AJP - Heart and Circulatory Physiology, Vol 246, Issue 6 761-H767, Copyright © 1984 by American Physiological Society
Androgen and glucocorticoid mechanisms in exercise-induced cardiac hypertrophy
R. C. Hickson, T. M. Galassi, T. T. Kurowski, D. G. Daniels and R. T. Chatterton Jr
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
[3H]methyltrienolone (R1881), were not significantly different from control
values in the exercised groups. Glucocorticoid cytosol receptor binding
capacity in ventricular tissue, determined using [3H]dexamethasone, 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.
