This commentary demonstrates that VO2max depends, in part, on diffusive O2 transport; exercise hyperemia is necessary but not sufficient. Experiments and new mathematical models place the principal site of resistance to O2 diffusion between the surface of a red cell and the sarcolemma. The large drop in PO2 over this short distance is caused by high flux density and absence of heme protein O2 carrier in this region. PO2 gradients within red myocytes are shallow at high VO2 because myoglobin acts as O2 carrier and PO2 buffer. At high VO2 cell PO2 is less than 5 torr, the myoglobin P50. Low cell PO2 relative to blood PO2 is essential to a) maintain the driving force on diffusion as capillary PO2 falls, and b) to increase myoglobin-facilitated diffusion and the overall O2 conductance. O2 per se does not limit mitochondrial ATP production under normal circumstances because the low O2 drive on electron transport is compensated by greater phosphorylation and redox drives. These metabolic adaptations support transcapillary diffusion by defending VO2 at the low cell PO2 required to extract O2 from blood. Thus aerobic capacity is a distributed property, dependent on the interaction of transport and metabolism as a system.