Cardiorespiratory responses to exercise in acute hypoxia, hyperoxia and normoxia.

There is a prevailing hypothesis that an acute change in the fraction of oxygen in inspired air (F(I)O2) has no effect on maximal cardiac output (Qcmax), although maximal oxygen uptake (VO2max) and exercise performance do vary along with F(I)O2. We tested this hypothesis in six endurance athletes during progressive cycle ergometer exercise in conditions of hypoxia (FI(O)2 = 0.150), normoxia (F(I)O2 = 0.209) and hyperoxia (F(I)O2=0.320). As expected, VO2max decreased in hypoxia [mean (SD) 3.58 (0.45)l.min(-1), P<0.05] and increased in hyperoxia [5.17 (0.34) l.min(-1), P<0.05] in comparison with normoxia [4.55 (0.32)l.min(-1)]. Similarly, maximal power (Wmax) decreased in hypoxia [334 (41) W, P< 0.05] and tended to increase in hyperoxia [404 (58) W] in comparison with normoxia [383 (46) W]. Contrary to the hypothesis, Qcmax was 25.99 (3.37) l.min(-1) in hypoxia (P<0.05 compared to normoxia and hyperoxia), 28.51 (2.36) l.min(-1) in normoxia and 30.13 (2.06)l.min(-1) in hyperoxia. Our results can be interpreted to indicate that (1) the reduction in VO2max in acute hypoxia is explained both by the narrowing of the arterio-venous oxygen difference and reduced Qcmax, (2) reduced Qcmax in acute hypoxia may be beneficial by preventing a further decrease in pulmonary and peripheral oxygen diffusion, and (3) reduced Qcmax and VO2max in acute hypoxia may be the result rather than the cause of the reduced Wmax and skeletal muscle recruitment, thus supporting the existence of a central governor.