Glucocorticoid-induced cardiac hypertrophy: additive effects of exercise

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Abstract
Female rats were divided into a sedentary control and an exercise group that was trained by treadmill running 100 min/day for 13–15 wk. During the last 12 days of training, they were further subdivided into trained and sedentary groups that received either daily subcutaneous injections of cortisone acetate (CA) (100 mg/kg body wt) or the vehicle, 1% (wt/vol) carboxymethylcellulose. As a result of the exercise program, ventricular weights were 15% (P less than 0.01) heavier in the vehicle-treated runners than in the vehicle-treated controls, but there were no changes in cardiac androgen (methyltrienolone, R1881) or glucocorticoid (dexamethasone, DEX) cytosol-specific binding concentrations. Body weights were decreased by 11–12% in both CA-treated groups. Ventricular weights of the CA-treated controls were 11% (P less than 0.01) heavier than the weights of the vehicle-treated controls. The combination of exercise and glucocorticoid treatments resulted in ventricular weights that were 21% heavier than those in the vehicle-treated controls and 8 and 5% (P less than 0.05) greater than those resulting from CA and endurance training individually. Both R1881 and DEX binding were decreased in hearts of CA-treated animals from those of vehicle-treated animals, and exercise did not modify this response. These results show that glucocorticoid treatment can induce cardiac enlargement, and the combination of glucocorticoids and exercise can have additive effects on the growth, yet their mechanisms appear different.