The present series of studies were conducted to investigate the relationship between exercise performance and oxygen uptake (VO2) by altering the fraction of oxygen in inspired air (FIO2) in an attempt to elucidate the mechanisms that regulate and limit physical work capacity. A total of 29 endurance athletes were examined in hyperoxia (FIO2 0.293 - 0.622), normoxia (FIO2 0.209) and hypoxia (FIO2 0.150-0.166). Hypoxia impaired (mean 14.7%) and hyperoxia improved (12.2%) maximal oxygen uptake (VO2max) in comparison with normoxia. Impaired VO2max was accompanied by a decrement in exercise performance (Pmax) in hypoxia (7.3%). Also, Pmax tended to be higher in hyperoxia (3.6%) than in normoxia. Thus, in both hypoxia and hyperoxia, the change in VO2max exceeded the change in Pmax. Maximal cardiac output (Qmax) was reduced (8.8%) in acute hypoxia when compared with normoxia. The reduction in VO2max in acute hypoxia is therefore explained both by the narrowing of the arterio-venous O2 difference and reduced Qmax. The reduced Qmax in hypoxia and the finding that hypoxia had a tendency to diminish the sum of integrated electromyography signals during maximal exercise in comparison with normoxia and hyperoxia both suggest that the central nervous system (CNS) is among those factors that limit exercise performance and VO2max in acute hypoxia. Therefore, reduced Qmax and VO2max in acute hypoxia may be the result rather than the cause of reduced Pmax and skeletal muscle recruitment, which can be interpreted to support the "central governor" hypothesis. However, further studies are needed to indicate the existence and mode of action of the proposed "central governor". This study indicates that some of those responses that previously were expected to occur only in chronic hypoxia can also be seen in acute phase, at least in highly trained endurance athletes. This study also indicates that exercise performance and VO2max may not be dependent only on the O2 delivery and utilization, but also on other factors including factors possibly linked to CNS function.
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