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Ascent to high altitude is associated with alterations in lung function. The mechanisms of these changes and whether they reflect early stages of high-altitude pulmonary edema (HAPE) has been debated. Therefore, we investigated the time course of pulmonary function in relation to hemodynamics and clinical symptoms in mountaineers ascending rapidly to high altitude.In 26 unacclimatized subjects we assessed spirometry, single-breath nitrogen washout, diffusing capacity (DLCO), and Doppler echocardiography in Zurich, 490 m, after climbing within 24 h to Monte Rosa, 4559 m, and after one night at 4559 m.Mean (± SD) FVC fell from 103 ± 9% predicted in Zurich to 96 ± 10% predicted at 4559 m, FEV1/FVC increased from 0.82 ± 0.06 to 0.84 ± 0.08, and closing volume increased from 0.35 ± 0.14 to 0.44 ± 0.11 L above residual volume (P < 0.05, all changes). On the following day at 4559 m, closing volume remained elevated in 9 of 21 subjects who had a lower DLCO but similar pulmonary artery systolic pressures compared with the remaining 12 subjects (40 ± 8 vs 43 ± 7 mm Hg, P = NS). None of the subjects had overt HAPE.We conclude that changes in pulmonary function after rapid ascent to high altitude were consistent with interstitial fluid accumulation, but they were not related to changes in pulmonary artery pressure. Individual lung function responses to high-altitude exposure varied largely and did not predict subsequent HAPE.