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Abstract Title:

The benefit of a supplement with the antioxidant melatonin on redox status and muscle damage in resistance trained athletes.

Abstract Source:

Appl Physiol Nutr Metab. 2017 Feb 13. Epub 2017 Feb 13. PMID: 28192673

Abstract Author(s):

Roberto C Leonardo-Mendonça, Javier Ocaña-Wilhelmi, Tomás de Haro, Carlos de Teresa-Galván, Eduardo Guerra-Hernández, Iryna Rusanova, Marisol Fernández-Ortiz, Ramy Ka Sayed, Germaine Escames, Darío Acuña-Castroviejo

Article Affiliation:

Roberto C Leonardo-Mendonça

Abstract:

Previous data showed that the administration of high doses of melatonin improved the circadian system in athletes. Here, we investigated in the same experimental paradigm whether the antioxidant properties of melatonin has also beneficial effects against exercise-induced oxidative stress and muscle damage in athletes. Twenty-four athletes were treated with 100 mg.day-1 of melatonin or placebo 30 min before bedtime during four weeks in a randomized double-blind scheme. Exercise intensity was higher during the study that before starting it. Blood samples were collected before and after treatment, and plasma was used for oxygen radical absorption capacity (ORAC), lipid peroxidation (LPO), nitrite plus nitrate (NOx), and advanced oxidation protein products (AOPP) determinations. Glutathione (GSH), glutathione disulphide (GSSG) levels, and glutathione peroxidase (GPx) and reductase (GRd) activities, were measured in erythrocytes. Melatonin intake increased ORAC, reduced LPO and NOx levels, and prevented the increase of AOPP, compared to placebo group. Melatonin was also more efficient than placebo in reducing GSSG.GSH-1 and GPx.GRd-1 ratios. Melatonin, but not placebo, reduced creatine kinase, lactate dehydrogenase, creatinine, and total cholesterol levels. Overall, the data reflect a beneficial effect of melatonin treatment in resistance-training athletes, preventing extra- and intracellular oxidative stress induced by exercise, and yielding further skeletal muscle protection against exercise-induced oxidative damage.

Study Type : Human Study

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