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

Abstract

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% O₂) 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% O₂). Arterial desaturation (ΔSaO₂) was calculate by the difference between SaO₂ at normoxia-at each level of hypoxia (%). HVR was calculate by differences in pulmonary ventilation between normoxia and each level of hypoxia against ΔSaO₂ (L min^-1 %^-1 kg^-1). Similarly, HCR was calculated by differences in heart rate between normoxia and each level of hypoxia against ΔSaO₂ (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. ΔSaO₂ from normoxia to 18% or 15% O₂ and HCR between normoxia and 12% O₂ 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% O₂ and ΔSaO₂ at 15% O₂ were explanatory variables (adjusted R² = 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.