Effect of different pedal rates on oxygen uptake slow component during constant-load cycling exercise

AIM: We hypothesized that an extremely high pedal rate would induce much more type II muscle fibers recruitment even at an early phase of the same absolute work rate compared with normal pedal rates, and would result in changed amplitude of the pulmonary oxygen uptake slow component (VO(2)SC) during heavy constant-load exercise. METHODS: Two square-wave transitions of constant-load exercise were carried out at an exercise intensity corresponding to a VO(2) of 130% of the ventilatory threshold. The amplitude of the VO(2)SC in phase III during heavy constant-load exercise was determined at normal (60 rpm) and extremely high pedal rates (110 rpm). The VO(2) kinetics were analyzed by nonlinear regression. RESULTS: Although the absolute work rates were almost identical in the two pedal rates cycling exercise, the amplitude of the VO(2) in phase II (phase II amplitude), end-exercise VO(2) (EEVO(2)) and blood lactate accumulation ([La]) were significantly greater at 110 rpm than at 60 rpm (2 260+/-242 vs 1.830+/-304 mL.min(-1) for phase II amplitude; P<0.01, 2 350+/-265 vs 1 709+/-342 mL.min(-1) for EEVO(2); P<0.01, 6.4+/-1.3 vs 3.2+/-1.3 mmol.L(-1) for [La]; P<0.01, respectively). The amplitude of the VO(2)SC in phase III also revealed a significantly higher value at 110 rpm compared with 60 rpm (416+/-73 vs 201+/-89 mL.min(-1), P<0.01). In spite of the appearance of greater VO(2)SC at 110 rpm, no corresponding changes in integrals of the electromyography (EMG) signal and mean power frequency were observed. CONCLUSIONS: The results of this study indicate that the amplitude of the VO(2)SC was greater in higher pedal rate during the same work rate constant-load cycling exercise, which might be associated with a progressive increase in the adenosine triphosphate requirement of already recruited muscle fibers in exercising muscle.     

Effect of glycogen depletion on the oxygen uptake slow component in humans

Previous studies have indicated that the (.-)VO(2) slow component is related to the recruitment of type II muscle fibres. We therefore hypothesised that an exercise and dietary regimen designed to deplete type I muscle fibres of glycogen would result in a greater contribution of type II muscle fibres to the exercise power output and therefore a larger amplitude of the (.-)VO(2) slow component. Eight male subjects took part in this study. On day 1, the subjects reported to the laboratory at 8 a.m., and completed a 9 min constant-load cycling test at a work rate equivalent to 85 % (.-)VO(2) peak. On day 2 at 12 p.m., the subjects were fed a 4200 kJ meal (60 % protein, 40 % fat); at 6 p.m. they completed a 2 h cycling test at 60 % (.-)VO(2) peak. On day 3 at 8 a.m., the subjects performed an exercise test identical to that of day 1. Metabolic and respiratory measurements indicated that our experimental design was effective in reducing the muscle glycogen content. (.-)VO(2) was significantly higher (by approximately 140 ml x min (-1)) throughout exercise following glycogen depletion but no appreciable changes in (.-)VO(2) kinetics were found: neither the time constant of the primary response (from 35.4 +/- 2.5 to 33.2 +/- 4.4 s) nor the amplitude of the slow component (from 404 +/- 95 to 376 +/- 81 ml x min (-1)) was significantly altered. Therefore, we suggest that the increased (.-)VO(2) throughout exercise and the unaltered (.-)VO(2) slow component following glycogen depletion might be explained by a shift towards a greater reliance on fat metabolism in type I muscle fibres with no appreciable change in fibre type recruitment patterns.     

Electromyographic activity in lower limb muscles is temporally associated with the slow phase of oxygen uptake during cycling

Although the “slow” phase of pulmonary oxygen uptake () appears to represent energetic processes in contracting muscle, electromyographic evidence tends not to support this. The present study assessed normalized integrated electromyographic (NIEMG) activity in eight muscles that act about the hip, knee and ankle during 8 min of moderate (<ventilatory threshold) and very heavy (>ventilatory threshold) cycling in six male cyclists. was measured breath by breath during four repeated trials at each of the two intensities. Moderate and very heavy exercise followed a 4‐min period of light exercise (50 W). During moderate exercise the slow phase was absent and NIEMG in all muscles did not increase after the first minute of exercise. During very heavy exercise, the slow phase emerged (time delay=58 ± 16 s) and increased progressively (time constant=120 ± 35 s) to an amplitude (0.83 ± 0.16 L/min) that was approximately 21% of the total response. This slow phase coincided with a significant increase in NIEMG in most muscles, and differences in NIEMG activities between the two intensities revealed “slow” muscle activation profiles that differed between muscles in terms of the onset, amplitude and shape of these profiles. This supports the hypothesis that the slow phase is a function of these different slow muscle activation profiles.     

Relationship between the slow component of oxygen uptake and the potential reduction in maximal power output during constant-load exercise.

BACKGROUND: The purpose of the present study was to examine the relationship between the slow component of oxygen uptake (VO2) and muscle fiber fatigue. Maximal power output (MPO) was used as an index of muscle fiber fatigue. METHODS: Two constant exercises were carried out at exercise intensities of 40% and 80% of maximal oxygen uptake (VO2max). Each exercise was repeated three times, once for the measurement for VO2, and the other two times for MPO testing, at 3 and 6 minutes after work output. RESULTS: Reproducibility of MPO at rest was assessed by correlation coefficient. Its value was 0.933. At 40% VO2max, MPO did not significantly decrease from the resting value. At 80% VO2max, MPO significantly decreased by 129+/-77 watts at 3 min and by 178+/-108 watts at 6 min. The VO2 kinetic at 40% VO2 was well described by a monoexponential function with a time constant of 0.432 min. However, at 80% VO2max, a slow component of the form of a linear drift superimposed on a monoexponential function with an essentially equal time constant (0.469 min) was unambiguously detected. This slow component was significantly related to the decrease in MPO (r=0.567). CONCLUSIONS: The present results suggested that the fatigue of muscle fibers may be one of the factors that produce the slow component of VO2 during high intensity exercise.     

Ventilatory threshold and maximal oxygen uptake during cycling and running in triathletes

VO2max and the ventilatory threshold (Tvent) were measured during cycle ergometry (CE) and treadmill running (TR) in a group of 10 highly trained male triathletes. Tvent was indicated as the VO2 at which the ventilatory equivalent for oxygen increased without a marked rise in the ventilatory equivalent for carbon dioxide. Triathletes achieved a significantly higher VO2max for TR (75.4 +/- 7.3 ml.kg-1.min-1) than for CE (70.3 +/- 6.0 ml.kg-1.min-1). Mean CE VO2max was 93.2% of the TR value. Average VO2max values for CE and TR compared favorably with values reported for elite single-sport athletes and were greater than those previously reported for other male triathletes. CE Tvent occurred at 3.37 +/- 0.32 l.min-1 or 66.8 +/- 3.7% of CE VO2max, while TR Tvent was detected at 3.87 +/- 0.33 l.min-1 or 71.9 +/- 6.6% of TR VO2max. The VO2 (l.min-1) at which Tvent occurred for TR was significantly higher than for CE (P less than 0.001). Although the VO2 values at TR Tvent expressed as a percentage of VO2max were consistently higher than for CE, the difference between the means did not reach statistical significance (P greater than 0.05). The average Tvent for CE (as %VO2max) was nearly identical to Tvent values reported in the literature for competitive male cyclists, whereas TR Tvent was lower than recently reported values for elite distance runners and marathoners. We speculate that triathlon training results in general (cross-training) adaptations which enhance maximal oxygen uptake values, whereas anaerobic threshold adaptations occur primarily in the specific muscle groups utilized in training.     

Ventilatory threshold and maximal oxygen uptake during cycling and running in female triathletes

Maximal oxygen uptake (VO2max) and the ventilatory threshold (Tvent) were measured during cycle ergometry (CE) and treadmill running (TR) in a group of 10 highly trained female triathletes. Tvent was defined as the VO2 at which the ventilatory equivalent for oxygen increased without a marked rise in the ventilatory equivalent for carbon dioxide. Female triathletes achieved a significantly higher mean (+/- SE) relative VO2max for running (63.6 +/- 1.2 ml.kg-1.min-1) than for cycling (59.9 +/- 1.3 ml.kg-1.min-1). When oxygen uptake measured at the ventilatory threshold was expressed as a percent of VO2max, the mean value obtained for TR (74.0 +/- 2.0% of VO2max) was significantly greater than the value obtained for CE (62.7 +/- 2.1% of VO2max). This occurred even though the total training time and intensity were similar for the two modes of exercise. Female triathletes had average running and cycling VO2max values that compared favorably with maximal oxygen uptake values previously reported for elite female runners and cyclists, respectively. However, mean running and cycling Tvent values (VO2 Tvent as%VO2max) were lower than recently reported values for single-sport athletes. The physiological variability between the triathletes studied and single-sport athletes may be attributed in part to differences in training distance or intensity, and/or to variations in the number of years of intense training in a specific mode of exercise. It was concluded that these triathletes were well-trained in both running and cycling, but not to the same extent as female athletes who only train and compete in running or cycling.     

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.     

Lactate, oxygen uptake, and cycling performance in triathletes

To assess the relationship of exercise test variables to each other and to bike race times in an ultra-distance triathlon, we studied 24 participants (14 men, 10 women) in the 1985 Hawaii Ironman Triathlon, using a graded, maximal cycle ergometer test with gas exchange and blood lactate (LA) measurements at each work load. Exercise test variables were oxygen uptake (VO2) and heart rate (HR) at the lactate and ventilatory thresholds. Lactate threshold (LT-1) was defined as the exercise intensity that elicited a 1 mM increase in blood lactate concentration above the value measured during the first work load for each subject. Variables were also examined at the lactate thresholds of 2 mM and 4 mM. Ventilatory thresholds (VT) were identified as the points at which the ventilatory equivalent of oxygen (VE/VO2) increased without a corresponding increase in the ventilatory equivalent of carbon dioxide (VE/VCO2). Mean peak oxygen uptake (peak VO2) for this sample of Ironman triathletes was 57.4 ml.kg-1.min-1. Cycle peak VO2 was inversely correlated, r = 0.68 (P less than 0.0002) with bike finish time. VO2 and HR as well as the respective percentages of maximum were higher at all lactate thresholds than at VT (P less than 0.0001). Therefore VT should not be used to identify a lactate threshold in ultra-endurance triathletes. VO2 values at the lactate and ventilatory thresholds were not highly related to bike finish time (r = -0.26 to -0.58). Fractional utilization of peak VO2 (% peak VO2), HR, and % peak HR at thresholds were not related to bike finish time (r = -0.01 to 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of prior high-intensity cycling exercise on the VO2 kinetics during high-intensity cycling exercise is situated at the additional slow component

In previous studies conclusions about the effect of prior exercise on VO2 kinetics of subsequent high-intensity exercise are generally based on observed changes in the overall VO2 response without considering the effects on the VO2 fast and slow component. The aim of the present study was to examine the effect on the VO2 fast and slow component separately. Therefore 10 subjects performed an exercise protocol consisting of an initial 3 min period of unloaded cycling followed by two constant-load work bouts at a work rate corresponding to 90% VO2peak, separated by 3 min of rest and 3 min of unloaded cycling. VO2 was measured on a breath-by-breath basis, and the response curves were analysed by a biexponential model. To increase signal-to-noise ratio, subjects performed four repetitions of the exercise protocol, each separated by at least one day. There was no significant alteration in VO2 kinetic parameters of the primary, fast component after high-intensity exercise. However, there was a significant effect of prior high-intensity exercise on the VO2 kinetic parameters of the slow component. The time constant and the amplitude of the slow component were reduced by respectively 44% (from 231.0 +/- 111.7 s to 130.1 +/- 50.4 s) and 49% (from 824 +/- 270 ml x min(-1) to 417 +/- 134 ml x min(-1)). The results of this study indicate that the effect of high-intensity exercise on the VO2 kinetics of a subsequent high-intensity exercise is probably limited to an effect on the slow component.     

Auxiliary muscles and slow component during rowing

The aim of this study was to investigate the contribution of the auxiliary muscles, utilized to sustain the subject's position on the ergometer, to the oxygen uptake slow component phenomenon. Three tests were performed at the same severe relative intensity on a rowing ergometer: a standard rowing exercise test, a rowing exercise performed with the arms and one performed with the legs only. During the three exercise modalities, oxygen uptake, local oxyhemoglobin saturation and surface electromyography signals of the trapezius and vastus lateralis muscles were measured. The slow component amplitude, in absolute values, resulted statistically lower for rowing (343.9 ml . min (-1)) than for arms (795.6 ml . min (-1)) and legs (695.8 ml . min (-1)) exercise modes. The same result was found when the slow component amplitude was calculated as percentage of V O (2peak) (7.1 % for rowing; 17.2 % for arms; 17.3 % for legs). The lower slow component amplitude measured for the rowing exercise mode with respect to both arms and legs modes, demonstrates that the auxiliary muscles involved in the exercise contribute to the increasing energetic cost due to the slow component.     

The slow component of O2 uptake kinetics during high-intensity exercise in trained and untrained prepubertal children

The aim of the present study was to investigate the O2 uptake slow component in prepubertal children of different aerobic capacity during high intensity exercise. Twenty-three (12 well-trained, T and 11 untrained, U subjects) 10-13 year old prepubertal children took part in 3 tests: one incremental test to determine the maximal aerobic power (PMA) and anaerobic threshold (LAT); two constant-power tests performed at intensities corresponding to 80%LAT and 90%PMA. Oxygen uptake (VO2), heart rate, ventilation (VE) and lactate ([L]s) were evaluated during each test. A monoexponential + linear term model (starting after phase 1) was used to assess VO2 kinetics during both constant-power tests. Our results showed that a slow component, represented by the linear coefficient (S) of the mathematical model, was present during the 90%PMA test only (S = 0.86 +/- 0.48 ml x min(-2) x kg(-1) for the whole population). No relationships were found between either S and VE or [L]s, showing that, at least in prepubertal children, these factors play a minor role in the explanation for the VO2 slow component. The slow component contributed approximately to the same amount of the total VO2 response in both groups (T: 21.4 +/- 8.0, U: 19.3 +/- 3.9%, ns). In conclusion, as previously described in adults, our data demonstrated the existence of a slow component in prepubertal children during high-intensity exercise. Moreover, this slow component was similar in trained and untrained children, exercising at the same relative intensity.     

The role of cadence on the VO2 slow component in cycling and running in triathletes.

The purpose of this study was to compare the effect of two different types of cyclic severe exercise (running and cycling) on the VO2 slow component. Moreover we examined the influence of cadence of exercise (freely chosen [FF] vs. low frequency [LF]) on the hypothesis that: 1) a stride frequency lower than optimal and 2) a pedalling frequency lower than FF one could induce a larger and/or lower VO2 slow component. Eight triathletes ran and cycled to exhaustion at a work-rate corresponding to the lactate threshold + 50% of the difference between the work-rate associated with VO2max and the lactate threshold (delta 50) at a freely chosen (FF) and low frequency (LF: - 10 % of FF). The time to exhaustion was not significantly different for both types of exercises and both cadences (13 min 39 s, 15 min 43 s, 13 min 32 s, 15 min 05 s for running at FF and LF and cycling at FF and LF, respectively). The amplitude of the VO2 slow component (i.e. difference between VO2 at the last and the 3rd min of the exercise) was significantly smaller during running compared with cycling, but there was no effect of cadence. Consequently, there was no relationship between the magnitude of the VO2 slow component and the time to fatigue for a severe exercise (r = 0.20, p = 0.27). However, time to fatigue was inversely correlated with the blood lactate concentration for both modes of exercise and both cadences (r = - 0.42, p = 0.01). In summary, these data demonstrate that: 1) in subjects well trained for both cycling and running, the amplitude of the VO2 slow component at fatigue was larger in cycling and that it was not significantly influenced by cadence; 2) the VO2 slow component was not correlated with the time to fatigue. If the nature of the linkage between the VO2 slow component and the fatigue process remains unclear, the type of contraction regimen depending on exercise biomechanic characteristics seems to be determinant in the VO2 slow component phenomenon for a same level of training.     

Oxygen uptake and muscle desaturation kinetics during intermittent cycling

PURPOSE: To investigate the kinetics of O2 uptake (VO2) and m. vastus lateralis [deoxyhemoglobin] ([Hb]) (near-infrared spectroscopy) for supramaximal intermittent cycling. METHODS: Six males performed a ramp test for determination of VO2peak and lactate threshold. On different days, they completed four intermittent "work:recovery" tests (10 s:20 s, 30 s:60 s, 60 s:120 s, 90 s:180 s) for 30 min or to the tolerable limit; "work" = 120% peak work rate (WRpeak) attained on the ramp, "recovery" = 20 W. RESULTS: Arterialized capillary [lactate] ([L]c) profiles were dependent on duty-cycle length and resembled those for constant-load exercise classically used to assign exercise intensity: 10 s:20 s-no increase (i.e., "moderate", with first-order VO2 kinetics); 30 s:60 s-increased but stable (i.e., "heavy," with first-order VO2 kinetics supplemented by a slow component (VO2 sc) that stabilizes); 60s:120s-progressive increase that was more marked for 90 s:180 s (i.e., "very heavy" or "severe," with first-order VO2 kinetics supplemented by a VO2 sc projecting to VO2peak). VO2 and Delta[Hb] oscillated with WR, the ensemble-averaged single-cycle oscillation amplitudes (peak-to-nadir) for each individual subject increasing with WR duty-cycle duration. In the 30-s:60-s test, with [L]c being elevated, there was also a tendency towards a modest VO2 sc, with an increase in individual VO2 peak values early in the test and VO2 not fully recovering back to baseline in recovery. This was more marked for the 60-s:120-s duty cycle: VO2 failed to recover completely back to baseline, and the peaks of the VO2 oscillations increased significantly with time (F = 30.7, P < 0.001); in some cases, VO2peak was attained and exhaustion rapidly ensued. CONCLUSION: VO2 kinetics in intermittent exercise over a range of duty-cycle durations tended to associate with blood [lactate] profiles, similarly to previous demonstrations for sustained constant-load exercise.     

Muscle activation during the tennis volley.

PURPOSE: To broaden our understanding of muscle function during the tennis volley under different ball placement and speed conditions by examining the activity of selected superficial muscles of the stroking arm and shoulder (flexor carpi radialis, extensor carpi radialis, triceps brachii, deltoids, and pectoralis major) and muscles related to postural support (left and right external oblique, lumbar erector spinae, and gastrocnemius) during the volley. METHODS: Seven skilled tennis players were asked to perform volley strokes under 18 experimental conditions, including variations in lateral contact location (forehand and backhand), ball contact height (high, middle, and low), and ball speed (fast, medium, and slow). A ball machine was modified so that the subjects could not predict the ball trajectory before it was released from the machine. Muscle activity was determined using surface electromyographic (EMG) techniques, and the critical instants of a volley were determined using two force platforms and two high-speed (120 Hz) video cameras. Average EMG values for different phases of the volley, defined by the critical instants, were computed. RESULTS AND CONCLUSIONS: In general, muscle activity increased with increasing ball speed. The extensor carpi radialis was more active than the flexor carpi radialis during both forehand and backhand volleys, suggesting the importance of wrist extension/abduction and grip strength. The increase in EMG levels in the forearm muscles shortly before the ball impact indicated that the subjects did not tighten their grip and wrist until moments before ball impact. Both antero-middle and postero-middle deltoids were active in most stroke phases. However, the roles of the deltoid muscles during a volley cannot be determined without knowing the actions of the other shoulder joint muscles.     

Muscle deoxygenation and neural drive to the muscle during repeated sprint cycling

PURPOSE: To investigate muscle deoxygenation and neural drive-related changes during repeated cycling sprints in a fatiguing context. METHODS: Nine healthy male subjects performed a repeated-sprint test (consisting of 10 x 6-s maximal sprints interspaced by 30 s of recovery). Oxygen uptake was measured breath-by-breath; muscle deoxygenation of the vastus lateralis was assessed continuously using the near-infrared spectroscopy technique. Surface electromyograms (RMS) of both vastus lateralis and biceps femoris were also recorded. Furthermore, before and after the repeated-sprint test, the percentage of muscle activation by voluntary drive (twitch-interpolated method) was measured during a maximal voluntary contraction. RESULTS AND DISCUSSION: Consistent with previous research, our data showed a significant power decrement during repeated-sprint exercise. There was also a progressive muscle deoxygenation, but our data showed that the ability of the subjects to use available O2 throughout the entire repeated-sprint test was well preserved. Our data displayed a significant decrement in the RMS activity during the acceleration phase of each sprint across the repeated-sprint exercise. Moreover, decrement in motor drive was confirmed after exercise by a significant decrease in both percentage of voluntary activation and RMS/M-wave ratio during a maximal voluntary contraction. CONCLUSION: In this experimental design, our findings suggest that the ability to repeat short-duration (6 s) sprints was associated with the occurrence of both peripheral and central fatigue.     

Control of oxygen uptake during exercise

Other than during sleep and contrived laboratory testing protocols, humans rarely exist in prolonged metabolic steady states; rather, they transition among different metabolic rates (V O2). The dynamic transition of V O2 (V O2 kinetics), initiated, for example, at exercise onset, provides a unique window into understanding metabolic control. This brief review presents the state-of-the art regarding control of V O2 kinetics within the context of a simple model that helps explain the work rate dependence of V O2 kinetics as well as the effects of environmental perturbations and disease. Insights emerging from application of novel approaches and technologies are integrated into established concepts to assess in what circumstances O2 supply might exert a commanding role over V O2 kinetics, and where it probably does not. The common presumption that capillary blood flow dynamics can be extrapolated accurately from upstream arterial measurements is challenged. From this challenge, new complexities emerge with respect to the relationships between O2 supply and flux across the capillary-myocyte interface and the marked dependence of these processes on muscle fiber type. Indeed, because of interfiber type differences in O2 supply relative to V O2, the presence of much lower O2 levels in the microcirculation supplying fast-twitch muscle fibers, and the demonstrated metabolic sensitivity of muscle to O2, it is possible that fiber type recruitment profiles (and changes thereof) might help explain the slowing of V O2 kinetics at higher work rates and in chronic diseases such as heart failure and diabetes.     

Oxygen uptake response during maximal cycling in hyperoxia, normoxia and hypoxia

BACKGROUND: Oxygen uptake (VO2) on-kinetics is decelerated in acute hypoxia and accelerated in hyperoxia in comparison with normoxia during submaximal exercise. However, the effects of fraction of oxygen in inspired air (FIO2) on VO2 kinetics during maximal exercise are unknown. HYPOTHESIS: The effects of FIO2 on VO2 on-kinetics during maximal exercise are similar to submaximal exercise. METHODS: There were 11 endurance athletes who were studied during maximal 7-min cycle ergometer exercise in hyperoxia (FIO2 0.325), hypoxia (FIO2 0.166) and normoxia (FIO2 0.209). The individual VO2 data were fit to a curve by using a three exponential model. RESULTS: In hypoxia, VO2 on-response amplitude during Phase 2 (approximately 20-100 s from the beginning of exercise) was lower (p < 0.05) when compared with hyperoxia; time constant of VO2 Phase 3 (beyond approximately 100 s after beginning of exercise) was shorter (p < 0.05) when compared with hyperoxia; and mean response time (MRT, O-63%) for VO2peak was shorter (p < 0.05) when compared with normoxia and hyperoxia. VO2peak was higher in hyperoxia (4.80 +/- 0.48 L x min(-1), p < 0.05) and lower in hypoxia (4.03 +/- 0.46 L x min(-1), p < 0.05) than in normoxia (4.36 +/- 0.44 L x min(-1)). CONCLUSIONS: Moderate hypoxia or hyperoxia do not affect VO2 time constants at the onset of maximal exercise. However, MRT for VO2peak is shortened in hypoxia. It is suggested that the differences in VO2peak and power output during the latter half of the test and the point that FIO2 was modified only moderately might explain most of the discrepancy with the previous studies.