Abstract

The investigation was undertaken to evaluate whether endurance running of the type known to retard the muscle atrophy associated with glucocorticoid excess inhibits activation of glucocorticoid-receptor complexes to a DNA binding state. Female adrenalectomized rats received an injection of (3H)triamcinolone acetonide and remained sedentary or were immediately exercised by endurance running at 23 m/min for up to 90 min. Receptor activation, as quantified by binding to DNA-cellulose, steadily increased from 10-20 of the receptors capable of binding DNBA in uninjected controls to 25-45 by 5 min and to 53-80 by 90 min after receiving the hormone in all muscles studied (fast-twitch red and white vastus lat., slow-twitch soleus, mixed gastrocnemius, and heart). Exercise did not influence the time-course changes in percent activation. When activation was determined from changes in the conformational state of the receptor as measured by diethylaminoethyl-cellulose anion exchange chromatography, there was a similar time-dependent formation of activated receptor forms in all muscles types. However, exercise did not inhibit or delay the appearance of the activated receptor from the unactivated state. These results indicate that glucocorticoid receptor activation occurs at a rate that is independent of both fiber type and delivery of steroid to working muscles during exercise. If exercise alters receptor activation, a longer time period, beyond 90 min of running, or even additional training may be needed for inhibition to be expressed. V.-R.