“Physiological and pathological responses to hypoxia and high altitude, volume IV.” Mechanisms of reduction in VO2max in hypoxia/at altitude

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On Mt. Everest, maximal O 2 uptake ( V ˙ O 2 max ) in fit young subjects, around 4-5l/min at sea level, falls to only ~1l/min. The drop in PIO 2 itself as barometric pressure decreases with altitude would theoretically explain about half of that reduction. Limitations in the O 2 transport system (lungs, heart/circulation and muscles) increase with altitude and account for the rest. Here the O 2 transport system is analyzed using both physiological theory and published experimental data to show that O 2 diffusion limitation in the lungs and muscles appears to be the primary basis for this, as the laws of diffusion would dictate, based on ever smaller O 2 diffusion gradients with altitude. On the other hand, changes in the convective processes in O 2 transport (ventilation and blood flow) appear not to explain most of the fall in V ˙ O 2 max with altitude. Maximal ventilation is well-maintained at sea level values despite the low V ˙ O 2 max , causing arterial PCO 2 to fall to single digit values. While maximal cardiac output falls with altitude, multidisciplinary studies show preserved cardiac function even at the Everest summit. Additionally, both theoretical calculations and experimental data suggest that lower maximal cardiac output is not likely a major factor in the reduction in V ˙ O 2 max . The increase in hemoglobin concentration with time at altitude has also been shown not to affect V ˙ O 2 max . The ongoing debate about the role of the cardiovascular system in limiting V ˙ O 2 at altitude will likely continue until a study can be devised that restores cardiac output at altitude to sea level norms.