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Biomedical subjects

Andrew M Jones

Publications and source records attributed to Andrew M Jones.

At least 55 records · Page 3Linked to original sources
PubMed2004

Influence of DCA on pulmonary (.-)V(O2) kinetics during moderate-intensity cycle exercise.

PURPOSE: To test the hypothesis that pharmacological activation of the pyruvate dehydrogenase enzyme complex (PDC) with dichloroacetate (DCA) would speed phase II pulmonary oxygen uptake ((.-)V(O2)) kinetics after the onset of subsequent moderate-intensity (40-45% ((.-)V(O2)) peak) cycle exercise. METHODS: Seven healthy males (mean +/- SD age 25 +/- 4 yr, body mass 75.3 +/- 9.4 kg) performed four "square-wave" transitions from unloaded cycling to a work rate requiring 90% of the predetermined gas exchange threshold either with or without prior infusion of DCA (50 mg x kg body mass in 50 mL saline). Pulmonary ((.-)V(O2)) was measured breath-by-breath in all tests and ((.-)V(O2)) kinetics were determined from the averaged individual response to each condition using nonlinear regression techniques. RESULTS: The blood [lactate] measured immediately before the onset of exercise was significantly reduced in the DCA condition (C: 1.1 +/- 0.3 vs DCA: 0.6 +/- 0.3 mM; P < 0.01) consistent with successful activation of the PDC. However, DCA had no discernible effect on the rate at which ((.-)V(O2)) increased toward the steady state after the onset of exercise as reflected in the phase II time constant (C: 28.5 +/- 11.8 vs DCA: 29.4 +/- 14.9 s). CONCLUSIONS: The results suggest that PDC activation does not represent a principal intramuscular limitation to ((.-)V(O2)) kinetics after the onset of moderate-intensity exercise.

Adult↗
PubMed2003

Dichloroacetate does not speed phase-II pulmonary VO2 kinetics following the onset of heavy intensity cycle exercise.

We hypothesised that pharmacological activation of the pyruvate dehydrogenase enzyme complex (PDC) by dichloroacetate (DCA) would speed phase-II pulmonary O2 uptake (VO2) kinetics following the onset of high-intensity, sub-maximal exercise. Eight healthy males (aged 19-33 years) completed two "square-wave" transitions of 6 min duration from unloaded cycling to a work-rate equivalent to approximately 80% of peak VO2 either with or without prior i.v. infusion of DCA (50 mg kg(-1) body mass in 50 ml saline). Pulmonary VO2 was measured breath-by-breath throughout all tests, and VO2 kinetics were determined using non-linear regression techniques from the averaged individual response to each of the conditions. Infusion of DCA resulted in significantly lower blood [lactate] during the baseline cycling period (means+/-SEM: control 0.9+/-0.1, DCA 0.5+/-0.1 mM; P<0.01) consistent with successful activation of PDC. However, DCA had no discernible effect on the rate at which VO2 increased towards the initially anticipated steady state following the onset of exercise as reflected in the time constant of the fundamental VO2 response (control 26.7+/-4.1, DCA 27.7+/-2.8 s). These results indicate that the principal limitation to oxidative metabolism following the onset of high-intensity, sub-maximal cycle exercise lies downstream from PDC and/or that muscle O2 consumption is primarily under "feedback" control via the concentration of one or more of the reactants associated with ATP hydrolysis.

Adult↗
PubMed2003

Influence of L-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise.

We hypothesized that inhibition of nitric oxide synthase (NOS) by N(G)-nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (Vo(2)) by nitric oxide and result in a speeding of phase II pulmonary Vo(2) kinetics at the onset of heavy-intensity exercise. Seven men performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and peak Vo(2) with and without prior intravenous infusion of L-NAME (4 mg/kg in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath by breath, and Vo(2) kinetics were determined from the averaged response to two exercise bouts performed in each condition. There were no significant differences between the control (C) and L-NAME conditions (L) for baseline Vo(2), the duration of phase I, or the amplitude of the primary Vo(2) response. However, the time constant of the Vo(2) response in phase II was significantly smaller (mean +/- SE: C: 25.1 +/- 3.0 s; L: 21.8 +/- 3.3 s; P < 0.05), and the amplitude of the Vo(2) slow component was significantly greater (C: 240 +/- 47 ml/min; L: 363 +/- 24 ml/min; P < 0.05) after L-NAME infusion. These data indicate that inhibition of NOS by L-NAME results in a significant (13%) speeding of Vo(2) kinetics and a significant increase in the amplitude of the Vo(2) slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component Vo(2) kinetics after L-NAME infusion indicates that at least part of the intrinsic inertia to oxidative metabolism at the onset of heavy-intensity exercise may result from inhibition of mitochondrial Vo(2) by nitric oxide. The cause of the larger Vo(2) slow-component amplitude with L-NAME requires further investigation but may be related to differences in muscle blood flow early in the rest-to-exercise transition.

Adult↗
PubMed2003

Influence of muscle fibre type and pedal rate on the VO2-work rate slope during ramp exercise.

We hypothesised that the ratio between the increase in oxygen uptake and the increase in work rate (Delta VO(2)/DeltaWR) during ramp cycle exercise would be significantly related to the percentage type II muscle fibres at work rates above the gas exchange threshold (GET) where type II fibres are presumed to be active. We further hypothesised that ramp exercise at higher pedal rates, which would be expected to increase the proportional contribution of type II fibres to the total power delivered, would increase the Delta VO(2)/DeltaWR slope at work rates above the GET. Fourteen healthy subjects [four female; mean (SD): age 25 (3) years, body mass 74.3 (15.1) kg] performed a ramp exercise test to exhaustion (25 W min(-1)) at a pedal rate of 75 rev min(-1), and consented to a muscle biopsy of the vastus lateralis. Eleven of the subjects also performed two further ramp tests at pedal rates of 35 and 115 rev min(-1). The Delta VO(2)/DeltaWR slope for exercise GET ( S(2)) was significantly correlated to percentage type II fibres ( r=0.54; P=0.05). The ratio between the Delta VO(2)/DeltaWR slopes for exercise above and below the GET ( S(2)/ S(1)) was significantly greater at the pedal rate of 115 rev min(-1) [1.22 (0.09)] compared to pedal rates of 35 rev min(-1) [0.96 (0.02)] and 75 rev min(-1) [1.09 (0.05), ( P<0.05)]. The greater increase in S(2) relative to S(1) in subjects (1) with a high percentage type II fibres, and (2) at a high pedal rate, suggests that a greater recruitment of type II fibres contributes in some manner to the "xs" VO(2) observed during ramp exercise.

Adult↗
PubMed2003

Inhibition of nitric oxide synthase by L-NAME speeds phase II pulmonary .VO2 kinetics in the transition to moderate-intensity exercise in man.

There is evidence that the rate at which oxygen uptake (.VO2) rises at the transition to higher metabolic rates within the moderate exercise intensity domain is modulated by oxidative enzyme inertia, and also that nitric oxide regulates mitochondrial function through competitive inhibition of cytochrome c oxidase in the electron transport chain. We therefore hypothesised that inhibition of nitric oxide synthase (NOS) by nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial .VO2 by nitric oxide and result in a speeding of .VO2 kinetics at the onset of moderate-intensity exercise. Seven males performed square-wave transitions from unloaded cycling to a work rate requiring 90 % of predetermined gas exchange threshold with and without prior intravenous infusion of L-NAME (4 mg kg-1 in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath-by-breath and .VO2 kinetics were determined from the averaged response to four exercise bouts performed in each condition using a mono-exponential function following elimination of the phase I response. There were no significant differences between the control and L-NAME conditions for baseline .VO2 (means +/- S.E.M. 797 +/- 32 vs. 794 +/- 29), the duration of phase I (15.4 +/- 0.8 vs. 17.2 +/- 0.6), or the steady-state increment in .VO2 above baseline (1000 +/- 83 vs. 990 +/- 85 ml min-1), respectively. However, the phase II time constant of the .VO2 response was significantly smaller following L-NAME infusion (22.1 +/- 2.4 vs. 17.9 +/- 2.3; P < 0.05). These data indicate that inhibition of NOS by L-NAME results in a significant (19 %) speeding of pulmonary .VO2 kinetics in the transition to moderate-intensity cycle exercise in man. At least part of the intrinsic inertia to oxidative metabolism at the onset of moderate-intensity exercise may result from competitive inhibition of mitochondrial .VO2 by nitric oxide at cytochrome c oxidase, although other mechanisms for the effect of L-NAME on .VO2 kinetics remain to be explored.

Adult↗
PubMed2003

Oxygen uptake kinetics during moderate, heavy and severe intensity "submaximal" exercise in humans: the influence of muscle fibre type and capillarisation.

The purpose of the present study was to test the hypothesis that muscle fibre type influences the oxygen uptake (.VO(2)) on-kinetic response (primary time constant; primary and slow component amplitudes) during moderate, heavy and severe intensity sub-maximal cycle exercise. Fourteen subjects [10 males, mean (SD) age 25 (4) years; mass 72.6 (3.9) kg; .VO(2peak) 47.9 (2.3) ml kg(-1) min(-1)] volunteered to participate in this study. The subjects underwent a muscle biopsy of the vastus lateralis for histochemical determination of muscle fibre type, and completed repeat "square-wave" transitions from unloaded cycling to power outputs corresponding to 80% of the ventilatory threshold (VT; moderate exercise), 50% (heavy exercise) and 70% (severe exercise) of the difference between the VT and .VO(2peak). Pulmonary .VO(2) was measured breath-by-breath. The percentage of type I fibres was significantly correlated with the time constant of the primary .VO(2) response for heavy exercise (r=-0.68). Furthermore, the percentage of type I muscle fibres was significantly correlated with the gain of the .VO(2) primary component for moderate (r=0.65), heavy (r=0.57) and severe (r=0.57) exercise, and with the relative amplitude of the .VO(2) slow component for heavy (r=-0.74) and severe (r=-0.64) exercise. The influence of muscle fibre type on the .VO(2) on-kinetic response persisted when differences in aerobic fitness and muscle capillarity were accounted for. This study demonstrates that muscle fibre type is significantly related to both the speed and the amplitudes of the .VO(2) response at the onset of constant-load sub-maximal exercise. Differences in contraction efficiency and oxidative enzyme activity between type I and type II muscle fibres may be responsible for the differences observed.

Adaptation, Physiological↗
PubMed2003

Inequalities in self-reported health: validation of a new approach to measurement.

This paper assesses the internal validity of using the McMaster 'Health Utility Index Mark III' (HUI) to scale the responses on the typical self-assessed health (SAH) question, "how do you rate your health status in general?" It compares alternative procedures to impose cardinality on the ordinal responses. These include OLS, ordered probit and interval regression approaches. The cardinal measures of health are used to compute and to decompose concentration indices for income-related inequality in health. These results are validated by comparison with the individual variation in the 'benchmark' HUI responses obtained from the Canadian 'National Population Health Survey 1994-1995'. The interval regression approach, which exploits a mapping from the empirical distribution function (EDF) of HUI into SAH, outperforms the other approaches. In addition, we show how the method can be extended to allow for differences in SAH thresholds across different groups of people and to measuring and decomposing 'pure' health inequality.

Bias↗
PubMed2003

Prior heavy exercise enhances performance during subsequent perimaximal exercise.

PURPOSE: To test the hypothesis that prior heavy exercise increases the time to exhaustion during subsequent perimaximal exercise. METHODS: Seven healthy males (mean +/- SD 27 +/- 3 yr; 78.4 +/- 0.7 kg) completed square-wave transitions from unloaded cycling to work rates equivalent to 100, 110, and 120% of the work rate at VO2peak (W-[VO2peak) after no prior exercise (control, C) and 10 min after a 6-min bout of heavy exercise at 50% Delta (HE; half-way between the gas exchange threshold (GET) and VO2peak), in a counterbalanced design. RESULTS: Blood [lactate] was significantly elevated before the onset of the perimaximal exercise bouts after prior HE (approximately 2.5 vs approximately 1.1 mM; P < 0.05). Prior HE increased time to exhaustion at 100% (mean +/- SEM. C: 386 +/- 92 vs HE: 613 +/- 161 s), 110% (C: 218 +/- 26 vs HE: 284 +/- 47 s), and 120% (C: 139 +/- 18 vs HE: 180 +/- 29 s) of W-VO2peak, (all P < 0.01). VO2 was significantly higher at 1 min into exercise after prior HE at 110% W-VO2peak (C: 3.11 +/- 0.14 vs HE: 3.42 +/- 0.16 L x min(-1); P < 0.05), and at 1 min into exercise (C: 3.25 +/- 0.12 vs HE: 3.67 +/- 0.15; P < 0.01) and at exhaustion (C: 3.60 +/- 0.08 vs HE: 3.95 +/- 0.12 L x min(-1); P < 0.01) at 120% of W-VO2peak. CONCLUSIONS: This study demonstrate that prior HE, which caused a significant elevation of blood [lactate], resulted in an increased time to exhaustion during subsequent perimaximal exercise presumably by enabling a greater aerobic contribution to the energy requirement of exercise.

Adult↗
PubMed2003

Effects of prior exercise on metabolic and gas exchange responses to exercise.

'Warm-up' activity is almost universally performed by athletes prior to their participation in training or competition. However, relatively little is known about the optimal intensity and duration for such exercise, or about the potential mechanisms primed by warm-up that might enhance performance. Recent studies demonstrate that vigorous warm-up exercise that normally results in an elevated blood and presumably muscle lactate concentration has the potential to increase the aerobic energy turnover in subsequent high-intensity exercise. The reduced oxygen deficit is associated with a reduction in both the depletion of the intramuscular phosphocreatine stores and the rate at which lactic acid is produced. Furthermore, the oxygen uptake 'slow component' that develops during high-intensity, ostensibly submaximal, exercise is attenuated. These factors would be hypothesised to predispose to increased exercise tolerance. Interestingly, the elevation of muscle temperature by prior exercise does not appear to be implicated in the altered metabolic and gas exchange responses observed during subsequent exercise. The physiological mechanism(s) that limit the rate and the extent to which muscle oxygen uptake increases following the onset of exercise, and which are apparently altered by the performance of prior heavy exercise, are debated. However, these mechanisms could include oxygen availability, enzyme activity and/or availability of metabolic substrate, and motor unit recruitment patterns. Irrespective of the nature of the control mechanisms that are influenced, 'priming' exercise has the potential to significantly enhance exercise tolerance and athletic performance. The optimal combination of the intensity, duration and mode of 'warm-up' exercise, and the recovery period allowed before the criterion exercise challenge, remain to be determined.

Acidosis, Lactic↗
PubMed2003

Comparing the efficiency of national health systems: a sensitivity analysis of the WHO approach.

The World Health Organization (WHO) has used econometric methods to measure the efficiency of health care systems. We assess the robustness of WHO results to definitions of efficiency and statistical procedures. Originally analysed by the WHO, the data are for 1997 (50 countries) and 1993-1997 (141 countries). The efficiency of each country in promoting population health is estimated after taking into account health care expenditure, all other expenditure and education levels. Efficiency scores are compared under different definitions of efficiency and different estimation methods. The results show that the country rankings and efficiency scores are sensitive to the definition of efficiency and choice of model specification. We conclude that econometric methods can yield insights into complex socioeconomic phenomena. However, the lack of robust results to reasonable alternative specifications suggests that it is premature to use the methods adopted by the WHO to construct league tables of health systems.

Data Collection↗
PubMed2002

Effect of pedal rate on primary and slow-component oxygen uptake responses during heavy-cycle exercise.

We hypothesized that a higher pedal rate (assumed to result in a greater proportional contribution of type II motor units) would be associated with an increased amplitude of the O(2) uptake (Vo(2)) slow component during heavy-cycle exercise. Ten subjects (mean +/- SD, age 26 +/- 4 yr, body mass 71.5 +/- 7.9 kg) completed a series of square-wave transitions to heavy exercise at pedal rates of 35, 75, and 115 rpm. The exercise power output was set at 50% of the difference between the pedal rate-specific ventilatory threshold and peak Vo(2), and the baseline power output was adjusted to account for differences in the O(2) cost of unloaded pedaling. The gain of the Vo(2) primary component was significantly higher at 35 rpm compared with 75 and 115 rpm (mean +/- SE, 10.6 +/- 0.3, 9.5 +/- 0.2, and 8.9 +/- 0.4 ml. min(-1). W(-1), respectively; P < 0.05). The amplitude of the Vo(2) slow component was significantly greater at 115 rpm (328 +/- 29 ml/min) compared with 35 rpm (109 +/- 30 ml/min) and 75 rpm (202 +/- 38 ml/min) (P < 0.05). There were no significant differences in the time constants or time delays associated with the primary and slow components across the pedal rates. The change in blood lactate concentration was significantly greater at 115 rpm (3.7 +/- 0.2 mM) and 75 rpm (2.8 +/- 0.3 mM) compared with 35 rpm (1.7 +/- 0.4 mM) (P < 0.05). These data indicate that pedal rate influences Vo(2) kinetics during heavy exercise at the same relative intensity, presumably by altering motor unit recruitment patterns.

Adult↗
PubMed2002

Effect of prior heavy arm and leg exercise on VO2 kinetics during heavy leg exercise.

The aim of the present study was to examine the effect of prior exercise at a remote site on the VO(2) kinetics during subsequent heavy cycle exercise using a model that allowed us to discriminate between the VO(2) fast and slow component responses. Ten male subjects completed a constant-load exercise of 6 min cycling at 90% of the VO(2)peak in three conditions: without prior exercise (LE-C), after heavy cycling exercise (6 min at 90% of the VO(2)peak) (LE-L) and after heavy arm-cranking exercise (6 min at 90% of the arm VO(2)peak) (LE-A). Subjects performed four repetitions of each exercise protocol, separated by at least 1 day. VO(2) was measured on a breath-by-breath basis and VO(2) kinetics were determined with a biexponential model. There were no significant differences in the VO(2) fast component parameters between LE-C, LE-L and LE-A. However, the VO(2) slow component amplitude was significantly reduced in LE-L and LE-A compared to LE-C, but the reduction was less pronounced in LE-A [the value of the VO(2) slow exponential term at the end of exercise, A(2)', was 657 (SD 200) ml x min(-1) in LE-C versus 384 (SD 136) ml x min(-1) in LE-L and 551 (SD 169) m x min(-1) in LE-A; P<0.05]. The results of this study demonstrate that prior heavy arm exercise alters VO(2) kinetics during cycling exercise by reducing the VO(2)slow component amplitude, though this reduction is smaller than the reduction observed following prior heavy leg exercise. These data indicate that the primary factor causing changes in the VO(2) kinetics is probably located in the involved muscle.

Adaptation, Physiological↗
PubMed2002

Oxygen uptake kinetics during high-intensity arm and leg exercise.

The purpose of the present study was to examine the oxygen uptake kinetics during heavy arm exercise using appropriate modelling techniques, and to compare the responses to those observed during heavy leg exercise at the same relative intensity. We hypothesised that any differences in the response might be related to differences in muscle fibre composition that are known to exist between the upper and lower body musculature. To test this, ten subjects completed several bouts of constant-load cycling and arm cranking exercise at 90% of the mode specific V(O(2)) peak. There was no difference in plasma [lactate] at the end of arm and leg exercise. The time constant of the fast component response was significantly longer in arm exercise compared to leg exercise (mean+/-S.D., 48+/-12 vs. 21+/-5 sec; P < 0.01), while the fast component gain was significantly greater in arm exercise (12.1+/-1.0 vs. 9.2+/-0.5 ml min(-1) W(-1); P < 0.01). The V(O(2)) slow component emerged later in arm exercise (126+/-27 vs. 95+/-20 sec; P < 0.01) and, in relative terms, increased more per unit time (5.5 vs. 4.4% min(-1); P < 0.01). These differences between arm crank and leg cycle exercise are consistent with a greater and/or earlier recruitment of type II muscle fibres during arm crank exercise.

Adult↗
PubMed2002

Maximal lactate steady state, critical power and EMG during cycling.

We hypothesised that: (1) the maximal lactate steady state (MLSS), critical power (CP) and electromyographic fatigue threshold (EMG(FT)) occur at the same power output in cycling exercise, and (2) exercise above the power output at MLSS (P-MLSS) results in continued increases in oxygen uptake (VO(2)), blood lactate concentration ([La]) and integrated electromyogram (iEMG) with time. Eight healthy subjects [mean (SD) age 25 (3) years, body mass 72.1 (8.2) kg] performed a series of laboratory tests for the determination of MLSS, CP and EMG(FT). The CP was determined from four exhaustive trials of between 2 and 15 min duration. The MLSS was determined as the highest power output at which the increase in blood [La] was less than 1.0 mM across the last 20 min of a series of 30-min trials. The EMG(FT) was determined from four trials of 2 min duration at different power outputs. The surface electromyogram was recorded continuously from the vastus lateralis muscle. The CP was significantly higher than the P-MLSS [242 (25) vs. 222 (23) W; P<0.05], although the two variables were strongly correlated (r=0.95; P<0.01). The EMG(FT) could not be determined in 50% of the subjects. Blood [La], VO(2) and minute ventilation all increased significantly with time for exercise at power outputs above the P-MLSS. In conclusion, the P-MLSS, and not the CP, represents the upper limit of the heavy exercise domain in cycling. During exercise above the P-MLSS, there is no association between changes in iEMG and increases in VO(2) and blood [La] with time.

Adult↗
PubMed2002

Oxygen uptake kinetics during horizontal and uphill treadmill running in humans.

The aim of this study was to examine the effect of increasing the ratio of concentric to eccentric muscle activation on oxygen uptake (VO(2)) kinetics during treadmill running. Nine subjects [2 women; mean (SD) age 29 (7) years, height 1.77 (0.07) m, body mass 73.0 (7.5) kg] completed incremental treadmill tests to exhaustion at 0% and 10% gradients to establish the gradient-specific ventilatory threshold (VT) and maximal oxygen uptake (VO(2max)). Subsequently, the subjects performed repeated moderate intensity (80% of gradient-specific VT) and heavy intensity (50% of the difference between the gradient specific VT and VO(2max)) square-wave runs with the treadmill gradient set at 0% and 10%. For moderate intensity exercise, there were no significant differences between treadmill gradients for VO(2) kinetics. For heavy intensity exercise, the amplitude of the primary component of VO(2) was not significantly different between 0% and 10% treadmill gradients [mean (SEM) 2,940 (196) compared to 2,869 (156) ml x min(-1), respectively], but the amplitude of the VO(2) slow component was significantly greater at the 10% gradient [283 (43) compared to 397 (37) ml x min(-1); P < 0.05]. These results indicate that the muscle contraction regimen (i.e. the relative contribution of concentric and eccentric muscle action) significantly influences the amplitude of the VO(2) slow component.

Adult↗
PubMed2002

Effects of prior heavy exercise, prior sprint exercise and passive warming on oxygen uptake kinetics during heavy exercise in humans.

Prior heavy exercise (above the lactate threshold, Th(la)) increases the amplitude of the primary oxygen uptake (VVO(2)) response and reduces the amplitude of the VO(2) slow component during subsequent heavy exercise. The purpose of this study was to determine whether these effects required the prior performance of an identical bout of heavy exercise, or if prior short-duration sprint exercise could cause similar effects. A secondary purpose of this study was to determine the effect of elevating muscle temperature (through passive warming) on VO(2) kinetics during heavy exercise. Nine male subjects performed a 6-min bout of heavy exercise on a cycle ergometer 6 min after: (1) an identical bout of heavy exercise; (2) a 30-s bout of maximal sprint cycling; (3) a 40-min period of leg warming in a hot water bath at 42 degrees C. Prior sprint exercise elevated blood [lactate] prior to the onset of heavy exercise (by aproximately 5.6 mM) with only a minor increase in muscle temperature (of approximately 0.7 degrees C). In contrast, prior warming had no effect on baseline blood lactate concentration, but elevated muscle temperature by approximately 2.6 degrees C. Both prior heavy exercise and prior sprint exercise significantly increased the absolute primary VO(2) amplitude (by approximately 230 ml x min(-1) and 260 ml x min(-1), respectively) and reduced the amplitude of the VO(2) slow component (by approximately 280 ml x min(-1) and 200 ml x min(-1), respectively) during heavy exercise, whereas prior warming had no significant effect on the VO(2) response. We conclude that the VO(2) response to heavy exercise can be markedly altered by both sustained heavy-intensity submaximal exercise and by short-duration sprint exercise that induces a residual acidosis. In contrast, passive warming elevated muscle temperature but had no effect on the VO(2) response.

Adult↗