Muscle energetics and ultrastructure in chronic hypoxia.

High-altitude exposure impairs both maximal aerobic and anaerobic (lactic and alactic) performances. The maximal aerobic power (VO2max) decreases exponentially with increasing altitude. At 5,350 m, a sudden rise in inspired O2 pressure (PIO2) was found to raise the VO2max of acclimatized lowlanders from 70 to only 92% of the control sea-level value. Since the hemoglobin concentration was about 35% higher than that of the controls, hemoglobin O2 saturation was restored to about 100%, and maximal cardiac output was only 10-20% lower than at sea level, the above result can only be the consequence: (1) of a reduced muscle mass and/or of muscle deterioration, and (2) of impaired muscle perfusion. In muscle biopsies taken from the vastus lateralis muscles of mountaineers after a 6- to 8-week sojourn at high altitude, a reduction in the fiber cross-sectional area was found which was accompanied by a decrease in the volume density of the mitochondria and by a lower tissue oxidative capacity. In acclimatized lowlanders, the maximal blood lactate concentration after exhausting exercise was halved compared to sea-level conditions. On the other hand, the peak anaerobic power was not affected by severe hypoxia within the first 3 weeks of exposure; thereafter, it decreased by about 25%, probably as a consequence of muscle deterioration. It is concluded that, whereas in acute hypoxia VO2max is primarily reduced by a lack of O2, in chronic hypoxia muscle deterioration may become an important factor contributing to the limitation of the maximal aerobic performance.