Limiting factors for exercise at extreme altitudes

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Abstract
Man can only survive and do work in the severe oxygen deprivation of great altitudes by an enormous increase in ventilation which has the advantage of defending the alveolar PO2 against the reduced inspired PO2. Nevertheless the arterial PO2 on the summit of Mt Everest at rest is less than 30 Torr, and it decreases with exercise because of diffusion limitation within the lung. One of the consequences of the hyperventilation is that the marked respiratory alkalosis increases the oxygen affinity of the haemoglobin and assists in loading of oxygen by the pulmonary capillary. Although ventilation is greatly increased, it is a paradox that cardiac output for a given work level is the same in acclimatized subjects at high altitude as at sea level. Stroke volume is reduced but not because of impaired myocardial contractility because this is preserved up to extreme altitudes. Indeed the normal myocardium is one of the few tissues whose function is unimpaired by the very severe hypoxia. There is evidence that oxygen delivery to exercising muscle is diffusion limited along the pathway between the peripheral capillary and the mitochondria. At the altitude of Mt Everest, maximal oxygen uptake is reduced to 20-25% of its sea level value, and it is exquisitely sensitive to barometric pressure. Seasonal variations of barometric pressure affect the ability of man to reach the summit without supplementary oxygen. In spite of the greatly reduced aerobic capacity, anaerobiosis is greatly curtailed, and it is predicted that above 7500 m, there is no rise in blood lactate on exercise. The paradoxically low lactate is possibly related to plasma bicarbonate depletion.

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