Sauna exposure immediately prior to short-term heat acclimation accelerates phenotypic adaptation in females.

OBJECTIVES: Investigate whether a sauna exposure prior to short-term heat acclimation (HA) accelerates phenotypic adaptation in females. DESIGN: Randomised, repeated measures, cross-over trial. METHODS: Nine females performed two 5-d HA interventions (controlled hyperthermia Tre≥38.5°C), separated by 7-wk, during the follicular phase of the menstrual cycle confirmed by plasma concentrations of 17-ß estradiol and progesterone. Prior to each 90-min HA session participants sat for 20-min in either a temperate environment (20°C, 40% RH; HAtemp) wearing shorts and sports bra or a hot environment (50°C, 30% RH) wearing a sauna suit to replicate sauna conditions (HAsauna). Participants performed a running heat tolerance test (RHTT) 24-h pre and 24-h post HA. RESULTS: Mean heart rate (HR) (85±4 vs. 68±5 bpm, p≤0.001), sweat rate (0.4±0.2 vs. 0.0±0.0Lh-1, p≤0.001), and thermal sensation (6±0 vs. 5±1, p=0.050) were higher during the sauna compared to temperate exposure. Resting rectal temperature (Tre) (-0.28±0.16°C), peak Tre (-0.42±0.22°C), resting HR (-10±4 bpm), peak HR (-12±7 bpm), Tre at sweating onset (-0.29±0.17°C) (p≤0.001), thermal sensation (-0.5±0.5; p=0.002), and perceived exertion (-3±2; p≤0.001) reduced during the RHTT, following HAsauna; but not HAtemp. Plasma volume expansion was greater following HAsauna (HAsauna, 9±7%; HAtemp, 1±5%; p=0.013). Sweat rate (p≤0.001) increased and sweat NaCl (p=0.006) reduced during the RHTT following HAsauna and HAtemp. CONCLUSIONS: This novel strategy initiated HA with an attenuation of thermoregulatory, cardiovascular, and perceptual strain in females due to a measurably greater strain in the sauna compared to temperate exposure when adopted prior to STHA.

Motivational processes and well-being in cardiac rehabilitation: a self-determination theory perspective.

This research examined the processes underpinning changes in psychological well-being and behavioural regulation in cardiac rehabilitation (CR) patients using self-determination theory (SDT). A repeated measures design was used to identify the longitudinal relationships between SDT variables, psychological well-being and exercise behaviour during and following a structured CR programme. Participants were 389 cardiac patients (aged 36-84 years; M(age) = 64 ± 9 years; 34.3% female) referred to a 12-week-supervised CR programme. Psychological need satisfaction, behavioural regulation, health-related quality of life, physical self-worth, anxiety and depression were measured at programme entry, exit and six month post-programme. During the programme, increases in autonomy satisfaction predicted positive changes in behavioural regulation, and improvements in competence and relatedness satisfaction predicted improvements in behavioural regulation and well-being. Competence satisfaction also positively predicted habitual physical activity. Decreases in external regulation and increases in intrinsic motivation predicted improvements in physical self-worth and physical well-being, respectively. Significant longitudinal relationships were identified whereby changes during the programme predicted changes in habitual physical activity and the mental quality of life from exit to six month follow-up. Findings provide insight into the factors explaining psychological changes seen during CR. They highlight the importance of increasing patients' perceptions of psychological need satisfaction and self-determined motivation to improve well-being during the structured component of a CR programme and longer term physical activity.

A 3-min all-out cycling test is sensitive to a change in critical power.

PURPOSE: The aim of this investigation was to test the hypothesis that a 3-min all-out cycling test would detect a change in critical power (CP) after a 4-wk interval training intervention. METHODS: Nine habitually active subjects completed a ramp test, two 3-min all-out tests to establish the end power (EP) and the work done above EP (WEP), and three predicting trials to establish CP and W' using the work-time model (W = CPt + W'). After 12 supervised high-intensity interval training sessions over 4 wk, subjects repeated the testing procedures. RESULTS: The CP increased in all subjects after training (pretraining: 230 +/- 53 W; posttraining: 255 +/- 50 W; t8 = 7.47, P < 0.001), with no statistically significant effect on the W' (pretraining: 17.2 +/- 4.2 kJ; posttraining: 15.5 +/- 3.8 kJ; t8 = 2.03, P = 0.08). The all-out test EP was increased after training from 225 +/- 52 W to 248 +/- 46 W (t8 = 6.26, P < 0.001). The EP and CP estimates before and after training were not different and were highly correlated (pretraining: r = 0.96, P < 0.001; posttraining: r = 0.95, P < 0.001). In addition, the increase in EP was correlated with (r = 0.77, P = 0.016) and not different from (t8 = 0.60, P = 0.57) the increase in CP. There was no change in the WEP from pretraining to posttraining (t8 = 1.89, P = 0.10). CONCLUSIONS: The present study shows that the 3-min all-out test closely estimates CP across a wide range of aerobic fitness and is sensitive to training-induced changes in CP.

Physiological and performance effects of low- versus mixed-intensity rowing training.

PURPOSE: To examine the impact of low-intensity and a mixture of low- and high-intensity training on physiological and performance responses in rowing. METHODS: Eighteen experienced rowers undertook a 12-wk program of 100% < or = lactate threshold (LT) training (LOW) or 70% training at < or = LT and 30% at halfway (50%Delta) between the V O2 at LT and V O2peak (MIX). Responses were assessed before and after training by a progressive exercise test to exhaustion; multiple "square-wave" rest-to-exercise transitions of 6-min duration at 50%Delta; and a maximal 2000-m ergometer time trial. RESULTS: Improvements (P < 0.001) in 2000-m ergometer performance and V O2peak occurred independently of groups (P = 0.8 and 0.42, respectively). LOW improved the power at LT (23.5 +/- 12.2 vs 5.1 +/- 5.0 W, P = 0.013) and power at a [blood lactate] of 4 mM (32.3 +/- 6.9 vs 13.1 +/- 3.7 W, P = 0.03) compared with MIX. The time constant and gain of the primary component were unchanged with training, whereas the gain of the V O2 slow component was reduced with training, but independently of group. CONCLUSIONS: Both LOW and MIX training programs improved performance and V O2peak by the same magnitude, whereas LOW attenuated the blood lactate response to a given exercise intensity more so than MIX.

Robustness of a 3 min all-out cycling test to manipulations of power profile and cadence in humans.

The purpose of this study was to assess whether end-test power output (EP, synonymous with 'critical power') and the work done above EP (WEP) during a 3 min all-out cycling test against a fixed resistance were affected by the manipulation of cadence or pacing. Nine subjects performed a ramp test followed, in random order, by three cadence trials (in which flywheel resistance was manipulated to achieve end-test cadences which varied by approximately 20 r.p.m.) and two pacing trials (30 s at 100 or 130% of maximal ramp test power, followed by 2.5 min all-out effort against standard resistance). End-test power output was calculated as the mean power output over the final 30 s and the WEP as the power-time integral over 180 s for each trial. End-test power output was unaffected by reducing cadence below that of the 'standard test' but was reduced by approximately 10 W on the adoption of a higher cadence [244 +/- 41 W for high cadence (at an end-test cadence of 95 +/- 7 r.p.m.), 254 +/- 40 W for the standard test (at 88 +/- 6 r.p.m.) and 251 +/- 38 W for low cadence (at 77 +/- 5 r.p.m.)]. Pacing over the initial 30 s of the test had no effect on the EP or WEP estimates in comparison with the standard trial. The WEP was significantly higher in the low cadence trial (16.2 +/- 4.4 kJ) and lower in the high cadence trial (12.9 +/- 3.6 kJ) than in the standard test (14.2 +/- 3.7 kJ). Thus, EP is robust to the manipulation of power profile but is reduced by adopting cadences higher than 'standard'. While the WEP is robust to initial pacing applied, it is sensitive to even relatively minor changes in cadence.

Determination of critical power using a 3-min all-out cycling test.

PURPOSE: We tested the hypothesis that the power output attained at the end of a 3-min all-out cycling test would be equivalent to critical power. METHODS: Ten habitually active subjects performed a ramp test, two 3-min all-out tests against a fixed resistance to establish the end-test power (EP) and the work done above the EP (WEP), and five constant-work rate tests to establish the critical power (CP) and the curvature constant parameter (W') using the work-time and 1/time models. RESULTS: The power output in the 3-min trial declined to a steady level within 135 s. The EP was 287 +/- 55 W, which was not significantly different from, and highly correlated with, CP (287 +/- 56 W; P = 0.37, r = 0.99). The standard error for the estimation of CP using EP was approximately 6 W, and in 8 of 10 cases, EP agreed with CP to within 5 W. Similarly, the WEP derived from the 3-min test (15.0 +/- 4.7 kJ) was not significantly different from, and correlated with, W' (16.0 +/- 3.8 kJ; P = 0.35; r = 0.84). CONCLUSIONS: During a 3-min all-out cycling test, power output declined to a stable value in approximately the last 45 s, and this power output was not significantly different from the independently measured critical power.

Comparison of the oxygen uptake kinetics of club and olympic champion rowers.

PURPOSE: To test the hypothesis that elite rowers would possess a faster, more economic oxygen uptake response than club standard rowers. METHODS: Eight Olympic champion (ELITE) rowers were compared with a cohort of eight club standard (CLUB) rowers. Participants completed a progressive exercise test to exhaustion, repeated 6-min moderate and heavy square-wave transitions, and a maximal 2000-m ergometer time trial. RESULTS: The time constant (tau) of the primary component (PC) was faster for the ELITE group compared with CLUB for moderate-intensity (13.9 vs 19.4 s, P = 0.02) and heavy-intensity (18.7 vs 22.4 s, P = 0.005) exercise. ELITE rowers consumed less oxygen for moderate (14.2 vs 15.6 mL x min(-1) x W(-1); P = 0.009) and heavy (12.1 vs 13.7 mL x min(-1) x W(-1); P = 0.01) exercise. A greater absolute slow component was observed in the ELITE group (P = 0.009), but no differences were noted when the slow component was expressed relative to work rate performed (P = 0.14). Intergroup correlation with time trial performance speed was significant for tauPC during heavy-intensity exercise (r = -0.59, P = 0.02). CONCLUSIONS: Compared with CLUB rowers, the shorter time constant response and greater economy observed in ELITE rowers may suggest advantageous adjustment of oxidative processes from rest to work. Training status or performance level do not seem to be associated with a smaller slow component when comparing CLUB and ELITE oarsmen.

A 3-min all-out test to determine peak oxygen uptake and the maximal steady state.

PURPOSE: We tested the hypothesis that a 3-min all-out cycling test would provide a measure of peak oxygen uptake (VO2peak) and estimate the maximal steady-state power output. METHODS: Eleven habitually active subjects performed a ramp test, three 3-min all-out tests against a fixed resistance, and two further submaximal tests lasting up to 30 min, 15 W below or above the power output attained in the last 30 s of the 3-min test (the end-test power). RESULTS: The VO2peak measured during the 3-min all-out test (mean +/- SD: 3.78 +/- 0.68 L x min(-1)) was not different from that of the ramp test (3.84 +/- 0.79 L x min(-1); P = 0.75). The end-test power (257 +/- 49 W) was significantly lower than that at the end of the ramp test (368 +/- 73 W) and significantly higher than the power at the gas exchange threshold (169 +/- 55 W; P < 0.001). Nine subjects were able to complete 30 min of exercise at 15 W below the end-test power, and seven of these did so with a steady-state blood [lactate] and VO2 response profile. In contrast, when subjects exercised at 15 W above the end-test power, blood [lactate] and VO2 rose inexorably until exhaustion, which occurred in approximately 13 +/- 7 min. CONCLUSIONS: These data suggest that a 3-min all-out exercise test can be used to establish VO2peak and to estimate the maximal steady state.

Time required for the restoration of normal heavy exercise VO2 kinetics following prior heavy exercise.

Prior heavy exercise markedly alters the O2 uptake (VO2) response to subsequent heavy exercise. However, the time required for VO2 to return to its normal profile following prior heavy exercise is not known. Therefore, we examined the VO2 responses to repeated bouts of heavy exercise separated by five different recovery durations. On separate occasions, nine male subjects completed two 6-min bouts of heavy cycle exercise separated by 10, 20, 30, 45, or 60 min of passive recovery. The second-by-second VO2 responses were modeled using nonlinear regression. Prior heavy exercise had no effect on the primary VO2 time constant (from 25.9 +/- 4.7 s to 23.9 +/- 8.8 s after 10 min of recovery; P = 0.338), but it increased the primary VO2 amplitude (from 2.42 +/- 0.39 to 2.53 +/- 0.41 l/min after 10 min of recovery; P = 0.001) and reduced the VO2 slow component (from 0.44 +/- 0.13 to 0.21 +/- 0.12 l/min after 10 min of recovery; P < 0.001). The increased primary amplitude was also evident after 20-45 min, but not after 60 min, of recovery. The increase in the primary VO2 amplitude was accompanied by an increased baseline blood lactate concentration (to 5.1 +/- 1.0 mM after 10 min of recovery; P < 0.001). Baseline blood lactate concentration was still elevated after 20-60 min of recovery. The priming effect of prior heavy exercise on the VO2 response persists for at least 45 min, although the mechanism underpinning the effect remains obscure.

Influence of blood donation on O2 uptake on-kinetics, peak O2 uptake and time to exhaustion during severe-intensity cycle exercise in humans.

We hypothesized that the reduction of O2-carrying capacity caused by the withdrawal of approximately 450 ml blood would result in slower phase II O2 uptake (VO2) kinetics, a lower VO2peak and a reduced time to exhaustion during severe-intensity cycle exercise. Eleven healthy subjects (mean +/- S.D. age 23 +/- 6 years, body mass 77.2 +/- 11.0 kg) completed 'step' exercise tests from unloaded cycling to a severe-intensity work rate (80% of the difference between the predetermined gas exchange threshold and the VO2peak) on two occasions before, and 24 h following, the voluntary donation of approximately 450 ml blood. Oxygen uptake was measured breath-by-breath, and VO2 kinetics estimated using non-linear regression techniques. The blood withdrawal resulted in a significant reduction in haemoglobin concentration (pre: 15.4 +/- 0.9 versus post: 14.7 +/- 1.3 g dl(-1); 95% confidence limits (CL): -0.04, -1.38) and haematocrit (pre: 44 +/- 2 versus post: 41 +/- 3%; 95% CL: -1.3, -5.1). Compared to the control condition, blood withdrawal resulted in significant reductions in VO2peak (pre: 3.79 +/- 0.64 versus post: 3.64 +/- 0.61 l min(-1); 95% CL: -0.04, - 0.27) and time to exhaustion (pre: 375 +/- 129 versus post: 321 +/- 99 s; 95% CL: -24, -85). However, the kinetic parameters of the fundamental VO2 response, including the phase II time constant (pre: 29 +/- 8 versus post: 30 +/- 6 s; 95% CL: 5, -3), were not altered by blood withdrawal. The magnitude of the VO2 slow component was significantly reduced following blood donation owing to the lower VO2peak attained. We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and exercise tolerance but has no effect on the fundamental phase of the VO2 on-kinetics during severe-intensity exercise.

Effects of prior warm-up regime on severe-intensity cycling performance.

PURPOSE: The purpose of the present study was to determine the effect of three different warm-up regimes on cycling work output during a 7-min performance trial. METHODS: After habituation to the experimental methods, 12 well-trained cyclists completed a series of 7-min performance trials, involving 2 min of constant-work rate exercise at approximately 90% VO2max and a further 5 min during which subjects attempted to maximize power output. This trial was performed without prior intervention and 10 min after bouts of moderate, heavy, or sprint exercise in a random order. Pulmonary gas exchange was measured breath by breath during all performance trials. RESULTS: At the onset of the performance trial, baseline blood [lactate] was significantly elevated after heavy and sprint but not moderate exercise (mean +/- SD: control, 1.0 +/- 0.3 mM; moderate, 1.0 +/- 0.2 mM; heavy, 3.0 +/- 1.1 mM; sprint, 5.9 +/- 1.5 mM). All three interventions significantly increased the amplitude of the primary VO2 response (control, 2.59 +/- 0.28 L x min(-1); moderate, 2.69 +/- 0.27 L x min(-1); heavy, 2.78 +/- 0.26 L x min(-1); sprint, 2.78 +/- 0.30 L x min(-1)). Mean power output was significantly increased by prior moderate and heavy exercise but not significantly reduced after sprint exercise (control, 330 +/- 42 W; moderate, 338 +/- 39 W; heavy, 339 +/- 42 W; sprint, 324 +/- 45 W). CONCLUSIONS: These data indicate that priming exercise performed in the moderate- and heavy-intensity domains can improve severe-intensity cycling performance by ~2-3%, the latter condition doing so despite a mild lactacidosis being present at exercise onset.

Muscle glycogen depletion alters oxygen uptake kinetics during heavy exercise.

PURPOSE: To test the hypothesis that muscle fiber recruitment patterns influence the oxygen uptake (VO2) kinetic response, constant-load exercise was performed after glycogen depletion of specific fiber pools. METHODS: After validation of protocols for the selective depletion of Type I and II muscle fibers, 19 subjects performed square-wave exercise at 80% VT (moderate) and at 50% of the difference between VT and VO2max (heavy) without any prior depleting exercise (CON), after HIGH (10 x 1-min exercise bouts at 120% VO2max), and after LOW (3 h of exercise at 30% VO2max) exercise. RESULTS: Differences in VO2 kinetic parameters were only observed in heavy exercise AFTER HIGH: the VO2 primary component was higher (1.75 +/- 0.12 L x min) compared with CON (1.65 +/- 0.11 L x min, P < 0.05), and the VO2 slow component was lower (0.18 +/- 0.03 L x min) compared with CON (0.24 +/- 0.04 L x min, P < 0.05). CONCLUSIONS: The results indicate that the VO2 response to heavy constant-load exercise can be altered by depletion of glycogen in the Type II muscle fibers, lending support to the theory that muscle fiber recruitment influences both the VO2 primary and slow component amplitudes during heavy intensity exercise.

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.

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.

The effect of interdian and diurnal variation on oxygen uptake kinetics during treadmill running.

The aim of this study was to examine the variability of the oxygen uptake (VO2) kinetic response during moderate- and high-intensity treadmill exercise within the same day (at 06:00, 12:00 and 18:00 h) and across days (on five occasions). Nine participants (age 25 +/- 8 years, mass 70.2 +/- 4.7 kg, VO2max 4137 +/- 697 ml x min(-1); mean +/- s) took part in the study. Six of the participants performed replicate 'square-wave' rest-to-exercise transitions of 6 min duration at running speeds calculated to require 80% VO2 at the ventilatory threshold (moderate-intensity exercise) and 50% of the difference between VO2 at the ventilatory threshold and VO2max (50% delta; high-intensity exercise) on 5 different days. Although the amplitudes of the VO2 response were relatively constant (coefficient of variation approximately 6%) from day to day, the time-based parameters were more variable (coefficient of variation approximately 15 to 30%). All nine participants performed replicate square-waves for each time of day. There was no diurnal effect on the time-based parameters of VO2 kinetics during either moderate- or high-intensity exercise. However, for high-intensity exercise, the amplitude of the primary component was significantly lower during the 12:00 h trial (2859 +/- 142 ml x min(-1) vs 2955 +/- 135 ml x min(-1) at 06:00 h and 2937 +/- 137 ml x min(-1) at 18:00 h; P < 0.05), but this effect was eliminated when expressed relative to body mass. The results of this study indicate that the amplitudes of the VO2 kinetic responses to moderate- and high-intensity treadmill exercise are similar within and across test days. The time-based parameters, however, are more variable from day to day and multiple transitions are, therefore, recommended to increase confidence in the data.

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.

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.

Effects of prior heavy exercise on VO(2) kinetics during heavy exercise are related to changes in muscle activity.

We hypothesized that the elevated primary O(2) uptake (VO(2)) amplitude during the second of two bouts of heavy cycle exercise would be accompanied by an increase in the integrated electromyogram (iEMG) measured from three leg muscles (gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy men performed two 6-min bouts of heavy leg cycling (at 70% of the difference between the lactate threshold and peak VO(2)) separated by 12 min of recovery. The iEMG was measured throughout each exercise bout. The amplitude of the primary VO(2) response was increased after prior heavy leg exercise (from mean +/- SE 2.11 +/- 0.12 to 2.44 +/- 0.10 l/min, P < 0.05) with no change in the time constant of the primary response (from 21.7 +/- 2.3 to 25.2 +/- 3.3 s), and the amplitude of the VO(2) slow component was reduced (from 0.79 +/- 0.08 to 0.40 +/- 0.08 l/min, P < 0.05). The elevated primary VO(2) amplitude after leg cycling was accompanied by a 19% increase in the averaged iEMG of the three muscles in the first 2 min of exercise (491 +/- 108 vs. 604 +/- 151% increase above baseline values, P < 0.05), whereas mean power frequency was unchanged (80.1 +/- 0.9 vs. 80.6 +/- 1.0 Hz). The results of the present study indicate that the increased primary VO(2) amplitude observed during the second of two bouts of heavy exercise is related to a greater recruitment of motor units at the onset of exercise.

Oxygen uptake kinetics during treadmill running across exercise intensity domains.

The purpose of the present study was to examine comprehensively the kinetics of oxygen uptake (VO2) during treadmill running across the moderate, heavy and severe exercise intensity domains. Nine subjects [mean (SD age, 27 (7) years; mass, 69.8 (9.0) kg; maximum VO2, VO2max, 4,137 (697) ml x min(-1)] performed a series of "square-wave" rest-to-exercise transitions of 6 min duration at running speeds equivalent to 80% and 100% of the VO2 at lactate threshold (LT; moderate exercise); and at 20%, 40%, 60%, 80% and 100% of the difference between the VO2 at LT and VO2max (delta heavy and severe exercise). Critical velocity (CV) was also determined using four maximal treadmill runs designed to result in exhaustion in 2-15 min. The VO2 response was modelled using non-linear regression techniques. As expected, the amplitude of the VO2 primary component increased with exercise intensity [from 1,868 (136) ml x min-( 1) at 80% LT to 3,296 (218) ml x min-(1) at 100% delta, P < 0.05]. However, there was a non-significant trend for the "gain" of the primary component to decrease as exercise intensity increased [181 (7) ml x kg(-1) x km(-1) at 80% LT to 160 (6) ml x kg(-1) x km(-1) at 100% delta]. The time constant of the primary component was not different between supra-LT running speeds (mean value range = 17.9-19.1 s), but was significantly shorter during the 80% LT trial [12.7 (1.4) s, P < 0 .05]. The VO2 slow component increased with exercise intensity from 139 (39) ml x min(-1) at 20% delta to 487 (57) ml x min(-1) at 80% delta (P < 0.05), but decreased to 317 (84) ml x min(-1) during the 100% delta trial (P < 0.05). During both the 80% delta and 100% delta trials, the VO2 at the end of exercise reached VOmax [4,152 (242) ml x min(-1) and 4,154 (114) ml x min(-1), respectively]. Our results suggest that the "gain" of the primary component is not constant as exercise intensity increases across the moderate, heavy and severe domains of treadmill running. These intensity-dependent changes in the amplitudes and kinetics of the VO2 response profiles may be associated with the changing patterns of muscle fibre recruitment that occur as exercise intensity increases.