Exercise-induced cardiac hypertrophy in female rats was associated with increased ventricular glucocorticoid receptor binding capacity (39.3 vs 31.4 fmol/mg protein) rather than androgen changes.
Exercise-induced cardiac hypertrophy in female rats is associated with adaptive changes in glucocorticoid, rather than androgen, mechanisms.
Absolute Event Rate: 39.3% vs 31.4%
Female rats were trained daily by means of two 2-h-long bouts of swimming separated by a 30- to 40-min rest period. Absolute ventricular weights of the swimmers were increased above sedentary control values by 6% after 2 days, 15% after 7 days, and 30% after 35 days of exercise. Resting levels of total and free serum testosterone and total 5 alpha-dihydrotestosterone were not altered by the training. Total serum corticosterone concentrations at rest were significantly lower in the 7-day (149 +/- 16 ng/ml) and 35-day (169 +/- 24) swimmers compared with the controls (293 +/- 26). However, free corticosterone was not significantly reduced from controls in any of the swimming groups. Ventricular muscle cytosol androgen receptor binding dissociation constants and receptor binding capacities, measured using 3Hmethyltrienolone (R1881), were not significantly different from control values in the exercised groups. Glucocorticoid cytosol receptor binding capacity in ventricular tissue, determined using 3Hdexamethasone, was significantly increased as femtomoles per milligram protein (39.3 +/- 3.1 vs. 31.4 +/- 1.4) and femtomoles per milligram DNA (2,683 +/- 226 vs. 1,786 +/- 71). These findings show that glucocorticoids, rather than androgens, undergo adaptive changes in the circulation and in muscle during the development of exercise-induced cardiac hypertrophy.
Hickson et al. (Fri,) conducted a other in Exercise-induced cardiac hypertrophy. Exercise (swimming) vs. Sedentary controls was evaluated on Glucocorticoid cytosol receptor binding capacity in ventricular tissue (fmol/mg protein). Exercise-induced cardiac hypertrophy in female rats was associated with increased ventricular glucocorticoid receptor binding capacity (39.3 vs 31.4 fmol/mg protein) rather than androgen changes.