Data are presented which demonstrate that phasic/glycolytic muscles atrophy more than tonic/oxidative muscles in response to exogenously introduced glucocorticoids. Data are also presented demonstrating that immobilization makes a muscle unusually sensitive to glucocorticoid-induced atrophy and that remobilization of a previously immobilized muscle protects a muscle from glucocorticoid-induced atrophy. These observations are discussed within the context of the role of mechanical activity in the acquisition and maintenance of fiber-type characteristics. In addition, the available data on the glucocorticoid receptor population in skeletal muscles of various types and circumstance are reviewed within the context of the recent observations concerning the glucocorticoid induction of the enzyme glutamine synthetase in skeletal muscle. It is proposed here that atrophy is not necessarily the response of skeletal muscle to glucocorticoids. Rather, atrophy is a possible consequence of the glucocorticoid-induced increase in export of amino acid carbon from the muscle. Whether such export causes a muscle to atrophy or perhaps even hypertrophy will depend on the capacity of the muscle to sustain its free amino acid pools. Mechanical activity greatly promotes the uptake of free amino acids in skeletal muscle. Such promotion takes the form of both contraction-induced uptake and increased insulin sensitivity. Within this perspective, it is suggested that tonic muscles and remobilized muscles are protected from atrophy by exogenous glucocorticoids because their high level of mechanical activity allows them to maintain their free amino acid pools.