[Skeletal muscle aging and mitochondrial dysfunction: an update]

Abstract

One of the most obvious and deleterious changes occurring with aging is a progressive loss of skeletal muscle mass and strength, a physiological process named sarcopenia. Amongst the multiple theories that have been put forward to explain sarcopenia, the mitochondrial theory of aging, which postulates that the accumulation of mitochondrial dysfunctions with aging plays a causal role in muscle atrophy, has focused intense research effort and attention in the past decades. The generally accepted view of this theory is that, due to the reactive oxygen species (ROS) production inherent to respiratory chain activity, oxidative damage to mitochondrial proteins, lipids and DNA accumulates with aging. This damage is thought to (i) exacerbate mitochondrial ROS production, (ii) impair the capacity of mitochondria to adequately match the cellular ATP demand and (iii) trigger mitochondrial-mediated apoptosis. Although very appealing, this theory remains controversial. The aims of the present review are (i) to provide the reader with a short, but comprehensive review of the current literature linking mitochondrial dysfunction and sarcopenia and (ii) to briefly discuss the potential mechanisms underlying the accumulation of mitochondrial dysfunction with muscle aging.