Air to Muscle O2 Delivery during Exercise at Altitude

Calbet, Jose, and Carsten Lundby. High Alt. Med. & Biol. 10.123-134, 2009.-Hypoxia-induced hyperventilation is critical to improve blood oxygenation, particularly when the arterial Po(2) lies in the steep region of the O(2) dissociation curve of the hemoglobin (ODC). Hyperventilation increases alveolar Po(2) and, by increasing pH, left shifts the ODC, increasing arterial saturation (Sao(2)) 6 to 12 percentage units. Pulmonary gas exchange (PGE) is efficient at rest and, hence, the alveolar-arterial Po(2) difference (Pao(2)-Pao(2)) remains close to 0 to 5mm Hg. The (Pao(2)-Pao(2)) increases with exercise duration and intensity and the level of hypoxia. During exercise in hypoxia, diffusion limitation explains most of the additional Pao(2)-Pao(2). With altitude, acclimatization exercise (Pao(2)-Pao(2)) is reduced, but does not reach the low values observed in high altitude natives, who possess an exceptionally high DLo(2). Convective O(2) transport depends on arterial O(2) content (Cao(2)), cardiac output (Q), and muscle blood flow (LBF). During whole-body exercise in severe acute hypoxia and in chronic hypoxia, peak Q and LBF are blunted, contributing to the limitation of maximal oxygen uptake (Vo(2max)). During small-muscle exercise in hypoxia, PGE is less perturbed, Cao(2) is higher, and peak Q and LBF achieve values similar to normoxia. Although the Po(2) gradient driving O(2) diffusion into the muscles is reduced in hypoxia, similar levels of muscle O(2) diffusion are observed during small-mass exercise in chronic hypoxia and in normoxia, indicating that humans have a functional reserve in muscle O(2) diffusing capacity, which is likely utilized during exercise in hypoxia. In summary, hypoxia reduces Vo(2max) because it limits O(2) diffusion in the lung.