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Journal Article

Citation

West JB. J. Appl. Physiol. 1982; 52(6): 1393-1399.

Copyright

(Copyright © 1982, American Physiological Society)

DOI

unavailable

PMID

7050056

Abstract

The history of man's attempts to learn more about the physiology of extreme altitudes is briefly reviewed. The earliest exploits were by balloonists who were often exposed to very severe hypoxia, sometimes with fatal consequences. A turning point was the work by Paul Bert using low-pressure chambers; he was able to prove that the deleterious effects of low barometric pressures were caused by the low PO2, though other explanations for mountain sickness such as a low aterial PCO2 continued to be promoted for some time. Many early physiologists believed that active secretion of oxygen by the lungs was necessary to explain man's tolerance of extreme altitudes. Indeed, Haldane championed this view until his death in 1936, though strong evidence to the contrary had accumulated since the work of Krogh and others in the first decade of the century. High climbs by mountaineers have stimulated much interest in the physiology of severe hypoxia. Norton reached over 8,500 m on Mt. Everest in 1924, but the summit was not attained without supplementary oxygen until 1978--the last 300 m took 54 years! This suggests that the summit, altitude 8,848 m, is very near the limit of human tolerance, and predictions based on maximal work levels measured at lower altitudes are consistent with this. The American Medical Research Expedition to Everest, 1981, was specifically planned to obtain data on human physiology at extreme altitudes, and a number of measurements were made over 8,000 m, including some on the summit itself. It is apparent that the mountain can be climbed without supplementary oxygen only because the barometric pressure at the summit is not as low as has often been predicted, and because of the extreme hyperventilation that man develops under these conditions.


Language: en

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