Disuse atrophy, plasma corticosterone, and muscle glucocorticoid receptor levels

A suspension model, characterized by differential atrophy of disused hindlimb skeletal muscles, was utilized to investigate plasma levels of and tissue sensitivity to glucocorticoids. The three objectives were determination of time course and extent of plasma corticosterone changes during 1 week of whole-body suspension; comparison of glucocorticoid receptor site concentrations in muscles differing in morphology and antigravity function; and investigation of the effect of disuse on tissue glucocorticoid receptor site concentrations. Plasma corticosterone increased significantly (p less than 0.01) on the first and third days of suspension, but returned to control levels by day 7. Muscle glucocorticoid receptors exhibited a characteristic hormonal specificity. In controls, receptor site concentration in the slow-twitch soleus (48 +/- 5 fmol/mg prot.) was comparable to that in the fast-twitch gastrocnemius (47 +/- 6) and plantaris (58 +/- 4) muscles but significantly (p less than 0.02) less than the extensor digitorum longus (66 +/- 5). Seven days of suspension resulted in significant differential effects on muscle receptor levels, with a large increase in the soleus (140%), lesser increments in the gastrocnemius (55%) and plantaris (45%), and only a small, statistically insignificant alteration in the EDL (10%). Receptor levels in the soleus remained elevated following 14 d of suspension, but levels in other muscles returned to control values. These results suggest that circulating glucocorticoids, as well as increased tissue hormonal sensitivity, may be related to muscle responses in this model of disuse.