Abstract
Significant progress has expanded our knowledge of the signaling pathways coordinatingmuscle protein turnover during various conditions including exercise. In this manuscript, the multiplemechanisms that govern the turnover of cellular components are reviewed, and their overall rolesin adaptations to exercise training are discussed. Recent studies have highlighted the central role ofthe energy sensor (AMP)-activated protein kinase (AMPK), forkhead box class O subfamily protein(FOXO) transcription factors and the kinase mechanistic (or mammalian) target of rapamycin complex(MTOR) in the regulation of autophagy for organelle maintenance during exercise. A new cellulartrafficking involving the lysosome was also revealed for full activation of MTOR and protein synthesisduring recovery. Other emerging candidates have been found to be relevant in organelle turnover,especially Parkin and the mitochondrial E3 ubiquitin protein ligase (Mul1) pathways for mitochondrialturnover, and the glycerolipids diacylglycerol (DAG) for protein translation and FOXO regulation.Recent experiments with autophagy and mitophagy flux assessment have also provided importantinsights concerning mitochondrial turnover during ageing and chronic exercise. However, data inhumans are often controversial and further investigations are needed to clarify the involvement ofautophagy in exercise performed with additional stresses, such as hypoxia, and to understand theinfluence of exercise modality. Improving our knowledge of these pathways should help developtherapeutic ways to counteract muscle disorders in pathological conditions.