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.
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.
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).
We conclude that a decrease in respiratory muscle strength may contribute to the decrease in FVC observed at high altitude.
1Department of Physiology, Faculty of Medicine, Free University of Brussels, BELGIUM; and 2Department of Physiology, Institute of Sports and Physiotherapy, Free University of Brussels, BELGIUM
Address for correspondence: Robert Naeije, Laboratory of Physiology, Erasmus Campus, CP 604, Route de Lennik 808, B-1070 Brussels, Belgium; E-mail: email@example.com.
Submitted for publication August 2004.
Accepted for publication December 2004.
The support of Col. Dr. van Stryndonck and the technical assistance of Gino D’Hondt were greatly appreciated.
We thank the Belgian Airforce for allowing us to use their hypobaric chamber.
This study was supported by grant no. 3.4613.04 from the Fonds de la Recherche Scientifique Médicale (FRSM), Belgium.