In vitro oxygen consumption of the muscles and hepatocytes was similar for 6 week old male obese and nonobese Zucker rats. Oxidative capacity, as measured by mitochondrial oxygen consumption and the activities of citrate synthase, succinate dehydrogenase, and cytochrome oxidase, was also phenotypically similar in the liver and muscles of these rats. In addition, muscle oxidative capacity was similar for obese and nonobese rats at 12 weeks of age, as was the change in muscle oxidative capacity in response to treadmill exercise. Total muscle mass, as measured by "empty carcass" protein, was phenotypically similar at 6 weeks of age, but was less in the obese rats at 13 weeks of age. Exercise did not reverse the defect in muscle mass accretion. However, exercise reduced, but did not normalize, hyperphagia and lipid accretion in the obese rat. The data indicate an absence of a defect in muscle or liver oxygen consumption as important contributors to the increased metabolic efficiency in the 6 week old obese Zucker rat. However, it is suggested that the decreased muscle mass may contribute to the increased metabolic efficiency of the 12 week old obese rat. The data further show that regular strenuous aerobic exercise will not significantly reverse the development of the obese state in the Zucker rat.