ABSTRACT
In the face of the reduction in the inspired PO2 encountered at high altitude, exercise in this environment makes enormous demands on the transfer of oxygen from the air to the blood in the lung and eventually to the mitochondria of the exercise muscles. Consequently, reduced exercise tolerance is one of the most obvious features of exposure to high altitude. Maximal exercise is accompanied by extremely high ventilations (measured at body temperature and pressure); these can approach 200 L min1 at extreme altitudes, which is close to the maximum voluntary ventilation. Diffusion-limitation of oxygen transfer across the blood-gas barrier is also an important limiting factor. As a result, arterial PO2 levels typically fall greatly as the work rate is increased. Some additional ventilation-perfusion inequality also often develops, possibly because of subclinical pulmonary edema. Maximal cardiac output is reduced at high altitude, although in acclimatized subjects, the relationship between cardiac output and work rate is the same as at sea level, and oxygen consumption for a given work rate is inde-
in acclimatized subjects falls from about 4-5 L min1
at sea level to just over 1 L min1 at the Everest summit. Part of the reduction in VO2,max can be ascribed to diffusion limitation within the exercising muscle as well as a limited blood flow to the muscles of locomotion because of the increased demand of the respiratory muscles. Although aerobic performance is greatly impaired at high altitude, there is no change in maximal anaerobic peak power (for example, as measured by a standing jump) unless muscle mass is reduced.
