Evidence for Peripheral Tissue Diffusion Limitation of Maximal O2 Uptake

摘要

Maximum oxygen uptake (VO2max) is often said to be limited by blood O2 transport at sea level and by pulmonary diffusion disequilibrium at altitude. Neither of these mechanisms directly addresses the role of peripheral tissue O2 extraction. A retrospective analysis of directly measured mixed venous PO2 (PvO2) during exercise at both sea level and simulated altitude in 15 normal subjects revealed that PvO2 at VO2max was very different at sea level compared to altitude. While even at submaximal workloads PvO2 at altitude readily fell below 20 torr, even at maximal workloads it remained at or above 20 torr at sea level in spite of a much higher VO2max at sea level. Moreover, the relationship between VO2max and PvO2 was linear through the origin in all subjects. On the assumption that at VO2max, average effluent muscle capillary PO2 is proportional to PvO2, these data are compatible with the notion of tissue diffusion limitation of VO2max. This argument is based on Fick's 1st law of diffusion further assuming that at VO2max, mitochondrial PO2 is sufficiently close to zero to be negligible. Thus, one would predict that VO2max is linearly dependent on the head of pressure (PO2) in the muscle capillary and by altering this PO2 during altitude simulation, such linearity was demonstrated. We found no difference in the PvO2/VO2max relationship at altitude according to whether altitude exposure was acute or chronic.