A worm's life: AMPK links muscle mitochondrial dynamics to physical fitness and healthy aging in Caenorhabditis elegans.

Abstract

Mitochondrial dynamics is driven by a balance between fusion and fission[1,2]. Fusion connects individual mitochondria to form a network of highly energy-efficient organelle systems. Fission drives fragmentation of the mitochondrial network resulting in less energy-efficient organelles. Nevertheless, fission is critical for the removal of damaged mitochondria and the mitigation of oxidative stress. Well-defined factors that control fusion (mitofusin-1/2, optical atrophy protein-1/2) and fission (dynamin-related protein 1, mitochondrial fusion factor, fission protein 1) regulate mitochondrial connectivity dynamics. Mitochondrial dynamics is critical for energy homeostasis, particularly in the skeletal muscle[1], one of the most plastic organs in adulthood amenable to remodeling by exercise, as well as a sedentary lifestyle and aging[3]. Exercise has long been known to be necessary for healthy aging and energy efficiency, as well as for delaying cardiovascular and metabolic diseases[4]. Exercise benefits are partly mediated by boosting energy metabolism[1]. However, molecular mechanisms of age-related decline in physical fitness, and its counterdelay by exercise, are poorly defined. Skeletal muscle is an excellent organ system for obtaining molecular insights into the interaction between exercise and aging, particularly as it is related to mitochondrial dynamics, muscle quality, and fitness. So far, studies in