Antioxidants in Sport Sarcopenia

Abstract

The decline of skeletal muscle mass and strength that leads to sarcopenia is a pathology that might represent an emergency healthcare issue in future years. Decreased muscle mass is also a condition that mainly affects master athletes involved in endurance physical activities. Skeletal muscles respond to exercise by reshaping the biochemical, morphological, and physiological state of myofibrils. Adaptive responses involve the activation of intracellular signaling pathways and genetic reprogramming, causing alterations in contractile properties, metabolic status, and muscle mass. One of the mechanisms leading to sarcopenia is an increase in reactive oxygen and nitrogen species levels and a reduction in enzymatic antioxidant protection. The present review shows the recent experimental models of sarcopenia that explore molecular mechanisms. Furthermore, the clinical aspect of sport sarcopenia will be highlighted, and new strategies based on nutritional supplements, which may contribute to reducing indices of oxidative stress by reinforcing natural endogenous protection, will be suggested.

Keywords: antioxidant; muscle cells; nutritional supplements; sport sarcopenia.

Figure 1

Sarcopenia induced by glucocorticoid-treated skeletal muscle cells in vitro. (a) Protein kinase B (Akt) causes phosphorylation and nuclear exclusion of Forkhead box protein O (FoxO) family, which suppresses atrogene (muscle atrophy F-box, MAFbx) expression and proteolysis. Dexamethasone prevents Akt-mediated phosphorylation of FoxO (FoxO-P), inducing its transfer to the nucleus and the consequent MAFbx upregulation and protein degradation. (b) The skeletal muscle structure. (c) Representative images of human myotube after dexamethasone (Dexa) treatment (50 µM for 48 h), showing fluorescence double labeling, using an anti-myosin heavy chain-2 antibody (green), and Hoechst (nuclei in blue). Scale bar = 100 µm.

Figure 2

A schema of the intracellular pathway activated by physical exercise in skeletal muscle cells, showing protein synthesis (blue) and protein degradation pathway (pink). The solid line represents direct reaction; the broken line represents the intermediate pathway and products of reaction. Phosphoinositide 3-kinase (PI3), protein kinase B (Akt), mammalian target of the rapamycin (mTOR), mTOR complex 1 (mTORC1), Forkhead box protein O (FoxO) and phosphorylated forkhead box protein O (FoxO-P).

Figure 3

Antioxidant enzyme activity to counteract reactive oxygen species (ROS) production and accumulation in skeletal muscle cells after exercise. Exhaustive exercise induces an increased production of reactive oxygen species: superoxide anion (O^2-), hydrogen peroxide (H₂O₂) and hydroxyl radical (OH.) according to the Fenton reaction. Catalase (CAT), glutathione transferase (GSH), glutathione peroxidase (Px), and superoxide dismutase (SOD), work to maintain a state of oxidative balance, producing water and oxygen. Glutathione disulfide (GSSG), Glutathione reductase (GR), nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) and nicotinamide adenine dinucleotide phosphate (NADP).