Enrique Roche

Physical activity results in oxidative stress, as evidenced by the increased production of reactive oxygen, nitrogen species, and inflammatory mediators. The management of these components is instrumental for antioxidant adaptation to exercise and post-exercise recovery. Therefore, the present report aims to study the antioxidant response to two types of exercise (a 2000 m run and a burpee test) in healthy volunteers after a long period of inactivity (1–2 months). Antioxidant enzyme activities and oxidative stress markers (protein carbonyls and malondialdehyde content) were measured in neutrophils, peripheral blood mononuclear cells, and plasma. These parameters were determined under basal conditions and immediately post-exercise. Compared to those in basal state, neutrophil superoxide dismutase (28.3 vs. 22.9 pkat/109 cells), glutathione peroxidase (147.5 vs. 120.1 nkat/109 cells), and catalase (106.3 vs. 57.9 k/109 cells) were activated significantly (p < 0.05) after the burpee test. Peripheral blood mononuclear cells exhibited only significant (p < 0.05) catalase activation (113.6 vs. 89.4 k/109 cells) after the burpee test. Other enzymes, such as glutathione reductase and myeloperoxidase, tended to increase post-exercise, although the differences from baseline were not significant. Finally, compared to basal conditions, the protein carbonyl (24.5 vs. 14.5 mmol/L) and malondialdehyde (39.6 vs. 18.3 mmol/L) contents increased significantly (p < 0.05) in neutrophils and in plasma (115.1 vs. 97.8 and 130.2 vs. 123.4 μmol/L, respectively) after the burpee test. In conclusion, high-intensity exercise seems to induce immediate oxidative stress in inactive individuals, and the acute antioxidant response was slightly greater after the burpee test than after the 2000 m run. Glutathione-dependent antioxidant systems are activated immediately as protective mechanisms.

Exercise-induced muscle damage results in decreased physical performance that is accompanied by an inflammatory response in muscle tissue. The inflammation process occurs with the infiltration of phagocytes (neutrophils and macrophages) that play a key role in the repair and regeneration of muscle tissue. In this context, high intensity or long-lasting exercise results in the breakdown of cell structures. The removal of cellular debris is performed by infiltrated phagocytes, but with the release of free radicals as collateral products. L-carnitine is a key metabolite in cellular energy metabolism, but at the same time, it exerts antioxidant actions in the neuromuscular system. L-carnitine eliminates reactive oxygen and nitrogen species that, in excess, alter DNA, lipids and proteins, disturbing cell function. Supplementation using L-carnitine results in an increase in serum L-carnitine levels that correlates positively with the decrease in cell alterations induced by oxidative stress situations, such as hypoxia. The present narrative scoping review focuses on the critical evaluation of the efficacy of L-carnitine supplementation on exercise-induced muscle damage, particularly in postexercise inflammatory and oxidative damage. Although both concepts appear associated, only in two studies were evaluated together. In addition, other studies explored the effect of L-carnitine in perception of fatigue and delayed onset of muscle soreness. In view of the studies analyzed and considering the role of L-carnitine in muscle bioenergetics and its antioxidant potential, this supplement could help in postexercise recovery. However, further studies are needed to conclusively clarify the mechanisms underlying these protective effects.