Maximal exercise at extreme altitudes was studied during the course of the American Medical Research Expedition to Everest. Measurements were carried out at sea level [inspired O2 partial pressure (PO2) 147 Torr], 6,300 m during air breathing (inspired PO2 64 Torr), 6,300 m during 16% O2 breathing (inspired PO2 49 Torr), and 6,300 m during 14% O2 breathing (inspired PO2 43 Torr). The last PO2 is equivalent to that on the summit of Mt. Everest. All the 6,300 m studies were carried out in a warm well-equipped laboratory on well-acclimatized subjects. Maximal O2 uptake fell dramatically as the inspired PO2 was reduced to very low levels. However, two subjects were able to reach an O2 uptake of 1 l/min at the lowest inspired PO2. Arterial O2 saturations fell markedly and alveolar-arterial PO2 differences increased as the work rate was raised at high altitude, indicating diffusion limitation of O2 transfer. Maximal exercise ventilations exceeded 200 l/min at 6,300 m during air breathing but fell considerably at the lowest values of inspired PO2. Alveolar CO2 partial pressure was reduced to 7-8 Torr in one subject at the lowest inspired PO2, and the same value was obtained from alveolar gas samples taken by him at rest on the summit. The results help to explain how man can reach the highest point on earth while breathing ambient air.

At very high altitude, exercise performance in the human sojourner may depend on a sufficient hypoxic ventilatory response (HVR). To study the relationship of HVR to exercise performance at high altitude, we studied HVR at sea level and 5,400 m and exercise ventilation at sea level, 5,400 m, and 6,300 m in nine members of the American Medical Research Expedition to Everest. The relationship of HVR between individuals was maintained when HVR was repeated after acclimatization to 5,400 m (P less than 0.05). There was a significant correlation in all subjects between HVR and ventilatory equivalent during exercise at sea level (r = 0.704, P less than 0.05). Subjects were then grouped into high (H) and low (L) HVR responders (ventilation increase to end-tidal PO2 of 40 Torr = 21.2 +/- 5.4 and 5.6 +/- 0.9 1 X min-1, respectively. At low and moderate levels of exercise, ventilation at sea level and after acclimatization to 6,300 m was higher in the high HVR group. At 6,300 m blood O2 saturation (Sao2%) decreased from rest to maximum exercise: H = 8.3 +/- 1.8%, L = 20.0 +/- 2.5% (P less than 0.01). HVR correlated inversely in all subjects with the decrease in Sao2 from rest to maximum exercise (P less than 0.05). Climbers with the highest HVR values reached and slept at higher altitudes. We conclude that the relative value of HVR in our group of climbers was not significantly altered after acclimatization; HVR predicts exercise ventilation at sea level and high altitude; the drop in Sao2% that occurs with exercise is inversely related to HVR; and sojourners with high HVR may perform better at extreme altitude.

In established cases of acute mountain sickness, treatment with acetazolamide relieves symptoms, improves arterial oxygenation, and prevents further impairment of pulmonary gas exchange.

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