Abstract

In 1978, Peter Habeler and Reinhold Messner climbed Everest without supplemental O2. Subsequently, Oelz et al. (Oelz O, Howald H, Di Prampero PE, Hoppeler H, Claassen H, Jenni R, Bühlmann A, Ferretti G, Brückner JC, Veicsteinas A, Gussoni M, Cerretelli P. J Appl Physiol (1985) 60: 1734-1742, 1986) assessed their cardiopulmonary function, finding no advantageous physiological attributes to explain their success, and leading West (West JB. High Life: A History of High-Altitude Physiology and Medicine. New York: Oxford University, 1998) to suggest that grit and determination were more important. In 1985, Charlie Houston, John Sutton, and Al Cymerman hosted a scientific project assessing a simulated ascent of Everest (OE II) at the U.S. Army Research Institute of Environmental Medicine. Included were measurements of O2 transport. In particular, mixed venous Po2 was measured at/near maximal exercise, for calculating pulmonary O2-diffusing capacity. A serendipitous observation was made: while both V̇o2max and mixed venous Po2 fell with altitude (as expected), it was how they fell-in direct proportion-that was remarkable. It later became clear that this reflected diffusion limitation of O2 transport from muscle microvessels to the mitochondria, and that this last step in O2 transport plays a major role in limiting V̇o2max. Thus, how Habeler and Messner made it up Everest without bottled O2 and no special cardiopulmonary attributes might be explained if their muscle O2-diffusing capacity, which depends largely on muscle capillarity, was unusually high. Oelz et al. mention that muscle capillary density was substantially-40%-above normal, but did not suggest that this accounted for the climbers' success. Therefore, high muscle capillarity, enhancing diffusive unloading of O2, may have been a major enabling physiological attribute for Habeler and Messner and that OE II, by chance, played a key role in bringing this to light.

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