Objective: High intensity and prolonged exercise significantly enhances the levels of plasma ammonia, a metabolite with toxic effects on the central nervous system. The main purpose of the present study was to evaluate the metabolic response of athletes to glutamine (Gln) and alanine (Ala) supplementation, since these amino acids have a significant influence on both anaplerosis and gluconeogenesis. Methods: Professional soccer players were assigned to groups receiving either Gln or Ala supplementation (100 mg.Kg-1 body weight); this supplementation was either short- or long-term and was given immediately before exercise. The players were evaluated by two different exercise protocols, one with intervals (n=18) and the other with continuous intensity (n=12). Results: Both types of exercises increased ammonia, urate, urea and creatinine in blood. Chronic Gln supplementation partially protected against hyperammonemia after a soccer match (intermittent exercise; Gln - 140 ± 13% vs Ala - 240 ± 37%) and after continuous exercise at 80% of the maximum heart rate (Gln – 481 ± 44% vs placebo – 778 ± 99%). Urate increased by 10 to 20% in all groups, independently of supplementation. Glutamine one day supplementation induced a greater elevation in urate as compared to alanine at the end of the game; however, long-term supplementation provoked a lesser increment in urate. Exercise induced similar increases in creatinine as compared to their respective controls in either acute or chronic glutamine administration. Conclusions: Taken together, our results suggest that chronically supplemented Gln protects against exercise-induced hyperammonemia depending on exercise intensity and supplementation duration.
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