior moderate exercise did not increase the amplitude A 1 fior reduce the amplitude of the V O2 slow component, in contrast to the responses following prior heavy exercise. This is most clearly demonstrated in Fig. 5, which shows the superimposed responses to the two bouts of heavy exercise in the 6 min recovery protocol (panel A) and the superimposed responses to heavy exercise without prior exercise (bout 1) and following prior moderate exercise (bout 2; panel B) in subject 6. The responses in panel B are remarkably similar, demonstrating none of the characteristic differences in the response amplitudes shown in panel A. Finally, the blood lactate responses to heavy exercise following prior moderate exercise were again essentially identical to the initial bout of heavy exercise (Table 2). DISCUSSION The principal findings of the present study were that prior heavy exercise, followed by 12 min of recovery, increased the net amplitude of the phase II response (A 1 fi) and reduced the amplitude of the V O2 slow component (A 2 fi) during heavy exercise. These findings suggest that the increase in the absolute V O2 amplitude at the end of phase II previously observed during heavy exercise following 6 min of recovery from prior heavy exercise (Burnley et al. 2000) was a consequence of an increase in the net amplitude of the phase II response itself (A 1 fi) and was not caused simply by an elevation in baseline V O2. These results were therefore consistent with our first hypothesis that prior heavy excercise increases the amplitude of the phase II response independently of changes in the baseline V O2. In contrast to our second hypothesis that the amount of external work done Figure 4 Superimposed responses to the 6 min (A) and 12 min (B) recovery protocols in subject 1. Note the difference in baseline V O2 but the similar ontransient response, with an elevation in V O2 at ~ 2 min into exercise in the second exercise bouts. Note also the smaller V O2 slow component leading to a similar end-exercise V O2 in both plots.

7 Exp. Physiol Oxygen uptake kinetics during heavy exercise 423 during prior excercise is important, prior moderate exercise (in which the external work accomplished was identical to a standard 6 min bout of heavy exercise) had no effect on the subsequent heavy exercise V O2 responses. The results of this study therefore add to the growing body of evidence which suggests that the effect of prior exercise is only observed following exercise that induces a residual elevation in [lactate] blood (Gerbino et al. 1996; Burnley et al. 2000). Importantly, however, the data of the present investigation provide clear evidence that prior heavy exercise influences the V O2 response amplitudes (A 1 fi and the V O2 slow component), and not the phase II V O2 kinetics (r 1 ). The present study demonstrated that a 12 min recovery period, unlike the 6 min recovery period previously used, was sufficient to restore baseline V O2 (but not [lactate] blood ) to its initial value. It has been demonstrated that following a bout of intense exercise, the recovery time course of adrenaline, noradrenaline and potassium is complete within 6 min (Robach et al. 1997; Bohnert et al. 1998). In the present study, following both 6 and 12 min periods of recovery, [lactate] blood V O2 remained elevated prior to the onset of the second bout of exercise. Allsop et al (1991) demonstrated that the recovery of intramuscular ph was incomplete up to 30 min after a bout of high-intensity exercise. The similarity of the V O2 response profiles following 6 and 12 min of recovery, and the likely time courses of several putative metabolic mediators (Allsop et al. 1991; Robach et al. 1997; Bohnert et al. 1998), suggests that the effect of prior heavy exercise is only observed under conditions of metabolic acidosis. Previous investigators have demonstrated that heavy exercise V O2 kinetics are speeded by a prior bout of heavy exercise (Gerbino et al. 1996), and proposed that this speeding is the consequence of an increased vasodilatation and a greater O 2 availability during the second bout of heavy exercise (Ward et al. 1994). It is clear from the present study and our previous work (Burnley et al. 2000) that the phase II V O2 kinetics are not speeded by prior heavy exercise. Instead, the present study indicates that the net amplitude of the phase II response (A 1 fi) is increased by prior heavy exercise. This was clearly seen during heavy exercise following 12 min recovery. The similar increase in absolute V O2 at the end of phase II following 6 and 12 min recovery suggests that A 1 fi was increased following 6 min recovery but that this was difficult to identify due to the elevated baseline V O2 in this condition. The amplitude A 1 fi has been shown to increase as a linear function of power output during cycle exercise (Barstow et al. 1993), and has been termed the target amplitude as a result (Barstow et al. 1996). Koga et al. (1999) found that supine cycling exercise had no Figure 5 Superimposed responses to heavy exercise in the 6 min recovery protocol (A) and initial heavy exercise compared to heavy exercise following prior moderate exercise (B) in subject 6. Notice the similarity of the V O2 response following prior moderate exercise compared to the initial heavy exercise bout (B).

8 424 M. Burnley, J. H. Doust, H. Carter and A. M. Jones Exp. Physiol effect on r 1, but reduced A 1 fi and increased the amplitude of the V O2 slow component compared to the upright condition. This observation led the authors to suggest that A 1 fimay be more sensitive than r 1 to changes in O 2 delivery. Interestingly, this response is opposite to that shown in the present study during the second bout of heavy exercise following a 12 min period of recovery. MacDonald et al. (1997) showed that breathing a hyperoxic gas mixture (70% inspired O 2 fraction) during heavy exercise had no effect on the phase II time constant compared to normoxia, but instead increased the absolute V O2 amplitude at the end of phase II and reduced the amplitude of the slow component. It is therefore possible that the effect of prior heavy exercise could still be ascribed to the alleviation of an O 2 delivery limitation, as originally proposed (Gerbino et al. 1996). However, in order to accept this postulate it is important that evidence exists to suggest that A 1 fi is determined, in part, by a lag in O 2 delivery during upright cycle exercise. Engelen et al. (1996) provide convincing evidence against this possibility. These authors showed that acute hypoxia (imposed by altering the inspired O 2 fraction from 21% to 12%) slowed the phase II kinetics but had no effect on either A 1 fi or the amplitude of the slow component. This suggests that while a reduction in O 2 delivery can modulate the rate of adjustment toward the required amplitude at the end of phase II, this target amplitude itself will be unaltered. We contend, therefore, that an increase in O 2 availability is not itself able to explain the alterations in the V O2 response profile shown in the present data (increased A 1 fi and reduced V O2 slow component). It is possible that the increase in A 1 fi and the subsequent reduction in A 2 fi could be explained by an increase in motor unit recruitment at the onset of a second bout of heavy exercise. This would result in an increase in V O2 at the end of phase II, even though the external power output requirement has not changed, by virtue of an increase in cross-bridge turnover and Ca 2+ pump activity required to sustain the additional fibre recruitment, both of which are ATPase dependent (Meyer & Foley, 1996). This would necessitate an increase in the bulk O 2 supply to meet the increased O 2 demand, without necessarily altering the rate of adjustment of V O2 toward A 1 fi. This may be viewed as a positive adaptation because the initial target V O2 is closer to the true V O2 requirement of the exercise (as reflected by end-exercise V O2 ). The attenuation of the V O2 slow component may be a consequence of the increase in A 1 fi. It is possible that motor units that might have been recruited later in exercise, as the slow component developed in the initial heavy bout, would be recruited at exercise onset in the second bout. Recent preliminary evidence suggests that motor unit recruitment is increased at the onset of a second bout of heavy exercise (Bearden & Moffatt, 2000). Previous reports have suggested that the effect of prior exercise is intensity dependent (Gerbino et al. 1996; MacDonald et al. 1997; Burnley et al. 2000). That is, a prior bout of moderate exercise seems to have no significant effect on the V O2 kinetics during subsequent heavy exercise (Burnley et al. 2000). The present study showed that when the amount of work done during prior moderate and heavy exercise was equated, both the V O2 and [lactate] blood responses to heavy exercise following this prior moderate exercise were remarkably similar to the initial heavy bout (Table 2 and Fig. 5B). From the data of the present study, and those of previous reports (Gerbino et al. 1996; MacDonald et al. 1997; Burnley et al. 2000) we suggest that the effect of prior exercise is unequivocally intensity dependent. The lack of change in the kinetics of the V O2 response to heavy exercise following prior moderate exercise would seem to rule out the possibility that increased muscle temperature alone could mediate the effects observed following prior heavy exercise. Both moderate and heavy intensity exercise are capable of elevating muscle temperature (Poole et al. 1991; Koga et al. 1997). Koga et al. (1997) elevated intramuscular temperature by external heating, and reported no increase in the amplitude of the phase II V O2 response. We therefore note that the effect of prior exercise on V O2 kinetics (i.e. an increase in A 1 fi and a reduction in the amplitude of the V O2 slow component) has only been demonstrated following an exercise-induced lactic acidosis. However, it is not clear exactly how an exerciseinduced lactic acidosis might influence the V O2 response to subsequent heavy exercise in the manner reported in the present work. In conclusion, prior heavy exercise resulted in an increase in the amplitude but no change in the kinetics of the phase II V O2 response during subsequent heavy exercise. The amplitude of the V O2 slow component was reduced by a similar magnitude to the increase in the phase II amplitude. Importantly, this effect was still apparent following 12 min of recovery, which was sufficient to restore pulmonary V O2, but not [lactate] blood, to its pre-exercise baseline value. Thus, the amplitude of the phase II V O2 response to heavy exercise had been increased by prior heavy exercise independent of the baseline V O2. In contrast, prior moderate exercise in which the same volume of work was accomplished as during a 6 min bout of heavy exercise had no effect on the subsequent heavy exercise V O2 response. We conclude, therefore, that the V O2 response to heavy exercise is dependent on the intensity of any preceding exercise bout and that the effects on the amplitudes of the phase II and slow V O2 components persist for at least 12 min following prior heavy exercise. ALLSOP, P., JORFELDT, L., RUTBERG, H., LENNMARKEN, C. & HALL, G. M. (1991). Delayed recovery of muscle ph after short duration, high intensity exercise in malignant hyperthermia susceptible subjects. British Journal of Anaesthesia 66, BARSTOW, T. J., CASABURI, R. & WASSERMAN, K. (1993). O 2 uptake kinetics and the O 2 deficit as related to exercise intensity and blood lactate. Journal of Applied Physiology 75, BARSTOW, T. J., JONES, A. M., NGUYEN, P. H. & CASABURI, R. (1996). Influence of muscle fibre type and pedal frequency on oxygen uptake kinetics of heavy exercise. Journal of Applied Physiology 81, BARSTOW, T. J., LAMARRA, N. & WHIPP, B. J. (1990). Modulation of muscle and pulmonary O 2 uptakes by circulatory dynamics during exercise. Journal of Applied Physiology 68,

9 Exp. Physiol Oxygen uptake kinetics during heavy exercise 425 BARSTOW, T. J. & MOLE, P. A. (1991). Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise. Journal of Applied Physiology 71, BEARDEN, S. E. & MOFFATT, R. J. (2000). Oxygen uptake kinetics in repeated square-wave cycling. Medicine and Science in Sports and Exercise 32 (suppl.), S248. BOHNERT, B., WARD, S. A. & WHIPP, B. J. (1998). Effects of prior arm exercise on pulmonary gas exchange kinetics during highintensity exercise in humans. Experimental Physiology 83, BURNLEY, M., JONES, A. M., CARTER, H. & DOUST, J. H. (2000). Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics and the slow component during heavy exercise. Journal of Applied Physiology 89, ENGELEN, M., PORSZASZ, J., RILEY, M., WASSERMAN, K., MEAHARA, K. & BARSTOW, T. J. (1996). Effects of hypoxic hypoxia on O 2 uptake and heart rate kinetics during heavy exercise. Journal of Applied Physiology 81, GERBINO, A., WARD, S. A & WHIPP, B. J. (1996). Effects of prior exercise on pulmonary gas exchange kinetics during high-intensity exercise in humans. Journal of Applied Physiology 80, GRASSI, B. (2000). Skeletal muscle V O2 on-kinetics: set by O 2 delivery or O 2 utilisation? New insights on an old issue. Medicine and Science in Sports and Exercise 32, KOGA, S., SHIOJIRI, T., KONDO, N. & BARSTOW, T. J. (1997). Effects of increased muscle temperature on oxygen uptake kinetics during exercise. Journal of Applied Physiology 83, KOGA, S., SHIOJIRI, T., SHIBASAKI, M., KONDO, N., FUKUBA, Y. & BARSTOW, T. J. (1999). Kinetics of oxygen uptake during supine and upright heavy exercise. Journal of Applied Physiology 87, LINNARSSON, D. (1974). Dynamics of pulmonary gas exchange and heart rate changes at start and end of exercise. Act. Physiologica Scandinavica 415 (suppl.), MACDONALD, M., PEDERSEN, P. K. & HUGHSON, R. L. (1997). Acceleration of V O2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise. Journal of Applied Physiology 83, MEYER, R. A. & FOLEY, J. M. (1996). Cellular processes integrating metabolic response to exercise. In Handbook of Physiology, section 12, Exercise: Regulation and Integration of Multiple Systems, ed. ROWELL, L. B. & SHEPHERD, J. T., pp American Physiological Society, Bethesda, MD, USA. PATERSON, D. H. & WHIPP, B. J. (1991). Asymmetries of oxygen uptake transients at the on- and offset of heavy exercise in humans. Journal of Physiology 443, POOLE, D. C., SCHAFFARTZIK, W., KNIGHT, D. R., DERION, T., KENNEDY, B., GUY, H., PREDILETTO, R. & WAGNER, P. D. (1991). Contribution of the exercising legs to the slow component of oxygen uptake kinetics in humans. Journal of Applied Physiology 71, ROBACH, P., BIOU, D., HERRY, J.-P., DEBERNE, D., LETOURNEL, M., VAYSSE, J. & RICHALET, J.-P. (1997). Recovery processes after repeated supramaximal exercise at the altitude of 4,350 m. Journal of Applied Physiology 82, WARD, S. A., SKASICK, A. & WHIPP, B. J. (1994). Skeletal muscle oxygenation profiles and oxygen uptake kinetics during highintensity exercise in humans. Federation Proceedings 8, A288. WHIPP, B. J. & WARD, S. A. (1990). Physiological determinants of pulmonary gas exchange kinetics during exercise. Medicine and Science in Sports and Exercise 22, WHIPP B. J. & WASSERMAN, K. (1972). Oxygen uptake kinetics for various intensities of constant-load work. Journal of Applied Physiology 33,