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This work evaluated the anticatabolic capacity of androgenic-anabolic steroids and exercise (contractile activity) in inhibiting skeletal muscle atrophy associated with excessive levels of circulating glucocorticoids. With androgenic-anabolic steroids, most binding studies indicate that they have very low binding specificity for the glucocorticoid receptor. Androgens may interact through their own receptor to interfere with glucocorticoid functioning at the gene level, but this remains unproven. Current literature suggests that androgens do not prevent atrophy but may retard growth suppression accompanying glucocorticoid treatment. With exercise, functional overload, resistance, and endurance types of training are capable of preventing muscle atrophy from glucocorticoids. Androgen and glucocorticoid-receptor binding and glucocorticoid-receptor activation studies have, thus far, not established that atrophy prevention is mediated through the receptor. In conclusion, the role of androgenic-anabolic steroids as glucocorticoid antagonists requires further study. Study of the effects of exercise on muscle gene expression of glucocorticoid-inducible proteins is needed to gain additional understanding of this mechanism of atrophy prevention.