Reactive oxygen species generation and skeletal muscle wasting - Implications for sarcopenia

Abstract

Frailty in the elderly is largely caused by loss of muscle mass and strength, increased susceptibility to injury, and impaired recovery following -damage, particularly contraction-induced damage. The mechanisms responsible for the age-related loss of muscle mass and function are unclear although -modified generation of Reactive Oxygen and Nitrogen Species (RONS) have been -implicated in age-related tissue dysfunction. Many studies have provided evidence for the pivotal role of ROS in signal transduction and recognized these molecules as second messengers. Aberrant generation of RONS in the mitochondria and cytosol of cells and tissues of old mammals leads to an altered activation of crucial redox-responsive transcription factors at rest, following acute stress or during the regenerative process. Data suggest that targeted interventions to suppress altered mitochondrial ROS generation in muscle of old individuals are necessary to restore the signal for adaptive responses to contractions. Interventions based on antioxidant supplementation will suppress ROS signals in both mitochondrial and cytosolic compartments and hence be ineffective at prevention of age-related loss of muscle mass and function.