Hypoxic-induced resting ventilatory and circulatory responses under multistep hypoxia is related to decline in peak aerobic capacity in hypoxia

BACKGROUND: Several factors have been shown to contribute to hypoxic-induced declined in aerobic capacity. In the present study, we investigated the effects of resting hypoxic ventilatory and cardiac responses (HVR and HCR) on hypoxic-induced declines in peak oxygen uptake ([Formula: see text] O(2peak)). METHODS: Peak oxygen uptakes was measured in normobaric normoxia (room air) and hypoxia (14.1% O(2)) for 10 young healthy men. The resting HVR and HCR were evaluated at multiple steps of hypoxia (1 h at each of 21, 18, 15 and 12% O(2)). Arterial desaturation (ΔSaO(2)) was calculate by the difference between SaO(2) at normoxia—at each level of hypoxia (%). HVR was calculate by differences in pulmonary ventilation between normoxia and each level of hypoxia against ΔSaO(2) (L min(−1) %(−1) kg(−1)). Similarly, HCR was calculated by differences in heart rate between normoxia and each level of hypoxia against ΔSaO(2) (beats min(−1) %(−1)). RESULTS: [Formula: see text] O(2peak) significantly decreased in hypoxia by 21% on average (P < 0.001). HVR was not associated with changes in [Formula: see text] O(2peak). ΔSaO(2) from normoxia to 18% or 15% O(2) and HCR between normoxia and 12% O(2) were associated with changes in [Formula: see text] O(2peak) (P < 0.05, respectively). The most optimal model using multiple linear regression analysis found that ΔHCR at 12% O(2) and ΔSaO(2) at 15% O(2) were explanatory variables (adjusted R(2) = 0.580, P = 0.02). CONCLUSION: These results suggest that arterial desaturation at moderate hypoxia and heart rate responses at severe hypoxia may account for hypoxic-induced declines in peak aerobic capacity, but ventilatory responses may be unrelated.