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

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... 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.