Effects of long-term cocaine administration and exercise on cardiac metabolism and isomyosin expression

Although chronic cocaine use is cardiotoxic, its use remains problematic in athletics. Hence adaptive changes induced in the heart by superimposing chronic cocaine use on an exercise training are of interest but remain poorly understood. Therefore this study investigated the effects of cocaine treatment combined with exercise training on the metabolic and contractile properties of the heart. Male Sprague-Dawley rats were assigned to one of four groups: normal sedentary (NS, n = 6), cocaine sedentary (CS, n = 6), normal trained (NT, n = 6), and cocaine trained (CT, n = 6). Trained animals were sprint trained 4 times/week. CS and CT animals received cocaine (25 mg/kg, ip) 6 times/week, 15 min before each exercise bout and 2 additional times per week. After 12 weeks, all animals were sacrificed, and the hearts were removed and analyzed for citrate synthase activity, 3-hydroxyacyl-CoA dehydrogenase activity, Ca(2+)-activated myofibrillar ATPase activity, and myosin isoform distribution. None of the groups demonstrated altered cardiac metabolic properties, but cocaine alone and in conjunction with exercise reduced myofibrillar ATPase activity (p < 0.05) and increased expression of the low ATPase myosin isoform, V3. These data suggest that the potential of the citric acid cycle and beta-oxidation is not sensitive to chronic cocaine treatment, but the distribution of cardiac myosin among its three isoforms is affected. Furthermore, high-intensity treadmill training does not interact with cocaine to further alter these properties.