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

Abstract

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 ($$\dot{\mathrm V}$$ V ˙ O2peak). 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 $$\dot{\mathrm V}$$ V ˙ O2peak significantly decreased in hypoxia by 21% on average (P < 0.001). HVR was not associated with changes in $$\dot{\mathrm V}$$ V ˙ O2peak. ΔSaO2 from normoxia to 18% or 15% O2 and HCR between normoxia and 12% O2 were associated with changes in $$\dot{\mathrm V}$$ V ˙ O2peak (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.