To evaluate the effect of extreme altitude on cardiac function in normal young men, electrocardiograms were recorded at rest and during maximal exercise at several simulated altitudes up to the equivalent of the summit of Mt. Everest (240 torn or 8,848 m). The subjects spent 40 days in a hypobaric chamber as the pressure was gradually reduced to simulate an ascent. Changes in the resting electrocardiogram were evident at 483 torr (3,660 m) and were more marked at 282 torr (7,620 m) and 240 torr (8,848 m). They consisted of an increase in resting heart rate from 63 ± 5 to a maximum of 89 ± 8 beats/min; increase in P-wave amplitude in inferior leads; right-axis shift in the frontal plane; increased S/R ratio in the left precordial leads; and increased T negativity in V1 and V2. No significant arrhythmias or conduction defects were observed. Most changes reverted to normal within 12 hours of return to sea level, with the exception of the frontal-plane axis and T-wave alterations. Maximal cycle ergometer exercise at 282 torr (7,620 m) and 240 torr (8,848 m) resulted in a heart rate of 138 ± 7 and 119 ± 6 beats/min at the 2 altitudes, respectively. No ST depression or T-wave changes suggestive of ischemia occurred despite a mean arterial oxygen saturation of 49% and a mean pH of 8 during peak exercise. Occasional ventricular premature beats were observed during exercise in 2 subjects. It is concluded that extreme altitude exposure results in electrocardlographic changes compatible with pulmonary hypertension and that maximal exercise at 8,848 m is not accompanied by any electrocardlographic evidence of isdiemia despite severe hypoxemia and alkalosis.