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Journal of Applied Physiology, Vol 63, Issue 4 1504-1510, Copyright © 1987 by American Physiological Society
ARTICLES |
S. M. Czerwinski, T. G. Kurowski, T. M. O'Neill and R. C. Hickson
Department of Physical Education, University of Illinois, Chicago 60680.
This study was undertaken to examine whether exercise can prevent glucocorticoid-induced muscle atrophy in previously untrained individuals and to evaluate whether the time of hormone administration is a determinant in the muscle's response to glucocorticoids. Female rats were divided into five groups: 1) a sedentary group that received cortisol acetate (CA, 100 mg/kg body wt); 2) a sedentary group that received the dosing vehicle (1% aqueous carboxymethyl cellulose); 3) an exercise group that received CA immediately after each exercise session; 4) an exercise group that received CA 90 min after each exercise session; and 5) an exercise group that received the vehicle. Steroid treatment and exercise (28.7 m/min for 90 min/day) were performed for 11 consecutive days. Initiation of training prevented muscle mass loss by 60% in plantaris (P) muscles and by 25% in gastrocnemius (G) muscles. Time of steroid injection was not related to the muscle sparing response. In the glucocorticoid-treated exercised rats, the activities of citrate synthase, a training marker, increased 60% in P and 37% in G. Thus the exercise appeared to cause a greater recruitment of P muscles. These data support the hypothesis that entering into an exercise program can be effective in retarding glucocorticoid-induced muscle atrophy. The degree of atrophy prevention, however, may be related to the extent that specific muscles are recruited during exercise.
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