Systemic oxygen transport in rats artificially selected for running endurance

The relative contribution of genetic and environmental influences to individual exercise capacity is difficult to determine. Accordingly, animal models in which these influences are carefully controlled are highly useful to understand the determinants of intrinsic exercise capacity. Studies of systemic O2 transport during maximal treadmill exercise in two diverging lines of rats artificially selected for endurance capacity showed that, at generation 7, whole body maximal O2 uptake (V˙O2max) was 12% higher in high capacity (HCR) than in low capacity runners (LCR) during normoxic exercise. The difference in V˙O2max between HCR and LCR was larger during hypoxic exercise. Analysis of the linked O2 conductances of the O2 transport system showed that the higher V˙O2max was not due to a higher ventilatory response, a more effective pulmonary gas exchange, or an increased rate of O2 delivery to the tissue by blood. The main reason for the higher V˙O2max of HCR was an increased tissue O2 extraction, due largely to a higher tissue diffusive O2 conductance. The enhanced tissue O2 diffusing capacity was paralleled by an increased capillary density of a representative locomotory skeletal muscle, the gastrocnemius, in HCR. Activities of skeletal muscle oxidative enzymes citrate synthase and β-HAD were also higher in HCR than LCR. Thus, the functional characteristics observed during exercise are consistent with the structural and biochemical changes observed in skeletal muscle that imply an enhanced capacity for muscle O2 uptake and utilization in HCR. The results indicate that the improved V˙O2max is solely due to enhanced muscle O2 extraction and utilization. However, the question arises as to whether it is possible to maintain a continually expanding capacity for O2 extraction at the tissue level with successive generations, without a parallel improvement in the capacity to deliver O2 to the exercising muscles.