Evidence of decrease in peak heart rate in acute hypoxia: effect of exercise-induced arterial hypoxemia.

This study focuses on the influence of the arterial oxygen saturation level at exhaustion on peak heart rate under acute moderate hypoxia, in endurance-trained subjects. Nineteen competing male cyclists performed exhaustive ramp exercise (cycle ergometer) under normoxia and normobaric hypoxia (15 % O (2)). After the normoxic trial, the subjects were divided into those demonstrating exercise-induced arterial hypoxemia during exercise (> 5 % decrease in SaO (2) between rest and the end of exercise, n = 10) and those who did not (n = 9). O (2) uptake, heart rate and arterial O (2) saturation (ear-oximeter) levels were measured. Under hypoxia, peak heart rate decreased for both groups (p < 0.001) and to a greater extent for hypoxemic subjects (p < 0.01). Arterial O (2) saturation under hypoxia was lower for the hypoxemic than for the non-hypoxemic subjects (p < 0.001) and it was correlated to the fall in peak heart rate between normoxia and hypoxia for all subjects (p < 0.01; r = 0.65). Hypoxemic subjects presented greater decrease in maximal O (2) uptake than non-hypoxemic ones (19.6 vs. 15.6 %; p < 0.05). The results confirm the greater decrement in arterial O (2) saturation under hypoxia in hypoxemic subjects and demonstrates a more pronounced reduction in peak heart rate in those subjects compared with non-hypoxemic ones. These data confirm the possible influence of arterial oxygenation on the decrease in peak heart rate in acute hypoxia.

A high blood lactate induced by heavy exercise does not affect the increase in submaximal VO2 with hyperoxia.

Few studies evidenced an enhancement in oxygen uptake (VO2) during submaximal exercise in hyperoxia. This O2 "overconsumption" seems to increase above the lactate threshold. The aim of this study was to determine whether the hyperoxia-induced enhancement in VO2 may be related to a higher metabolism of lactate. Nine healthy males (aged 23.1 years, mean VO2 max= 53.8 ml min-1 kg-1) were randomized to two series of exercise in either normoxia or hyperoxia corresponding to an inspired O2 fraction (FIO2) of 30%. Each series consisted of 6 min cycling at 50% VO2 max (Moderate1), 5 min cycling at 95%VO2 max (Near Max) and then 6 min at 50% VO2 max (Moderate2). In both series Near Max was performed in normoxia. VO2 was significantly greater under hyperoxia than in normoxia during Moderate1 (2192 +/- 189 vs. 2025 +/- 172 ml min-1) and during Moderate2 (2352 +/- 173 vs. 2180+ /- 193 ml min-1). However, the effect of the high FIO2 was not significantly different on VO2Moderate2 (+172+/-137 ml min-1 with [La] approximately 6 mmol l-1) compared to VO2Moderate1 (+166 +/- 133 ml min-1 with [La] approximately 2.4 mmol l-1). [La] at the onset of Moderate2 was not different between normoxia and hyperoxia (10.1 +/- 2.2 vs. 10.9 +/- 1.6 mmol l-1). The results show that VO2 is significantly increased during moderate exercise in hyperoxia. But this O2 overconsumption was not modified by a high [La] induced by a prior heavy exercise. It could be concluded that lactate accumulation is not directly responsible for the increase in O2 overconsumption with intensity during exercise in hyperoxia.