Effect of hypobaria on maximal ventilation, oxygen uptake, and exercise performance during running under hypobaric normoxic conditions

During exposure to high altitude, hypoxia develops because of reductions in barometric pressure and partial pressure of O(2). Although several studies have examined the effects of hypoxia on exercise performance and physiological responses, such as maximal minute ventilation ([Formula: see text] (Emax)) and maximal oxygen uptake ([Formula: see text] O(2max)), how barometric pressure reduction (hypobaria) modulates them remains largely unknown. In this study, 11 young men performed incremental treadmill running tests to exhaustion under three conditions chosen at random: normobaric normoxia (NN; 763 ± 5 mmHg of barometric pressure, equivalent to sea level), hypobaric hypoxia (HH; 492 ± 1 mmHg of barometric pressure, equivalent to 3500 m above sea level (m a.s.l.)), and hypobaric normoxia (HN; 492 ± 1 mmHg of barometric pressure while breathing 32.2 ± 0.1% O(2) to match the inspiratory O(2) content under NN). [Formula: see text] (Emax) was higher in HN than in NN (160.9 ± 10.7 vs. 150.7 ± 10.0 L min(−1), P < 0.05). However, no differences in [Formula: see text] O(2max) and arterial oxyhemoglobin saturation were observed between NN and HN (all P > 0.05). Time to exhaustion was longer in HN than in NN (932 ± 83 vs. 910 ± 79 s, P < 0.05). These results suggest that reduced air density during exposure to an altitude of 3500 m a.s.l. increases maximal ventilation and extends time to exhaustion without affecting oxygen consumption or arterial oxygen saturation.