Skeletal muscle aging: influence of oxidative stress and physical exercise

Abstract

Skeletal muscle abnormalities are responsible for significant disability in the elderly. Sarcopenia is the main alteration occurring during senescence and a key public health issue as it predicts frailty, poor quality of life, and mortality. Several factors such as reduced physical activity, hormonal changes, insulin resistance, genetic susceptibility, appetite loss, and nutritional deficiencies are involved in the physiopathology of muscle changes. Sarcopenia is characterized by structural, biochemical, molecular and functional muscle changes. An imbalance between anabolic and catabolic intracellular signaling pathways and an increase in oxidative stress both play important roles in muscle abnormalities. Currently, despite the discovery of new targets and development of new drugs, nonpharmacological therapies such as physical exercise and nutritional support are considered the basis for prevention and treatment of age-associated muscle abnormalities. There has been an increase in information on signaling pathways beneficially modulated by exercise; nonetheless, studies are needed to establish the best type, intensity, and frequency of exercise to prevent or treat age-induced skeletal muscle alterations.

Keywords: elderly; physical capacity; sarcopenia; training; treatment.

Figure 1. The effects of aging on the signalling pathways associated with protein synthesis and protein degradation

Red: catabolic pathways. Blue: anabolic pathways. Dash lines: inhibition. Dotted lines: no stimulation. The main alteration associated with aging is muscle atrophy. Muscle loss results from a disproportionate decrease in muscle protein synthesis and/or an increase in protein breakdown. Protein synthesis and degradation are regulated by several different stimuli, which activate multiple signaling pathways. See the main text for further details.