NEW INTERVENTIONS FOR SARCOPENIA

Abstract

Abstract: Sarcopenia of aging encompasses the loss of muscle mass and function and is associated with physical function decline and increased risk for frailty. Sarcopenia is a complex process with many proposed underlying pathogenic mechanisms which involves many tissues such as muscle and neuronal tissues as well as circulatory and systemic factors. Dysfunctional mitochondria and insufficient autophagy are common in muscle and neuronal tissues. The mitochondrial theory of aging is based on the premise that cumulative damage caused by the production of oxidants can alter mtDNA (e.g., point mutations and deletions) and leads to mitochondrial decay which can partly explain the loss of muscle fibers observed with age. It is well established that defects in mtDNA lead to a decline in mtDNA abundance (content) and a reduced number of genes encoding mitochondrial proteins that are essential for the proper assembly and maintenance of mitochondria. Additionally, lower mitochondrial protein synthesis rates, disturbances in mitochondrial enzyme activities, altered import protein machinery, and lower oxidative capacity and ATP synthesis have been documented to occur in aged tissues. Besides being less bioenergetically efficient, damaged mitochondria (aged) also produce increased amounts of reactive oxygen species, specifically under stressed conditions (ischemia, reperfusion, environmental toxins). The age-related accumulation of dysfunctional mitochondrial likely results from the combination of impaired clearance of damaged organelles by autophagy and inadequate replenishment of the cellular mitochondrial pool by mitochondriogenesis (partly caused by physical inactivity).