FIGURE 18.

Circadian regulation of skeletal muscle function and plasticity. A: circadian regulation of activity and muscle function. Circadian regulation of sleep-wake cycles, feeding, physical activity, or other zeitgebers is sensed and translated by the master clock in the suprachiasmatic nucleus as well as peripheral clocks in almost every cell in the human body. As a consequence, various physiological processes, e.g., muscle cell metabolism or contractile performance, can be affected in a circadian manner. B: interactions between core clock genes/proteins with regulators of muscle function and plasticity. Such cross talk pertains to the regulation of gene expression, protein-protein interactions, and/or enzymatic activity. Thereby, physiological processes in muscle might be affected by the core clock. Inversely, muscle fiber metabolism, contractile activity, oxygen availability, redox balance, and other perturbations could modulate the skeletal muscle clock. AMPK, AMP-dependent protein kinase; BMAL1, brain and muscle ARNT-like 1; CLOCK, circadian locomotor output cycles kaput; CREB, cAMP response element binding protein; CRY, cryptochrome circadian regulator; HIF-1α, hypoxia-inducible factor 1α; mTOR, mammalian target of rapamycin; NFE2L2, nuclear factor erythroid-derived 2-like 2; NF-κB, nuclear factor κB; PER, period; PGC-1α, peroxisome proliferator-activated receptor γ coactivator 1α; PPARα/β/δ, peroxisome proliferator-activated receptor α/β/δ; REV-ERB, nuclear receptor subfamily 1 group D member 1/2; ROR, retinoic acid-related orphan receptor; RORE, ROR elements; SIRT1, sirtuin 1. Image created with BioRender.com, with permission.