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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 ( 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: V ˙ O2peak significantly decreased in hypoxia by 21% on average (P < 0.001). HVR was not associated with changes in V ˙ O2peak. ΔSaO2 from normoxia to 18% or 15% O2 and HCR between normoxia and 12% O2 were associated with changes in 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. [ABSTRACT FROM AUTHOR]

Molecular hydrogen has been suggested to have a cytoprotective effect on the whole body and to enhance exercise performances. However, the effect of hydrogen-rich gas mixture (HG) inhalation on physiological responses has been poorly investigated. We examined the impact of acute HG inhalation on subsequent oxidative stress, muscle damage, and exercise performances during the recovery period after a strenuous exercise. This is a two-trial, double-blind, crossover, repeated measures study. Eight physically active male volunteers inhaled HG (estimated fraction of inspired oxygen and hydrogen were 21.57 and 4.08% at most, respectively) or normal gas (placebo, ambient air 400 m above sea level) during a 60-minute recovery phase after oxidative stress-inducing exercise) completion comprising 30-minute treadmill running at an intensity corresponding to 75% of maximal oxygen uptake and squat jumps (5 sets × 10 repetitions). Before oxidative stress-inducing exercise and 10 minutes after the post-exercise gas inhalation, blood and urine samples were obtained and exercise performances (jumping ability; pedaling power output; muscle strength) were evaluated. Post-exercise HG inhalation attenuated the increase in urinary 8-hydroxydeoxyguanosine excretion rate (P < 0.05), a DNA oxidation marker, and the reduction in the countermovement jump height (P < 0.05), compared with Placebo inhalation. Other exercise performances and blood oxidative stress and muscle damage markers did not differ between HG and Placebo inhalation. Moreover, the increase in urinary 8-hydroxydeoxyguanosine excretion rate was significantly associated with countermovement jump performance reduction (r = –0.78, P < 0.01). These findings suggested that HG inhalation during post-exercise recovery period might improve exercise performance via reducing systemic oxidative damage. The study was approved by the Human Research Ethics Committee of the University of Yamanashi (approval No. H29-006) on June 28, 2017. [ABSTRACT FROM AUTHOR]