Cardiorespiratory dynamics to hypoxia at the onset of cycling exercise in male endurance subjects.

AIM: It is well established that altering O2 delivering to contracting skeletal muscle affects human performance. In this respect, a reduced O2 supply (e.g., hypoxia) increases the rate of muscle fatigue. This study aimed to determine the effects of moderate hypoxia and exercise intensity on oxygen uptake (VO2) and cardiac output (CO) kinetics during moderate [below the ventilatory threshold (VT)] and heavy (above VT) constant work rate cycling exercises. METHODS: Eight trained males (age, mean+/-SD, 22+/-3 years; height 182+/-5 cm; body mass 71+/-12 kg) performed at the same relative intensity in normoxic (FIO2=0.21) and hypoxic (FIO2=0.13) conditions moderate and heavy exercises during which pulmonary gas exchange was determined breath-by-breath and CO was monitored beat-by-beat with Doppler echocardiography. RESULTS: The rate of increase (t63%, corresponding to time constant and time delay of a monoexponential response) in CO was significantly faster than that of VO2 in 3 out of 4 experimental conditions (p<0.05). Moreover VO2 kinetics were significantly slowed by hypoxia and speeded by exercise intensity, while CO responses were unaffected by such conditions. A slowed CO response was apparent in hypoxia compared to normoxia (p>0.05) in heavy exercise. CONCLUSIONS: These results suggest an absence of coupling between CO and VO2 kinetics, and that cardiorespiratory O2 delivery is likely different at exercise onset as a function of exercise intensity and FIO2.

Oxygen uptake kinetics during moderate and heavy intensity exercise in humans: the influence of hypoxia and training status.

This study examined the influence of moderate hypoxia on the oxygen uptake (V.O(2)) kinetic response (primary time constant and slow component amplitude) during moderate and heavy cycle exercise in twenty-seven male subjects with various training status. Nine endurance trained (21.5 +/- 2.6 yr), nine sprint trained (22.9 +/- 5.7 yr), and nine untrained controls (24.0 +/- 4.4 yr) completed incremental tests to exhaustion in normoxia (inspired gas concentration or FIO (2) = 21 % O(2)) and hypoxia (FIO (2) = 13 % O(2)) to establish the FIO (2)-specific ventilatory threshold (VT) and maximal VO(2). Subsequently, the subjects performed repeated constant work rate cycling exercises during 7 min at moderate intensity (80 % of FIO (2)-specific VT) and heavy intensity (midway between the FIO (2) specific VT and maximal VO(2)). Pulmonary gas exchange was measured breath-by-breath during all exercise sessions. For both moderate and heavy intensities, the time constant of the primary VO(2) component was significantly (p < 0.05) slowed by approximately 25 to 30 % in hypoxia compared to normoxia to the same extent in the three groups. Hypoxia produced a more important decrease in the amplitude of the slow component in endurance athletes (- 36 %) than in sprinters (- 30 %) and controls (- 12 %). These results suggest that both primary and slow components of VO(2) kinetics during the adjustment to moderate- and heavy-intensity exercise are sensitive to hypoxia while training status tended to modulate partly the slow component amplitude.

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.