Fig. 1

Potential underlying mechanisms of the protective effects of acute exercise preconditioning on disuse-induced muscular atrophy in aged muscle. HDAC4/Gadd45α axis plays an important role in disuse-induced muscle atrophy in aged skeletal muscle via preserving peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC-1α) expression and maintaining Akt phosphorylation during disuse. Other potential mechanisms of exercise-induced protection against the HDAC4/Gadd45α axis include the upregulation of microRNA (miR)-206 and the phosphorylation of AMP-activated protein kinase α (AMPKα) and calcium/calmodulin-dependent kinase II (CaMKII). Arrows represent the exercise effects based on the results from the previous study [14]