Effects of chronic exercise and ageing on regional energy metabolism in heart muscle

The effects of chronic running or swimming training and age on the regional distribution of glucose uptake, activities of several glycolytic and mitochondrial enzymes, and regional oxidative capacity were studied in rat hearts. Glucose uptake was measured in Langendorff-perfused hearts or in vivo, and enzyme activities and oxidative capacities were measured from tissue homogenates. Differences of cardiac glucose metabolism between males and females were also studied. Chronic swimming and running training increase both in vivo and in the isolated perfused heart the subepicardial glucose uptake, which normally is significantly lower than the subendocardial uptake in the hearts of young rats. This redistribution of glucose uptake probably mirrors a similar redistribution of cardiac work load. The distribution of glycolytic enzyme activities is not quite similar to that of glucose uptake, and training does not change these activities as clearly it changes the rate of glucose uptake. The adaptive change of glucose uptake to endurance training was even more clear in fem ale than in male rats: an opposite glucose uptake gradient was found, the subepicardial glucose uptake being higher than the subendocardial uptake. Also, most of the significant changes in enzyme activities were found in the hearts of female rats. Cessation of training restores the adaptive changes in transmural glucose uptake within two weeks. Glucose uptake measured in vivo increases during rest and exercise as a consequence of training. The increase seems to be independent of the actual work load or supply of major alternative myocardial substrates indicating that physical training increases the preference of glucose as a myocardial energy-yielding substrate. Regional differences exist in the oxidation capacity of various substrates, the subendocardial capacities tending to be higher than the subepicardial ones. Training enhances oxidation rates of succinate, pyruvate and palmitoylcarnitine in the subendocardium of young rats. On the basis of these results and results concerning glucose uptake, it seems that the myocardium adapts transmurally to chronic exercise by elevating mitochondrial ATP-production in the subendocardium and glycolytic ATP-production in the subepicardium. Ageing results in abolished gradients in the glucose uptake and in the oxidation rates of substrates, suggesting similar abolishment in the myocardial work load. Training-induced cardiac alterations are absent or small in aged rats.