Glucocorticoid cytosol binding in exercise-induced sparing of muscle atrophy

Female rats were initially divided into a sedentary or an exercise group that was trained by treadmill running to a final work rate of 31 m/min, 100 min/day, for 13-18 wk. During the last 12 days of training each of these groups were further subdivided into groups that received daily subcutaneous injections of cortisol acetate (CA) (100 mg/kg body wt) or the vehicle (1% carboxymethyl cellulose). Exercise prevented ~40% of the gastrocnemius muscle weight loss due to CA treatment. Training did not influence glucocorticoid cytosol-receptor binding concentrations, using [³H]triamcinolone acetonide (TA) as the labeled glucocorticoid in any of the skeletal muscle types investigated. TA-receptor binding capacities were depleted by the multiple injections but were higher in the red fiber types of the CA-treated trained than those in the CA-treated sedentary animals. In a second series of experiments in which receptor depletion and repletion rates were studied using a single injection of cortisol, TA binding capacities 2 h after the cortisol injection were higher in slow-twitch red soleus muscles of trained as compared with sedentary rats (36.4 ± 2.0 vs. 26.8 ± 2.5 fmol/mg protein). Similar patterns of TA binding were also observed at 2 h between trained and sedentary animals in the fast-twitch red muscle types, whereas no training related differences were observed in white muscle types. Total and free serum cortisol concentrations also returned to base-line values faster in the trained animals following the single injection protocol. The accelerated repletion kinetics in the red muscle types of the trained animals suggest that the residence time of the glucocorticoid-receptor complex within the nuclei is reduced and/or there is an increased reprocessing of the cytoplasmic form of the receptor. Thus glucocorticoid actions may be attenuated, at least in part, by alterations in receptor dynamics.