Oxygen Transport on Mount Everest: The Effects of Increased Hematocrit on Maximal O₂ Transport

Abstract

Maximal oxygen consumption (V̇O₂ ^max) urateirgoes a progressive reduction in hypoxia, both acute and chronic. Such decrease, for a pressure drop of half an athmosphere corresponding to a climb to about 5500 meters a.s.l., ranges, according to various Authors (1), between 30% and 45% and is apparently independent of the degree of acclimation (Fig. 1). Possible thoracic causes for the observed V̇O₂ ^max limitation in subjects exposed to low oxygen are:

• 1) the decreased arterial O2 pressure (PaO2) and blood O2 percent saturation (O2aHb%) of which, however, the latter may be more than compensated for in the acclimated, by the increased RBC and blood hemoglobin (Hb) concentration;

• 2) hypoxia of the myocardium, that may reduce maximal cardiac output (Q̇max) both in acute and chronic hypoxia;

• 3) limited to the acclimated, the effects on Q̇max of the increased blood relative viscosity (frem 5 to 11, according to personal measurements by the Ostwald viscometer) brought about by the high increase in the hematocrit (Hot).