Downing (23) has concluded that the effects of hypoxia on cardiac func tion are determined by the balance reached between extrinsic sympathetic stimulation and the direct depressant effect of hypoxia on the myocardium. During chronic hypoxia, this latter effect appears to predominate, and the reduced stroke volume is probably a manfestation of impaired myocardial oxygenation (1, 39). Just as this effect requires several days to become manifest, so it is also not readily reversible. In the man adapted to high altitude, acute restoration of the arterial oxygen tension to values normal for sea level by the administration of an oxygen-enriched gas mixture pro duces no increase in stroke volume. In fact, the decrease in heart rate which accompanies oxygen breathing results in a fall in the already subnor mal cardiac output (36, 39). However, when chronic hypoxia is relieved for ten days by actual descent to sea level, then stroke volume does increase (39).