Turnover of skeletal muscle contractile proteins in glucocorticoid myopathy.
Muscle weakness in glucocorticoid myopathy results mainly from muscle atrophy, the reason for which is the accelerated catabolism of muscle proteins. As the content of lysosomes in skeletal muscle, particularly in fast-twitch glycolytic fibers, is relatively low the non-lysosomal pathway makes a particularly significant contribution and has special importance in the initial rate-limiting steps in the catabolism of contractile proteins and in the regulation of their turnover rate. The turnover rate of actin and the myosin heavy chain is decreased in all types of muscle fibers, and more rapid turnover of the myosin light chain is registered in the fast-twitch glycolytic and oxidative-glycolytic fibers. Exercise and simultaneous glucocorticoid treatment is an effective measure in retarding skeletal muscle atrophy and provides protection against muscle wasting.
Seene
T
T
Institute of Exercise Biology, University of Tartu, Estonia.
D000818:Animals; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D008247:Lysosomes / Q000378:metabolism; D009119:Muscle Contraction; D009124:Muscle Proteins / Q000378:metabolism*; D009133:Muscular Atrophy / Q000139:chemically induced / Q000378:metabolism*
D005938:Glucocorticoids; D009124:Muscle Proteins