Purpose: High altitude exposure has consistently been reported to decrease forced vital capacity (FVC), but the mechanisms accounting for this observation remain incompletely understood. We investigated the possible contribution of a hypoxia-related decrease in respiratory muscle strength.
Methods: Maximal inspiratory and expiratory pressures (MIP and MEP), sniff nasal inspiratory pressure (SNIP), FVC, peak expiratory flow rate (PEF), and forced expiratory volume in 1 s (FEV1) were measured in 15 healthy subjects before and after 1, 6, and 12 h of exposure to an equivalent altitude of 4267 m in a hypobaric chamber.
Results: Hypoxia was associated with a progressive decrease in FVC (5.59 ± 0.24 to 5.24 ± 0.26 L, mean ± SEM, P < 0.001), MIP (130 ± 10 to 114 ± 8 cm H2O, P < 0.01), MEP (201 ± 12 to 171 ± 11 cm H2O, P < 0.001), and SNIP (125 ± 7 to 98 ± 7 cm H2O, P < 0.001). MIP, MEP, and SNIP were strongly correlated to FVC (r ranging from 0.77 to 0.92). FEV1 didn’t change, and PEF increased less than predicted by the reduction in air density (11–20% of sea-level value compared with 32% predicted).
Conclusion: We conclude that a decrease in respiratory muscle strength may contribute to the decrease in FVC observed at high altitude.