A clinically relevant decrease in contractile force differentially regulates control of glucocorticoid receptor translocation in mouse skeletal muscle

Abstract

Glucocorticoids induce significant skeletal muscle atrophy by activating the glucocorticoid receptor. Our work shows that muscle contractile force dictates glucocorticoid receptor nuclear translocation. We also show that blunting nuclear translocation by high force contractions coincides with the ability of muscle to mount an anabolic response characterized by increased muscle protein synthesis. This work further defines the therapeutic parameters of skeletal muscle contractions to blunt glucocorticoid-induced atrophy.