Gs. Morris et al., EFFECTS OF LONG-TERM COCAINE ADMINISTRATION AND EXERCISE ON CARDIAC METABOLISM AND ISOMYOSIN EXPRESSION, Canadian journal of physiology and pharmacology, 72(1), 1994, pp. 1-5
Although chronic cocaine use is cardiotoxic, its use remains problemat
ic in athletics. Hence adaptive changes induced in the heart by superi
mposing chronic cocaine use on an exercise training are of interest bu
t remain poorly understood. Therefore this study investigated the effe
cts of cocaine treatment combined with exercise training on the metabo
lic and contractile properties of the heart. Male Sprague-Dawley rats
were assigned to one of four groups: normal sedentary (NS, n = 6), coc
aine sedentary (CS, n = 6), normal trained (NT, n =6), and cocaine tra
ined (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 b
efore each exercise bout and 2 additional times per week. After 12 wee
ks, all animals were sacrificed, and the hearts were removed and analy
zed for citrate synthase activity, 3-hydroxyacyl-CoA dehydrogenase act
ivity, Ca2+-activated myofibrillar ATPase activity, and myosin isoform
distribution. None of the groups demonstrated altered cardiac metabol
ic properties, but cocaine alone and in conjunction with exercise redu
ced myofibrillar ATPase activity (p < 0.05) and increased expression o
f the low ATPase myosin isoform, V3. These data suggest that the poten
tial of the citric acid cycle and beta-oxidation is not sensitive to c
hronic 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 proper
ties.