Eleven healthy young men native to high altitude underwent haemodynamic studies at their original place of residence and after two years' residence at sea level. The investigation sought to determine the long-term effects of the suppression of the hypoxic stimulus upon heart rate, cardiac output, and pulmonary artery pressure of highlanders. For comparative purposes the influence of oxygen inhalation at high altitude was also studied.The heart rate fell at sea level and bradycardia was seen in most of the cases. The fall in heart rate is probably related to an increase in the predominance of the parasympathetic nervous system of highlanders after the relief of hypoxia. Oxygen inhalation at high altitude produced a smaller reduction in heart rate than after descending to sea level. The increase in heart rate during exercise was similar in both environments.Cardiac output increased moderately with the descent to sea level. This change was not associated with changes in oxygen uptake, but with a reduction in the values of haemoglobin, arterial oxygen content, and arteriovenous difference of oxygen. Stroke index increased significantly on descent to sea level, mainly as a consequence of the reduction in heart rate. At both altitudes exertion caused a similar increase in cardiac output which was related to the increase in heart rate rather than to stroke index which did not show significant variations. Oxygen inhalation at high altitude did not alter cardiac output and stroke index.Mean resting pulmonary arterial pressure fell to normal after two years' residence at sea level, but the pressure response to exercise was similar to that observed at high altitude and greater than that seen in healthy lowlanders. Oxygen inhalation at high altitude produced only a partial reduction in pulmonary hypertension. A recurrence ofpulmonary hypertension was observed on return to high altitude. These observations emphasize the importance of the structural characteristics of t the pulmonary vessels of highlanders in the mechanism of high altitude pulmonary hypertension.

The response elicited by exercise on pulmonary pressure, cardiac output, and arterial oxygen saturation in 35 lifetime residents of high altitude has been studied at high altitude (14,900 feet above sea level), and 22 residents of low altitude have been studied at sea level. A procedure combining cardiac catheterization, arterial cannulation, and spirometry was carried out. The exercise was moderate and was performed in supine position using a bicycle ergometer, the work load being 300 kg-m/min/m, 2 and the average increase of the oxygen uptake being 4.7 times at sea level and 4.8 times at high altitude. Both at sea level and at high altitude the cardiac output augmented during exercise proportionally to the increase in oxygen uptake, and thus followed the pattern of response described by other authors. The cardiac output as well as the oxygen intake, for the magnitude of exertion performed in this study, was almost the same at sea level and at high altitude. The cardiac output rose during exercise almost exclusively as a result of an increase in the heart rate, with the stroke volume remaining practically constant. Despite similar increase in cardiac output, the response of pulmonary pressure was smaller for sea-level subjects than for the high-altitude subjects. Increments of mean pulmonary pressure of nearly 50% and 100% were observed on exercise at sea level and at high altitude, respectively. During exercise the arterial oxygen saturation did not change in the sea-level studies, but decreased significantly in the high-altitude studies. The decrement observed in high-altitude residents is related to a fall in arterial pO 2 which at resting conditions is placed on the steep part of the oxygen dissociation curve.

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