A B S T R A C T Pulmonary hemodynamics and Rotta, Canepa, Hurtado, Velasquez, and Chavez in 1956 (1) and has been confirmed many times since, both in acclimatized natives (2, 3) and in newcomers (4). The relationship of this pulmonary hypertension to the development of high altitude pulmonary edema (HAPE) is uncertain, but pulmonary artery pressure is higher during episodes of HAPE than during control observations in the same individuals (5), and persons who have had such episodes previously have higher pulmonary artery pressures when reexposed to altitude than nonsusceptible individuals under the same conditions (6). Although it is recognized that the peak incidence of HAPE occurs 1-3 days after entry to high altitude (7), it has not been established whether pulmonary arterial pressure rises in a progressive fashion over the same time course. A progressive rise in pulmonary arterial pressure during a 6 wk period at 12,700 ft has been reported in steers, apparently associated with the right heart failure termed "brisket disease" (8), but was not observed in lambs in a matched experiment (9). Therefore, we decided to investigate in ourselves the time course of the pulmonary arterial pressure both at rest and during exercise at 12,470 ft and to examine other aspects of cardiovascular function over the same time span. We also explored the possibility suggested by Haab, Held, Ernst, and Farhi (10) and Reeves, Halpin, Cohn, and Daoud (11) that hypoxia widens the alveolar to arterial 02 difference.