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 omittedO.sub.2peak). Peak oxygen uptakes was measured in normobaric normoxia (room air) and hypoxia (14.1% O.sub.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.sub.2). Arterial desaturation (DELASaO.sub.2) was calculate by the difference between SaO.sub.2 at normoxia--at each level of hypoxia (%). HVR was calculate by differences in pulmonary ventilation between normoxia and each level of hypoxia against DELASaO.sub.2 (L min.sup.-1 %.sup.-1 kg.sup.-1). Similarly, HCR was calculated by differences in heart rate between normoxia and each level of hypoxia against DELASaO.sub.2 (beats min.sup.-1 %.sup.-1). formula omittedO.sub.2peak significantly decreased in hypoxia by 21% on average (P < 0.001). HVR was not associated with changes in formula omittedO.sub.2peak. DELASaO.sub.2 from normoxia to 18% or 15% O.sub.2 and HCR between normoxia and 12% O.sub.2 were associated with changes in formula omittedO.sub.2peak (P < 0.05, respectively). The most optimal model using multiple linear regression analysis found that DELAHCR at 12% O.sub.2 and DELASaO.sub.2 at 15% O.sub.2 were explanatory variables (adjusted R.sup.2 = 0.580, P = 0.02). 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.