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Effects of Glutamine and Alanine Supplementation on Central Fatigue Markers in Rats Submitted to Resistance Training

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      Abstract

      Recent evidence suggests that increased brain serotonin synthesis impairs performance in high-intensity intermittent exercise and specific amino acids may modulate this condition, delaying fatigue. This study investigated the effects of glutamine and alanine supplementation on central fatigue markers in rats submitted to resistance training (RT). Wistar rats were distributed in: sedentary (SED), trained (CON), trained and supplemented with alanine (ALA), glutamine and alanine in their free form (G + A), or as dipeptide (DIP). Trained groups underwent a ladder-climbing exercise for eight weeks, with progressive loads. In the last 21 days, supplementations were offered in water with a 4% concentration. Albeit without statistically significance difference, RT decreased liver glycogen, and enhanced the concentrations of plasma glucose, free fatty acids (FFA), hypothalamic serotonin, and ammonia in muscle and the liver. Amino acids affected fatigue parameters depending on the supplementation form. G + A prevented the muscle ammonia increase by RT, whereas ALA and DIP augmented ammonia and glycogen concentrations in muscle. DIP also increased liver ammonia. ALA and G + A reduced plasma FFA, whereas DIP increased this parameter, free tryptophan/total tryptophan ratio, hypothalamic serotonin, and the serotonin/dopamine ratio. The supplementations did not affect physical performance. In conclusion, glutamine and alanine may improve or impair central fatigue markers depending on their supplementation form.

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      Glutamine and glutamate--their central role in cell metabolism and function.

      Glucose is widely accepted as the primary nutrient for maintenance and promotion of cell function. However, we propose that the 5-carbon amino acids, glutamine and glutamate, should be considered to be equally important for maintenance and promotion of cell function. The functions of glutamine are many and include: substrate for protein synthesis, anabolic precursor for muscle growth, acid-base balance in the kidney, substrate for ureogenesis in the liver, substrate for hepatic and renal gluconeogenesis, an oxidative fuel for intestine and cells of the immune system, inter-organ nitrogen transport, precursor for neurotransmitter synthesis, precursor for nucleotide and nucleic acid synthesis and precursor for glutathione production. Many of these functions are connected to the formation of glutamate from glutamine. We propose that the unique properties regarding concentration and routes of metabolism of these amino acids allow them to be used for a diverse array of processes related to the specialized function of each of the glutamine utilizing cells. In this review we highlight the specialized aspects of glutamine/glutamate metabolism of different glutamine-utilizing cells and in each case relate key aspects of metabolism to cell function. Copyright 2002 John Wiley & Sons, Ltd.
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        Branched-chain amino acids and brain function.

        Branched-chain amino acids (BCAAs) influence brain function by modifying large, neutral amino acid (LNAA) transport at the blood-brain barrier. Transport is shared by several LNAAs, notably the BCAAs and the aromatic amino acids (ArAAs), and is competitive. Consequently, when plasma BCAA concentrations rise, which can occur in response to food ingestion or BCAA administration, or with the onset of certain metabolic diseases (e.g., uncontrolled diabetes), brain BCAA concentrations rise, and ArAA concentrations decline. Such effects occur acutely and chronically. Such reductions in brain ArAA concentrations have functional consequences: biochemically, they reduce the synthesis and the release of neurotransmitters derived from ArAAs, notably serotonin (from tryptophan) and catecholamines (from tyrosine and phenylalanine). The functional effects of such neurochemical changes include altered hormonal function, blood pressure, and affective state. Although the BCAAs thus have biochemical and functional effects in the brain, few attempts have been made to characterize time-course or dose-response relations for such effects. And, no studies have attempted to identify levels of BCAA intake that might produce adverse effects on the brain. The only "model" of very high BCAA exposure is a very rare genetic disorder, maple syrup urine disease, a feature of which is substantial brain dysfunction but that probably cannot serve as a useful model for excessive BCAA intake by normal individuals. Given the known biochemical and functional effects of the BCAAs, it should be a straightforward exercise to design studies to assess dose-response relations for biochemical and functional effects and, in this context, to explore for adverse effect thresholds.
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          Physiological hypertrophy of the FHL muscle following 8 weeks of progressive resistance exercise in the rat.

          In humans, progressive resistance exercise is recognized for its ability to induce skeletal muscle hypertrophy. In an attempt to develop an animal model which mimics human progressive resistance exercise, Sprague-Dawley rats were trained to climb a 1.1-m vertical (80 degree incline) ladder with weights secured to their tail. The rats were trained once every 3 days for 8 weeks. Each training session consisted of 4-9 (6.02 +/- 0.23) climbs requiring 8-12 dynamic movements per climb. Based on performance, the weight carried during each session was progressively increased. Over the course of 8 weeks, the maximal amount of weight the rats could carry increased 287%, p
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            Author and article information

            Affiliations
            [1 ]Department of Food and Experimental Nutrition, Faculty of Pharmaceutical Sciences, University of São Paulo, Avenida Professor Lineu Prestes 580, São Paulo SP 05508-000, Brazil; abonvini@ 123456usp.br (A.B.); jessicarrp3@ 123456gmail.com (J.R.R.P.); amandabogarcia@ 123456gmail.com (A.B.d.O.G.); rafael.souza.b.lara@ 123456hotmail.com (R.d.S.B.L.); tirapegu@ 123456usp.br (J.T.)
            [2 ]Department of Nutrition, Faculty of Public Health, University of São Paulo, Avenida Doutor Arnaldo 715, São Paulo SP 01246-904, Brazil; thaishypolito@ 123456gmail.com (T.H.); mmrogero@ 123456usp.br (M.M.R.)
            [3 ]Faculty of Nutrition, Federal University of Mato Grosso, Avenida Fernando Correa 2367, Cuiabá MT 78060-900, Brazil; allangodois@ 123456hotmail.com
            Author notes
            [* ]Correspondence: audreycoqueiro@ 123456hotmail.com (A.Y.C.); raqzel@ 123456usp.br (R.R.); Tel.: +55-11-3091-3309 (A.Y.C.)
            Journal
            Nutrients
            Nutrients
            nutrients
            Nutrients
            MDPI
            2072-6643
            25 January 2018
            February 2018
            : 10
            : 2
            29370091
            5852695
            10.3390/nu10020119
            nutrients-10-00119
            © 2018 by the authors.

            Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

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