We aimed to evaluate 1) the altitude where maximal heart rate (HRmax) decreases significantly in both trained and untrained subjects in moderate acute hypoxia, and 2) if the HRmax decrease could partly explain the drop of V·O2max. Seventeen healthy males, nine trained endurance athletes (TS) and eight untrained individuals (US) were studied. Subjects performed incremental exercise tests at sea level and at 5 simulated altitudes (1000, 1500, 2500, 3500, 4500 meters). Power output (PO), heart rate (HR), arterial oxygen saturation (SaO2), oxygen uptake (V·O2), arterialized blood pH and lactate were measured. Both groups showed a progressive reduction in V·O2max. The decrement in HRmax (ΔHRmax) was significant from 1000 m for TS and 2500 m for US and more important in TS than US (at 1500 m and 3500 m). At maximal exercise, TS had a greater reduction in SaO2 (ΔSaO2) at each altitude. ΔHRmax observed in TS was correlated with ΔSaO2. When the two groups were pooled, simple regressions showed that ΔV·O2max was correlated with both ΔSaO2 and ΔHRmax. However, a multiple regression analysis demonstrated that ΔSaO2 alone may account for ΔV·O2max. Furthermore, in spite of a greater reduction in SaO2 and HRmax in TS, no difference was evidenced in relative ΔV·O2max between groups. Thus, in moderate acute hypoxia, the reduction in SaO2 is the primary factor to explain the drop of V·O2max in trained and untrained subjects.
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