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

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.

Immunomodulatory role of branched-chain amino acids

“…33 Addition on an amino group to glutamate generates glutamine, a reaction catalyzed by glutamine synthetase. 33,34 The second step in BCAA catabolism is the irreversible oxidative decarboxylation of the respective BCKA, whereby the carbon skeletons of KIC, KMV and KIV are converted to isovaleryl-CoA, 3-methylbutyryl-CoA, and isobutyryl-CoA, respectively. 30 This reaction is 100 catalyzed by the branched-chain α-keto acid dehydrogenase (BCKD) complex, composed of several copies of branched-chain α-keto acid decarboxylase (E1), dihydrolipoamide acyltransferase (E2) and dihydrolipoamide dehydrogenase (E3) enzymes.…”

“…51 Both alanine and glutamine generated through the transamination process contribute to ammonia transportation in the body, carrying this metabolite from muscle to the liver and kidneys to be metabolized and excreted, respectively, avoiding its accumulation. 34,52,53 Considering that ammonia is toxic and its buildup is detrimental to the activity of several organ systems, such as the CNS, 54,55 the hyperammonemia state, common in liver diseases, contributes to the development of hepatic encephalopathy and the worsening of clinical conditions. 56,57 In addition, in chronic hepatopathies, there is a reduction in the plasma 161 concentration of BCAA and an increase in the plasma concentration of the aromatic amino 162 acids (AAA) tryptophan, phenylalanine, and tyrosine.…”

Effects of a commercially available branched-chain amino acid-alanine-carbohydrate-based sports supplement on perceived exertion and performance in high intensity endurance cycling tests

“…In addition to BCAA, other amino acids reputed to play a role in maintaining performance during endurance exercise are often included in sports supplements. Among these, Lalanine (Ala, another component of the product tested in the present study) is thought to support performance through several mechanisms [16], including the prevention of an exercise-induced decrease in many gluconeogenic amino acids and hence a metabolic profile that enhances performance [17]. Ala is consumed in quantities of 3 to 4 g/ day on average in a typical diet; however, no studies have assessed the long-term effects of its supplementation in humans alone or combined with BCAA [18].…”

Glutamine-to-glutamate ratio in the nucleus accumbens predicts effort-based motivated performance in humans

“…Although, to the best of our knowledge, no previous study assessed NAc metabolism in the context of fatigue, substantial influence relates fatigue with reduced Gln in blood [64] and potentially also with alterations in Gln metabolism in the brain [65]. Oral glutamine supplementation has been reported to reduce subjective fatigue and ratings of perceived exertion during demanding tasks [66,67] and to increase striatal Gln levels [68].…”