Sarcopenic obesity: satellite cells in the aging muscle

Current knowledge on satellite cells in relation to suggested mechanisms of loss of muscle mass and strength, induction of fat infiltration, and countermeasures is highlighted.

Consensus on the definition of sarcopenia and sarcopenic obesity is proposed. Human satellite cell heterogeneity has now unequivocally been verified in situ as well as an adipogenic potential, though in mice other muscle stem cells are the hot topic to induce adipogenesis upon muscle damage. Inflammation, oxidative stress, proteolytic degradation, and nuclear apoptosis are discussed as pathogenetic mechanisms of sarcopenia, although little evidence exists that they are important in human muscle. In rodents, exercise-induced muscle injury is a hallmark for sequential events leading to muscle fiber necrosis and sarcopenia. Exercise in humans, on the contrary, is the key event to countermeasure sarcopenia. Cautions to extrapolate observation in rodents to explain human conditions have been presented.

Human satellite cells are indispensable for maintenance of human muscle mass, but their implications in the pathogenesis of sarcopenia and sarcopenic obesity are still under debate. Nevertheless, satellite cell activation upon exercise seems unequivocally together with adequate nutrition to be the most effective countermeasure for sarcopenia and sarcopenic obesity.