Hormonal
Glucocorticoid administration induces skeletal muscle atrophy primarily by stimulating the ubiquitin-proteasome system (UPS) via FOXO transcription factors and downregulating IGF-I signaling, while simultaneously inhibiting protein synthesis through mTOR repression.
If you are prescribed glucocorticoids, muscle loss is driven by active molecular switches (FOXO, mTOR) rather than just inactivity. While you cannot stop the medication, being aware that this is a specific biological response helps in seeking targeted counter-measures (like specific nutritional or pharmacological interventions discussed in the paper) rather than assuming the loss is inevitable or purely due to lack of exercise.
Muscle proteolysis, in particular through the ubiquitin– proteasome system (UPS), is considered to play a major role in the catabolic action of glucocorticoids... Glucocorticoids also exert an anti-anabolic action by blunting muscle protein synthesis.
Why this rating
The paper is a comprehensive review citing numerous in vitro and in vivo studies establishing these pathways.
Source
Mechanisms of glucocorticoid-induced myopathy
O Schakman et al. · Journal of Endocrinology · 2008
DOI 10.1677/joe-07-0606
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