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O’Toole ML, Johnson KC: Calcium losses resulting from an acute bout of moderate intensity exercise. Int J Sport Nutr 1999, 9:275–284.PubMed 37. Montain SJ, Cheuvront SN, Lukaski HC: Sweat mineral-element responses during 7 h of exercise-heat stress. Int J Sport Nutr Exerc Metab 2007, 17:574–582.PubMed 38. Chinevere TD, Kenefick RW, Cheuvront SN, Lukaski HC, Sawka MN: Effect of heat acclimation on sweat minerals. Med Sci Sports Exerc 2008, 40:886–891.PubMedCrossRef 39. Barry DW, Hansen KC, see more Van Pelt RE, Witten M, Wolfe P, Kohrt WM: Acute calcium ingestion attenuates exercise-induced disruption of calcium homeostasis. Med Sci Sports Exerc 2011, 43:617–623.PubMed Competing interest LJL, JPK, JCR, SJC, KWW, AJY, and JPM,
no conflicts of interest. Authors’ contributions JPM and JPK designed research; JPK, SJC, KWW, and JPM conducted research; JCR processed biological samples; LJL and JPK conducted statistical analysis; LJL, AJY and JPM wrote the paper; JPM had primary responsibility for final content. All authors PND-1186 nmr read and approved the final manuscript.”
“Background Physical exercise causes diverse physiological challenges, including mechanical strain of the skeletal muscle [1] and molecular responses [2, 3], as well as metabolic changes. Among the metabolic changes induced by exercise, blood lactate concentration has been extensively investigated [4, 5]. It is well-known that protein breakdown is accelerated with intensive exercise [6]. Under high-intensity exercise, amino acids produced from muscle protein breakdown are partly used to produce energy [7]. It has been shown that the blood level of ammonia increased significantly in rats during resistance exercise and in humans during intense dynamic exercise [8, 9]. Several studies
have reported that an exercise bout causes a dramatic increase in ammonia concentration along with an increase in inosine-5´-monophosphate (IMP) and the ratio of IMP/AMP (adenosine monophosphate), demonstrating a deamination process from AMP to IMP under high energy MK-8931 cost turnover [10], which can remain above the baseline level after one hour of recovery [9]. Previous studies have CYTH4 attributed exercise-induced hyperammonemia to fatigue [11, 12]. Therefore, an ammonia accumulation caused by exercise is considered a negative factor for exercise tolerance. The effects of nutritional intervention, especially amino acid supplements, on physical performance have been reported [13]. It is evident that supplementation with specific amino acids, such as glutamate, reduces ammonia concentrations during exercise [14]. However, it is also evident that supplementation with branched-chain amino acids (BCAA) leads to a distinct elevation in arterial ammonia level during 60 min of exercise [15].
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