Oxygen transport during exercise at extreme altitude: Operation everest II

Eight male volunteers had rest and exercise measurements to determine the mechanisms of oxygen transport during a 40-day chamber, decompression simulating high-altitude exposure equivalent to the summit of Mt Everest. Five subjects completing the study decreased their maximum oxygen uptake by 72%. During maximal or near-maximal exercise, arterial PCO₂ fell as low as 8 mm Hg, defending the alveolar PO₂ and confirming marked hyperventilation. Alveolar-arterial diffusion did not improve and V/Q worsened. Cardiac function was unimpaired. Circulatory oxygen transport resembled that at sea level. The decrease in mixed venous PO₂ was not enough to preserve fractional oxygen utilization "on the summit". The PO₂ gradients from atmosphere to alveolus, alveolus to arterial blood, arterial to venous blood, and from venous (capillary) blood to mitochondria all decreased. However, hyperventilation appeared to be the primary adaptation that defended the maximum oxygen uptake.