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Ascent to high altitude leads to a number of changes in lung function. We studied 55 subjects at sea level and as they ascended from 2600m to 5300m over 8 to 14 days to investigate the possible time course of these changes. Using a turbine spirometer, previously validated at simulated altitude, subjects recorded their peak expiratory flow (PEF), forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) on arrival at each new attitude and again the next morning. Compared to sea level, PEF rose by 4.7% (95% confidence intervals (CI) 4.4-5.0, p=0.007), and FVC fell by 0.54% (95% CI 0.4-0.7, p=0.034), for every 1000m gain in altitude. FEV1 was unaffected by altitude change. These observations are in line with our previous findings (Pollard et al, Thorax, 1996;51:175-8). There was no significant change in lung function or acute mountain sickness (AMS) scores between arrival at each altitude and the next morning. Subjects with a greater fall in FVC on arrival at each attitude had higher AMS scores both on arrival and the next morning (Mood's median test, p=0.017). Furthermore, those with higher AMS scores had lower FVC at sea level (mean sea level FVC 4.81 (sd1.1) in those with AMS scores >4, vs. 5.51 (sd 0.9) in those with AMS scores <4 (p=0.018). Subjects with higher AMS scores had a smaller rise in PEF, although this did not reach significance (p=0.068). These results suggest that the fall in FVC may be related to acute mountain sickness, and that acute mountain sickness may be predicted from sea level FVC. The rise in PEF continued in two subjects studied after acclimatisation as they ascended to 6,400m, supporting the hypothesis that it is due to changes in air density. The fall in FVC was not progressive with further ascent, suggesting that it may be due to transient changes in the lung, such as sub-clinical pulmonary oedema, which resolved with acclimatisation.


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