WEST, John B.; University of California San Diego: Human Adaptation to Extreme Altitude

Humans who normally live near sea level make extraordinary short-term adaptations to extreme altitude, a process called acclimatization. The most important feature of the adaptation is intense hyperventilation which, on the summit of Mt. Everest, reduces the alveolar Pco₂ to less than 10 mmHg (normal sea level value is 40 mmHg). The hyperventilation maintains the alveolar Po₂ at about 35 mmHg, but the arterial Po₂ is only about 30 mmHg (normal is 90-100 mmHg) because of diffusion limitation across the blood-gas barrier. The hyperventilation causes a marked respiratory alkalosis with an arterial pH exceeding 7.7. Interestingly this increases the oxygen affinity of hemoglobin, a characteristic which is shared by many other animals that live in oxygen-deprived environments. The advantage of the increased oxygen affinity is that it assists in loading of oxygen in the pulmonary capillary. Maximal oxygen consumption on the summit is just over one l.min^-1, that is 20-25% of the sea level value. The oxygen cost of ventilation may be a limiting factor during exercise at extreme altitude. Surprisingly, in spite of the great reduction in anaerobic capacity, anaerobic glycolysis is also severely restricted in acclimatized humans. The oxygen deprivation of high altitude is caused by the low barometric pressure, and it is interesting that most of the high mountains of the world, for example the Himalayas and the Andes, enjoy a relatively high barometric pressure for a given altitude because of their low latitude. In fact if Mt. Everest were at a high latitude, for example, that of Mt. McKinley, it would probably be impossible for climbers to reach the summit without supplementary oxygen, a feat that has now been accomplished on Everest over 100 times. It is an extraordinary coincidence that they highest point on Earth is so close to the limit of human tolerance to hypoxia.