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Objective: Although glutamine and alanine have properties that could delay fatigue, recent evidence showed that these amino acids impaired central fatigue markers. Nevertheless, the effect of this intervention on muscle fatigue is unknown. The aim of this study was to investigate the effects of glutamine and alanine supplementation on muscle fatigue parameters in rats submitted to resistance training (RT)., Methods: Wistar rats were distributed into the following groups: sedentary (SED), exercised (CON), exercised and supplemented with alanine (ALA), glutamine and alanine in their free form (G+A) or l-alanyl-l-glutamine (DIP). Trained groups underwent a ladder-climbing exercise for 8 wk. In the last 3 wk of RT, supplementations were offered in water with a 4% concentration., Results: G+A and DIP supplementation increased the muscle content of glutamine and glutamate. DIP administration increased glycogen and lactate dehydrogenase (LDH) concentrations in muscle, whereas ALA and G+A supplementation reduced plasma LDH and creatine kinase levels. All trained groups presented higher levels of muscle glutathione (GSH) than SED. There was no difference between groups in lactate, xanthine, hypoxanthine, thiobarbituric acid reactive substances, 8-isoprostane and GSH in plasma; adenosine monophosphate deaminase, citrate synthase and monocarboxylate transporters 1 and 4 in muscle; and glycogen and GSH in the liver. Moreover, physical performance did not differ between groups., Conclusion: Glutamine and alanine supplementation improved muscle fatigue markers without affecting exercise performance., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Glutamine and alanine are lipogenic and could prevent the effects of resistance training (RT) in reducing adiposity and modulating lipid profile. Thus, we aimed to investigate the effects of RT and glutamine and alanine supplementation, in their free or conjugated form, on relative epididymal adipose tissue (EAT) and brown adipose tissue (BAT) weight, plasma lipid profile, and adipokines in EAT. Thirty Wistar rats, aged two months, were distributed into five groups: control (CTRL), trained (TRN), trained and supplemented with alanine (ALA), glutamine and alanine in their free form (GLN+ALA), or L-alanyl-L-glutamine (DIP). Trained groups underwent a ladder-climbing exercise for eight weeks, with progressive load increase. Supplementations were offered in a solution with a concentration of 4% in the last 21 days of training. Food consumption and body weight gain were decreased in the TRN group compared with CTRL. RT also reduced relative EAT and BAT weight, while supplementations, especially with ALA, increased adipose tissue mass. RT reduced total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-c) (TRN vs. CTRL), whereas glutamine and alanine supplementation increased TC and LDL-c, impairing lipid profile modulation by physical exercise. RT did not affect the concentrations of adipokines in EAT, but DIP supplementation increased interleukin- (IL-) 6 and IL-10. In conclusion, RT reduced adiposity and modulated lipid profile, whereas glutamine and alanine supplementation increased adiposity and impaired lipid profile but increased the concentration of the anti-inflammatory cytokines IL-6 and IL-10 in EAT.

Background: Loss of white adipose tissue (WAT), associated with type 1 diabetes (DM1), contributes to increased chronic systemic inflammation., Aim: The aim of this study was to investigate the effects of leucine supplementation and resistance training (RT) in attenuating WAT loss and improving inflammatory parameters and glucose metabolism in DM1 rats., Methods: Thirty-two male Wistar rats were distributed into four groups: DA (sedentary and supplemented with non-essential amino acids (NEAA)), DL (sedentary and supplemented with leucine), DTA (submitted to RT and supplemented with NEAA) and DTL (submitted to RT and supplemented with leucine). DM1 was induced by streptozotocin (STZ). An 8-week period of RT consisted of climbing a ladder with a progressively increased load, and supplementation was offered in the feed., Results: Glycemia, polyphagia and polydipsia were lower in DL, DTA and DTL groups compared with the DA group by approximately 20% ( p<.0001), 28% ( p=.004) and 64% ( p<.0001), respectively. Weight of total WAT and retroperitoneal adipose tissue (RPAT) were higher by approximately 21% ( p=.01) and 54% ( p=.0004), respectively, in DL, DTA and DTL groups compared with DA. However, gene expression of adiponectin and leptin in RPAT was only increased by RT (DTA and DTL) compared with DA and DL by approximately 93% ( p<.0001) and 78% ( p=.0002), respectively. Similarly, the levels of adiponectin in the serum, tissue IL-10 (RPAT) and serum IL-10 were only increased in DTA and DTL compared with DA and DL by approximately 31% ( p=.03), 45% ( p=.0009) and 35% ( p=.003), respectively., Conclusions: Both interventions, isolated or together, reduced hyperglycemia and excessive loss of WAT, but RT was the main factor responsible for attenuating inflammation.

We evaluated the effects of chronic oral supplementation with l-glutamine and l-alanine in their free form or as the dipeptide l-alanyl-l-glutamine (DIP) on muscle damage, inflammation and cytoprotection, in rats submitted to progressive resistance exercise (RE). Wistar rats (n 8/group) were submitted to 8-week RE, which consisted of climbing a ladder with progressive loads. In the final 21 d before euthanasia, supplements were delivered in a 4 % solution in drinking water. Glutamine, creatine kinase (CK), lactate dehydrogenase (LDH), TNF-α, specific IL (IL-1β, IL-6 and IL-10) and monocyte chemoattractant protein-1 (MCP-1) levels were evaluated in plasma. The concentrations of glutamine, TNF-α, IL-6 and IL-10, as well as NF-κB activation, were determined in extensor digitorum longus (EDL) skeletal muscle. HSP70 level was assayed in EDL and peripheral blood mononuclear cells (PBMC). RE reduced glutamine concentration in plasma and EDL (P<0·05 v. sedentary group). However, l-glutamine supplements (l-alanine plus l-glutamine (GLN+ALA) and DIP groups) restored glutamine levels in plasma (by 40 and 58 %, respectively) and muscle (by 93 and 105 %, respectively). GLN+ALA and DIP groups also exhibited increased level of HSP70 in EDL and PBMC, consistent with the reduction of NF-κB p65 activation and cytokines in EDL. Muscle protection was also indicated by attenuation in plasma levels of CK, LDH, TNF-α and IL-1β, as well as an increase in IL-6, IL-10 and MCP-1. Our study demonstrates that chronic oral l-glutamine treatment (given with l-alanine or as dipeptide) following progressive RE induces cyprotective effects mediated by HSP70-associated responses to muscle damage and inflammation.

Introduction: Brazil is the second country in the world with the largest number of gyms, currently accounting for approximately 30 thousand units. There is increasing evidence that a significant part of gym-goers develop excessive commitment to practicing physical exercises, which may even generate pathological dependence. Aim: To determine the association between physical exercise addiction (ED) and supplement intake among gym-goers. Method: The exercise addiction scale was employed for gym-goers older than 19 years of both sexes. Individual interview was made by using nutritional history to determine supplement intake profile; data related to anthropometry and participation in the gym were also assessed. Results: The frequency of ED at gyms was 66.5% and the prevalence of supplementation was 51.5%, while the chances for an exercise addict to be a supplement consumer were estimated at 4.53. Conclusion: The relationship between ED and supplement intake was proven, constituting an alert for health professionals, who should consider the risk factors for the development of more severe signs and symptoms, including obsessive weight control by means of excessive practice of exercises, diets with no nutritional basis and unnecessary supplementation. It is recommended to include nutritional assessment among the instruments to detect ED and supplementation so that, if necessary, campaigns can be promoted to elucidate diets, healthy body composition patterns and drastic changes in eating patterns, as well as other issues related to nutritional care.

Liver L-glutamine is an important vehicle for the transport of ammonia and intermediary metabolism of amino acids between tissues, particularly under catabolic situations, such as high-intensity exercise. Hence, the aim of this study was to investigate the effects of oral supplementations with L-glutamine in its free or dipeptide forms (with L-alanine) on liver glutamine-glutathione (GSH) axis, and 70 kDa heat shock proteins (HSP70)/heat shock transcription factor 1 (HSF1) expressions. Adult male Wistar rats were 8-week trained (60 min/day, 5 days/week) on a treadmill. During the last 21 days, the animals were daily supplemented with 1 g of L-glutamine/kg body weight per day in either l-alanyl-L-glutamine dipeptide (DIP) form or a solution containing L-glutamine and l-alanine in their free forms (GLN+ALA) or water (controls). Exercise training increased cytosolic and nuclear HSF1 and HSP70 expression, as compared with sedentary animals. However, both DIP and GLN+ALA supplements enhanced HSF1 expression (in both cytosolic and nuclear fractions) in relation to exercised controls. Interestingly, HSF1 rises were not followed by enhanced HSP70 expression. DIP and GLN+ALA supplements increased plasma glutamine concentrations (by 62% and 59%, respectively) and glutamine to glutamate plasma ratio in relation to trained controls. This was in parallel with a decrease in plasma ammonium levels. Supplementations increased liver GSH (by 90%), attenuating the glutathione disulfide (GSSG) to GSH ratio, suggesting a redox state protection. In conclusion, oral administration with DIP and GLN+ALA supplements in endurance-trained rats improve liver glutamine-GSH axis and modulate HSF1 pathway.

Several studies have highlighted the potential of leucine supplementation for the treatment of metabolic diseases including type 2 diabetes and obesity. Caloric restriction is a common approach to improve the health in diabetic and obese subjects. However, very few studies assessed the effects of leucine supplementation in calorie-restricted animals. Rats were subjected to a 30% calorie-restricted diet for 6 weeks to study the effects of leucine supplementation on protein status markers and lipid metabolism. Caloric restriction reduced the body weight. However, increased leucine intake preserved body lean mass and protein mass and improved protein anabolism as indicated by the increased circulating levels of albumin and insulin-like growth factor-1 (IGF-1), and the liver expression of albumin and IGF-1 messenger RNA. Leucine supplementation also increased the circulating levels of interleukin-6 and leptin but did not affect the tumour necrosis factor-α and monocyte chemotactic protein-1 concentrations. Ketone bodies were increased in rats consuming a leucine-rich diet, but we observed no changes in cholesterol or triglycerides concentrations. Caloric restriction reduced the liver expression of peroxisome proliferator activated receptor-α and glucose-6-phosphatase, whereas leucine supplementation increased the liver expression of 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA) reductase and sterol regulatory element-binding transcription factor 1. A leucine-rich diet during caloric restriction preserved whole body protein mass and improved markers of protein anabolism. In addition, leucine modulated the hepatic lipid metabolism. These results indicate that increased leucine intake may be useful in preventing excessive protein waste in conditions of large weight loss., (Copyright © 2013 John Wiley & Sons, Ltd.)

Sepsis is a leading cause of death in intensive care units worldwide. Low availability of glutamine contributes to the catabolic state of sepsis. L-Glutamine supplementation has antioxidant properties and modulates the expression of heat shock proteins (HSPs). This study investigated the effects of oral supplementation with L-glutamine plus L-alanine (GLN+ALA), both in the free form and L-alanyl-L-glutamine dipeptide (DIP), on glutamine-glutathione (GSH) axis and HSPs expression in endotoxemic mice. B6.129F2/J mice were subjected to endotoxemia (lipopolysaccharides from Escherichia coli, 5 mg.kg(-1), LPS group) and orally supplemented for 48 h with either L-glutamine (1 g.kg(-1)) plus L-alanine (0.61 g.kg(-1)) (GLN+ALA-LPS group) or 1.49 g.kg(-1) of DIP (DIP-LPS group). Endotoxemia reduced plasma and muscle glutamine concentrations [relative to CTRL group] which were restored in both GLN+ALA-LPS and DIP-LPS groups (P<.05). In supplemented groups were re-established GSH content and intracellular redox status (GSSG/GSH ratio) in circulating erythrocytes and muscle. Thiobarbituric acid reactive substance was 4-fold in LPS treated mice relative to the untreated CTRL group, and plasma TNF-α and IL-1β levels were attenuated by the supplements. Heat shock proteins 27, 70 and 90 (protein and mRNA) were elevated in the LPS group and were returned to basal levels (relative to CTRL group) in both GLN+ALA-LPS and DIP-LPS groups. Supplementations to endotoxemic mice resulted in up-regulation of GSH reductase, GSH peroxidase and glutamate cysteine ligase mRNA expression in muscle. In conclusion, oral supplementations with GLN+ALA or DIP are effective in reversing the conditions of LPS-induced deleterious impact on glutamine-GSH axis in mice under endotoxemia., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Leucine activates the intracellular mammalian target of the rapamycin (mTOR) pathway, and hypothalamic mTOR signaling regulates food intake. Although central infusion of leucine reduces food intake, it is still uncertain whether oral leucine supplementation is able to affect the hypothalamic circuits that control energy balance. We observed increased phosphorylation of p70s6k in the mouse hypothalamus after an acute oral gavage of leucine. We then assessed whether acute oral gavage of leucine induces the activation of neurons in several hypothalamic nuclei and in the brainstem. Leucine did not induce the expression of Fos in hypothalamic nuclei, but it increased the number of Fos-immunoreactive neurons in the area postrema. In addition, oral gavage of leucine acutely increased the 24 h food intake of mice. Nonetheless, chronic leucine supplementation in the drinking water did not change the food intake and the weight gain of ob/ob mice and of wild-type mice consuming a low- or a high-fat diet. We assessed the hypothalamic gene expression and observed that leucine supplementation increased the expression of enzymes (BCAT1, BCAT2 and BCKDK) that metabolize branched-chain amino acids. Despite these effects, leucine supplementation did not induce an anorectic pattern of gene expression in the hypothalamus. In conclusion, our data show that the brain is able to sense oral leucine intake. However, the food intake is not modified by chronic oral leucine supplementation. These results question the possible efficacy of leucine supplementation as an appetite suppressant to treat obesity.

Objective: Aging is characterized by alterations in body composition such as an increase in body fat and decreases in muscle mass (sarcopenia) and bone density (osteopenia). Leucine supplementation has been shown to acutely stimulate protein synthesis and to decrease body fat. However, the long-term effect of consistent leucine supplementation is not well defined. This study investigated the effect of leucine supplementation during aging., Methods: Six-month-old rats were divided into three groups: an adult group (n = 10) euthanized at 6 mo of age, a leucine group (n = 16) that received a diet supplemented with 4% leucine for 40 wk, and a control group (n = 19) that received the control diet for 40 wk. The following parameters were evaluated: body weight, food intake, chemical carcass composition, indicators of acquired chronic diseases, and indicators of protein nutritional status., Results: Body weight and fat were lower in the leucine group after 40 wk of supplementation compared with the control group but still higher than in the adult group. The lipid and glycemic profiles were equally altered in the control and leucine groups because of aging. In addition, leucine supplementation did not affect the changes in protein status parameters associated with aging, such as decreases in body and muscle protein and total serum protein., Conclusion: The results indicate that leucine supplementation attenuates body fat gain during aging but does not affect risk indicators of acquired chronic diseases. Furthermore, supplemented animals did not show signs of a prevention of the decrease in lean mass associated with aging., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Glutamine, one of the most abundant amino acids found in maternal milk, favors protein anabolism. Early-weaned babies are deprived of this source of glutamine, in a period during which endogenous biosynthesis may be insufficient for tissue needs in states of metabolic stress, mainly during infections. The objective of this study was to verify the effects of dietary glutamine supplementation on the body composition and visceral protein status of early-weaned mice inoculated with Mycobacterium bovis Bacillus Calmette-Guérin (BCG). Mice were weaned early on their 14th day of life and seperated into two groups, one of which was fed a glutamine-free diet (n = 16) and the other a glutamine-supplemented diet (40 g/kg diet) (n = 16). At 21 days of age, some mice were intraperitoneally injected with BCG. Euthanasia was performed at the 28th day of age. BCG inoculation significantly reduced body weight (P < 0.001), lean mass (P = 0.002), water (P = 0.006), protein (P = 0.007) and lipid content (P = 0.001) in the carcass. Dietary glutamine supplementation resulted in a significant increase in serum IGF-1 (P = 0.019) and albumin (P = 0.025) concentration, muscle protein concentration (P = 0.035) and lipid content (P = 0.002) in the carcass. In conclusion, dietary glutamine supplementation had a positive influence on visceral protein status but did not affect body composition in early-weaned mice inoculated with BCG.

An important role in protein-energy metabolism has been attributed to leucine because of its long-term effects on body fat reduction and on the improvement of some indicators of protein status in rodents. The present study investigated the influence of leucine supplementation on the body composition and protein status of rats during the early phase of weight loss, which is characterized by a rapid loss of body weight. Thirty adult male Wistar rats were divided into 2 groups, a control and a leucine group (diet supplemented with 0.59% L-leucine), and were submitted to 1 week of 50% food restriction. The following parameters were evaluated: chemical carcass composition, protein and RNA content in liver and gastrocnemius muscle, and serum concentrations of insulin-like growth factor-1 and corticosterone. A higher liver weight and liver protein content were observed in the supplemented group (p < 0.05). However, no difference in body fat was found between groups (p > 0.05). The results indicate that low-dose leucine supplementation favors liver protein status but does not reduce body fat in rats during the early phase of rapid weight loss.

Although many studies have shown that amino acid ingestion acutely stimulates protein anabolism, only few studies have investigated whether long-term supplementation promotes changes in body composition. We therefore tested the hypothesis that l-leucine (LEU) and l-phenylalanine (PHE) supplementation might have a positive impact on the body composition of rats submitted to intermittent periods of food restriction and refeeding (weight cycling or WC). The WC protocol comprised three cycles, each consisting of 1 week of 50% food restriction followed by 2 weeks of ad libitum ingestion. The groups submitted to WC ingested the control diet (WC-CON) or the diet supplemented with LEU+PHE (WC-AA). A pair-fed group receiving the control diet (PF-CON) was used as a reference for the effects of WC. Although food intake was the same in all groups, higher body weight and energy efficiency were observed in the WC-AA group compared to the PF-CON and WC-CON groups although not significantly in relation to the latter. These results were the consequence of a significant increase of lean body mass and body protein content in the WC-AA group compared to the PF-CON and WC-CON groups. The WC-CON and WC-AA groups presented 36.1% and 18.9% more body fat, respectively, than the PF-CON group but this difference was not significant. Neither fasting insulin nor glucose concentration nor postprandial insulin secretion was significantly affected by the supplemented diet. In conclusion, supplementation with LEU+PHE improved the body composition profile of rats submitted to WC, mainly by increasing lean body mass and body protein content.

The present study evaluated the acute effects of carbohydrate supplementation on heart rate (HR), rate of perceived exertion (RPE), metabolic and hormonal responses during and after sessions of high-intensity intermittent running exercise. Fifteen endurance runners (26 +/- 5 years, 64.5 +/- 4.9 kg) performed two sessions of intermittent exercise under carbohydrate (CHO) and placebo (PLA) ingestion. The sessions consisted of 12 x 800 m separated by intervals of 1 min 30 s at a mean velocity corresponding to the previously performed 3-km time trial. Both the CHO and PLA sessions were concluded within approximately 28 min. Blood glucose was significantly elevated in both sessions (123.9 +/- 13.2 mg dl(-1) on CHO and 147.2 +/- 16.3 mg dl(-1) on PLA) and mean blood lactate was significantly higher in the CHO (11.4 +/- 4.9 mmol l(-1)) than in the PLA condition (8.4 +/- 5.1 mmol l(-1)) (P < 0.05). The metabolic stress induced by the exercise model used was confirmed by the elevated HR (approximately 182 bpm) and RPE (approximately 18 on the 15-point Borg scale) for both conditions. No significant differences in plasma insulin, cortisol or free fatty acids were observed during exercise between the two trials. During the recovery period, free fatty acid and insulin concentrations were significantly lower in the CHO trial. Supplementation with CHO resulted in higher lactate associated with lipolytic suppression, but did not attenuate the cortisol, RPE or HR responses.

The objective of this study was to determine the effect of creatine supplementation on performance and body composition of swimmers. Eighteen swimmers were evaluated in terms of post-performance lactate accumulation, body composition, creatine and creatinine excretion, and serum creatinine concentrations before and after creatine or placebo supplementation. No significant differences were observed in the marks obtained in swimming tests after supplementation, although lactate concentrations were higher in placebo group during this period. In the creatine-supplemented group, urinary creatine, creatinine, and body mass, lean mass and body water were significantly increased, but no significant difference in muscle or bone mass was observed. These results suggest that creatine supplementation cannot be considered to be an ergogenic supplement ensuring improved performance and muscle mass gain in swimmers.

Creatine, a natural nutrient found in animal foods, is alleged to be an effective nutritional ergogenic aid to enhance sport or exercise performance. It may be formed in kidney and liver from arginina and glicina. Creatine may be delivered to the muscle, where it may combine readily with phosphate to form creatine phosphate, a high-energy phosphagen in the ATP-CP system, and is stored. The ATP-CP energy system is important for rapid energy production, such as in speed and power events. Approximately 120 g of creatine is found in a 70 kg male, 95% in the skeletal muscle. Total creatine exists in muscle as both free creatine (40%) and phosphocreatine (60%). It is only recently that a concerted effort has been undertaken to investigate its potential ergogenic effect relative to sport or exercise performance. It does appear that oral creatine monohydrate may increase muscle total creatine, including both free and phosphocreatine. Many, but not all studies suggest that creatine supplementation may enhance performance in high intensity, short-term exercise task that are dependent primarily on the ATP-CP energy system, particularly on laboratory test involving repeated exercise bouts with limited recovery time between repetitions. Short-term creatine supplementation appears to increase body mass, although the initial increase is most likely water associated with the osmotic effect of increased intramuscular total creatine. Chronic creatine supplementation in conjunction with physical training involving resistance exercise may increase muscle mass. However, confirmatory research data are needed. Creatine supplementation up to 8 weeks, with high doses, has not been associated with major health risks; with low doses, it was demonstrated that in 5 years period supplementation, there are no adverse effects. The decision to use creatine as a mean to enhance sport performance is left to the description to the individual athlete.

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Objective: The aim of the present study was to determine the effects of oral supplementation with L-glutamine plus L-alanine (GLN+ALA), both in the free form and L-alanyl-L-glutamine dipeptide (DIP) in endotoxemic mice. Methods: B6.129 F2/J mice were subjected to endotoxemia (Escherichia coli lipopolysaccharide [LPS], 5 mg/kg, LPS group) and orally supplemented for 48 h with either L-glutamine (1 g/kg) plus L-alanine (0.61 g/kg) (GLN+ALA-LPS group) or 1.49 g/kg DIP (DIP-LPS group). Plasma glutamine, cytokines, and lymphocyte proliferation were measured. Liver and skeletal muscle glutamine, glutathione (GSH), oxidized GSH (GSSG), tissue lipoperoxidation (TBARS), and nuclear factor (NF)- κB-interleukin-1 receptor-associated kinase 1 (IRAK1)-Myeloid differentiation primary response gene 88 pathway also were determined. Results: Endotoxemia depleted plasma (by 71%), muscle (by 44%), and liver (by 49%) glutamine concentrations (relative to the control group), which were restored in both GLN+ALA-LPS and DIP-LPS groups (P < 0.05). Supplemented groups reestablished GSH content, intracellular redox status (GSSG/GSH ratio), and TBARS concentration in muscle and liver (P < 0.05). T- and B-lymphocyte proliferation increased in supplemented groups compared with controls and LPS group (P < 0.05). Tumor necrosis factor-α, interleukin (IL)-6, IL-1 β, and IL-10 increased in LPS group but were attenuated by the supplements (P < 0.05). Endotoxemic mice exhibited higher muscle gene expression of components of the NF-κB pathway, with the phosphorylation of IkB kinase-α/β. These returned to basal levels (relative to the control group) in both GLN+ALA-LPS and DIP-LPS groups (P < 0.05). Higher mRNA of IRAK1 and MyD88 were observed in muscle of LPS group compared with the control and supplemented groups (P < 0.05). Conclusion: Oral supplementations with GLN+ALA or DIP are effective in attenuating oxidative stress and the proinflammatory responses induced by endotoxemia in mice. [ABSTRACT FROM AUTHOR]