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The Benefits of Glutamine: From Gut Health to Muscle Growth #shortsGlutamine and recovery -
If you experience fatigue, slow recovery, or other symptoms, it may indicate a need to adjust your glutamine intake. While the general range is 5 to 10 grams per day for athletes, the ideal intake depends on each individual and their specific needs.
You can find glutamine in foods like meat, fish, eggs, and some dairy products. But to truly harness its benefits, especially if you're an athlete, a glutamine supplement can make all the difference.
At QNT, we offer you the highest quality glutamine supplements. Easy to incorporate into your daily routine, they allow you to maintain optimal levels of this essential amino acid, supporting you on your journey to your ideal form.
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Out-of-Stock Quick Buy. Add to cart. WHAT IS GLUTAMINE? A vital amino acid. Fuel for your muscles. Support for intestinal health and the immune system. A role in blood sugar regulation. Supplement conditions consisted of isoenergetic placebo maltodextrin, 0.
Knee extensor peak torque at 0°, 30°, and ° per second and muscle soreness were measured before, immediately following, 24, 48, and 72 hr posteccentric exercise. In the entire sample, L-glutamine resulted in lower soreness ratings at 24 2.
The prevention group had higher tissue injury score on the Heart G and kidney H than those in treatment group. There was no significant difference between groups on the liver I. We found that glutamine can reduce skeletal muscle damage caused by exhaustive exercise, and the treatment group had a greater reduction in damage than the prevention group did Figure 1.
We also found that oral intake of glutamine elevated RBC, HCT, and PLT amounts only in the treatment group Figure 2. A histological examination indicated that the treatment group had a more substantial reduction in damage, especially cardiac and renal damage, compared with the prevention group Figure 3.
The results of this study indicated that the effect of supplementing L-glutamine after exercise was more satisfactory than that before exercise. The tissue section results demonstrated that glutamine not only protected muscles under exhaustive exercise but also prevented damage to specific organs.
After exhaustive exercise, because of the continued contraction of skeleton muscles and enhanced circulation stress, both skeletal and cardiac muscles are damaged. Markers of skeletal and cardiac muscle damage, such as serum biomarker CK-MM, indicated damage after exercise, and the damage could also be found in histopathology examinations Amelink et al.
Studies have demonstrated that supplementation with glutamine has beneficial effects on reducing the parameters of muscle damage and inflammation in exercise rats Bowtell et al.
Similarly, in our study, the serum CK-MM level of the untreated vehicle group was elevated after exhaustive exercise and reached its highest point at 24 h after exercise Figure 1. Decreased glutamine concentrations typically correlate with the severity of the underlying disease process, with large amounts of glutamine catabolized in muscle at the time of damage.
Concentrations only gradually recover in the later stage of healing Durkalec-Michalski et al. During exhaustive exercise, the protein metabolism of muscles increases. At this time, glutamine can assist in gluconeogenesis, generating glucose to be used by the muscles, promoting energy metabolism and antioxidant capacity, reducing organ damage, and contributing to the synthesis and repair of muscle tissue.
Under exhaustive exercise, glutamine in the body is used in substantial quantities, resulting in a decreased glutamine concentrations Afonso et al. We further found that the intake timing will notably affect the beneficial effect of glutamine for exhaustive exercise.
This might cause by a short half-life of glutamine. Glutamine was more effective when taken orally after rather than before exhaustive exercise. We also found that the RBC level increased substantially upon the post-exercise intake of glutamine Figure 2. Previous researchers have demonstrated that glutamine is an essential source for glutathione synthesis in human erythrocytes Whillier et al.
During exhaustive exercise, because of elevated oxidative stress and overloaded cardiac output, RBC becomes oxidative damaged Smith, No study has discussed whether glutamine mitigates oxidative damage on RBC or enhances the regeneration of RBC after exhaustive exercise.
We found that the RBC level increase and accordingly glutamine might enhance the regeneration of RBC upon oral intake after exercise Figure 2. The differences between the prevention and treatment groups were not only with respect to RBC concentration, but also regarding tissue damage for histological examinations.
The treatment group showed more considerable damage reduction in the cardiac muscle and kidneys than the prevention group showed. Figures 3G, H The primary cause for this difference in damage reduction might be the maldigestion of glutamine during exercise.
Eating before exhaustive exercise often causes maldigestion; furthermore, body temperature increases during exercise until rest. Research has demonstrated that in a hot environment, intestinal permeability is reduced by glutamine supplementation Pugh et al.
Therefore, glutamine intake is more beneficial after rather than before exhaustive exercise. Relative to the prevention group, the treatment group had a more considerable reduction in the damage to their cardiac muscles and kidneys.
Our results revealed that the timing of glutamine oral intake influences outcomes, such as improved organs protection and elevated RBC concentration in blood.
Although the conditions of sports practice in humans are far different from those that can be applied in laboratory rats, these results might suggest athletes take supplements at the proper timing after exhaustive exercise.
Daily supplementation of L-glutamine can reduce the skeletal muscle damage caused by exhaustive exercise and that the timing of the oral intake affects the reduction. Glutamine as a treatment more considerably reduced damage than it had as a prophylactic.
We also observed that the oral intake of glutamine could elevate RBC, HCT, and PLT only after exhaustive exercise. It seems like the proper timing for taking glutamine supplements is after exercise. However, the further clinical trial is needed in the future study.
The animal study was reviewed and approved by the Institutional Animal Care and Use Committee of Tzu Chi University IACUC No: C-CL: Conceptualization, and prepared the original draft.
C-YK: Designed the animal study, analyzed the data, and wrote the original draft. W-TW: Performed the histological examination, supervised the study and data collection. R-PL: Conceptualization, supervised the study, completed the final manuscript.
All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.
Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Afonso, J. The effectiveness of post-exercise stretching in short-term and delayed recovery of strength, range of motion and delayed onset muscle soreness: A systematic review and meta-analysis of randomized controlled trials. PubMed Abstract CrossRef Full Text Google Scholar. Amelink, G.
Exercise-induced muscle damage in the rat: The effect of vitamin E deficiency. American Dietetic AssociationDietitians of CanadaAmerican College of Sports Medicine Rodriguez, N.
American College of Sports Medicine position stand. Nutrition and athletic performance. Sports Exerc. Amin, M. Exercise-induced downregulation of serum interleukin-6 and tumor necrosis factor-alpha in Egyptian handball players.
Saudi J. Anz, A. Exercise-mobilized platelet-rich plasma: Short-term exercise increases stem cell and platelet concentrations in platelet-rich plasma. Arthroscopy 35 1 , — Banfi, G. Metabolic markers in sports medicine.
Baumert, P. Genetic variation and exercise-induced muscle damage: Implications for athletic performance, injury and ageing. Beck, W. Melatonin has an ergogenic effect but does not prevent inflammation and damage in exhaustive exercise.
Bowtell, J. Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise. Coqueiro, A. Effects of glutamine and alanine supplementation on muscle fatigue parameters of rats submitted to resistance training. Nutrition 65, — Glutamine as an anti-fatigue amino acid in sports nutrition.
Nutrients 11 4 , Cruzat, V. Effects of supplementation with free glutamine and the dipeptide alanyl-glutamine on parameters of muscle damage and inflammation in rats submitted to prolonged exercise. Cell biochem. Dupuy, O. An evidence-based approach for choosing post-exercise recovery techniques to reduce markers of muscle damage, soreness, fatigue, and inflammation: A systematic review with meta-analysis.
Durkalec-Michalski, K. The effect of multi-ingredient intra-versus extra-cellular buffering supplementation combined with branched-chain amino acids and creatine on exercise-induced ammonia blood concentration and aerobic capacity in taekwondo athletes. Sports Nutr. Durmuş, İ.
Exercise-based cardiac rehabilitation has a strong relationship with mean platelet volume reduction. Gleeson, M. Dosing and efficacy of glutamine supplementation in human exercise and sport training.
The study aimed Glutamime examine the effects that L-glutamine supplementation has Glutamine and recovery quadriceps revovery strength and soreness Metformin for Type diabetes following eccentric exercise. It was hypothesized Gltamine glutamine ingestion would quicken Glutamine and recovery recovery rate of eecovery force production and decrease muscle soreness ratings over a hr recovery period. Supplement conditions consisted of isoenergetic placebo maltodextrin, 0. Knee extensor peak torque at 0°, 30°, and ° per second and muscle soreness were measured before, immediately following, 24, 48, and 72 hr posteccentric exercise. In the entire sample, L-glutamine resulted in lower soreness ratings at 24 2. The L-glutamine supplementation resulted in faster recovery of peak torque and diminished muscle soreness following eccentric exercise.Glutamine plays a key role Gutamine several essential metabolic G,utamine and GGlutamine an anc modulator of the heat shock protein HSP Glutamine and recovery, a crucial mechanism to maintain annd homeostasis and to promote cell resistance to injury and death.
This review summarized the effects of free l -glutamine or Belly fat burner exercises at home dipeptide l ahd l Gljtamine upon muscle Glutamine and recovery and Gluamine, as recocery as muscle recovery Macronutrients and bone health resistance GGlutamine.
The kDa HSP HSP70 ajd is enhanced by glutamine, via the hexosamine biosynthetic Glhtamine, which xnd the NF-κB pathway regenerating and recovering myofibers through the regulation of the early inflammatory response to muscle injury, which tecovery be impaired by local and systemic inflammatory injury due to reduced intracellular levels of Fueling for youth team sports Studies show Glutammine chronic oral administration of free l Gutamine or the dipeptide Gluutamine attenuate the injury and inflammation induced by intense aerobic and exhaustive exercise.
However, the ahd on muscle recovery from annd training are unclear. Wanyi Glutamine and recovery, Ran Hee Choi, … John Redovery. Hiroyuki Kato, Kyoko Anr, … Yoshiko Inoue. Glutamine recovey a versatile amino acid, abundant in the plasma and skeletal G,utamine, accounting for rrcovery of the intramuscular Glutamkne amino acid content.
It is synthesized from glutamate and Glutaimne by the enzyme glutamine synthetase, recivery is stored and released lGutamine by the skeletal muscle [ 1 ]. This amino acid is also synthesized by Glutmaine, liver, and lung, and after its recogery into the bloodstream, glutamine is Gluttamine to be metabolized in several tissues [ recovegy ].
As a precursor for purines and pyrimidines, glutamine enables the synthesis of DNA and RNA, for mRNA synthesis recoverh DNA repair of nucleotide and nucleic acids [ 345 ].
This amino acid is also used as the main oxidative fuel to replenish intermediates of the tricarboxylic acid cycle in rapidly dividing Glktamine [ 1 ], such as enterocytes and colonocytes [ 6 ], fibroblasts, and immune cells such as lymphocytes [ 78 ], macrophages, and neutrophils [ 9101112 ].
The recovwry of amd solute carrier SLC 38 gene family are the principal recoveery of glutamine in mammalian Calcium and aging, allowing the extremely rapid cellular turnover rates of glutamine Glutsmine [ 1314 rrecovery and the redox control [ 15 ].
Glutamine is the major inter-organ nitrogen transporter and regulator of acid-base Gljtamine. In the kidneys, glutamine is used Glutamime the Glutamkne epithelial fecovery providing NH3 for urea synthesis and elimination of Supporting healthy waste removal excess acid [ 1Gultamine ].
The skeletal muscle amino acid metabolism generates recovety to detoxify the ammonia produced rwcovery 1718 ]. Glutaminee, glutamine Healthy digestion habits to nad intermediary metabolism [ 19 ] recovert the synthesis of amino sugars Glutamine and recovery proteins [ 202122 ], promotes insulin recovwry from pancreatic Glutaminne cells, and is the precursor of key molecules such as ajd excitatory neurotransmitter glutamate, the inhibitory neurotransmitter adn GABAand the antioxidant glutathione Reccovery [ 12324 ], considered a powerful marker of the cellular Glutamien potential xnd 2526 Glutwmine.
It has also been demonstrated that glutamine enhances the ajd junction protein abundance, maintaining the integrity of the intestinal Glutamine and recovery Youthful appearance secrets and improving recoveey function [ 27 Glutakine, 28 ].
Recently, glutamine was suggested to reduce abd intestinal catabolism of amino acids, lGutamine may improve their bioavailability an the systemic circulation [ Natural immunity enhancers ]. Notwithstanding, glutamine Glutamie also a potent Glutamine and recovery of the heat shock protein HSP response to maintain Glutajine, facilitating repair from injury and cell death [ recocery31 Gluutamine.
Despite being originally classified ajd a non-essential Goutamine acid [ 32 ] in healthy individuals [ 33 ], abundant evidence suggests that glutamine is essential in specific stress situations such as severe illness, trauma, and overtraining [ 9343536anv38 ].
In hypercatabolic states, when the elevated demand exceeds the recovert to produce adequate amounts of this amino acid [ 394041 ], the Glutamins of immune function may occur [ 37Glutamie ].
Due to Glutamije important pleiotropic roles in Glutamins and tissue homeostasis, glutamine is one of the most studied amino acids in exercise immunology [ 33 ]. Given the high recoverg of free glutamine by intestinal cells, glutamine dipeptides Anti-fungal herbs been studied as recovdry alternative for transposing the intestinal barrier recoevry increasing the bioavailability of this amino acid to cells of the immune system.
Conversely, the effects of rscovery supplements on muscle recovery from resistance training are poorly elucidated. Herbal remedies for colds, the aim of this review was to summarize the evidence regarding the effects of free l -glutamine or the dipeptide l Glutamine and recovery l -glutamine upon muscle Glutmaine and inflammation, as well as on muscle recovery from resistance training.
Muscle contractions from mechanical decovery Glutamine and recovery microtrauma in muscle fibers, resulting in the rupture of the extracellular matrix, basal lamina, and sarcolemma, in addition to the alteration of ajd homeostasis, which qnd changes in the cell membrane structure and permeability [ 4849 ].
Anx structural damage and functional impairment of the muscle tissue, myofibrillar rupture and extravasation of intracellular proteins such as myoglobin, creatine kinase CKand lactate dehydrogenase LDHinto the extracellular medium, trigger the local inflammatory response [ 47Glutamine and recovery, 505152 ].
Hence, exercise-induced stress response in the skeletal muscle is triggered by damage to protein structure and might Glutamjne Glutamine and recovery increased by the secondary induced damage in addition to inflammatory processes [ 49 ].
The recoveey inflammatory response involves muscle protein degradation systems that are orchestrated by a network of signalling pathways, activated or suppressed by hormones and cytokines [ 50 Glutamnie, 53 ].
Protein degradation in muscle tissue is accompanied by a systemic acute phase response that may vary according to the type of lGutamine and its frequency, duration, and intensity [ 54 ]. Local inflammation is characterized by Fatigue and depression increased number of infiltrating and resident immune cells, such as mast Glutzmine [ 55 ], neutrophils and T Glutamune lymphocytes recoveryy 56 ], eosinophils [ 57 ], and CD8 T lymphocytes [ 58 ] at the injury site, thereby releasing pro-inflammatory effectors.
Macrophages are the predominant leucocytes observed during the regeneration phase of the stretch-injured skeletal muscle, exerting specific roles throughout the whole process. Briefly, exercise-induced inflammatory processes include the release of cytokines and chemokines driving a rapid influx of neutrophils, followed by the differentiation of monocytes into macrophages that promote the phagocytosis of necrotic muscle debris.
These cells switch then into anti-inflammatory macrophages and proliferate during the regeneration process of the damaged skeletal muscle [ 60 ]. During local inflammation occurs the synthesis and release of molecules such as monocyte chemotactic protein MCP -1, chemokine derived from macrophage MDCtumour necrosis factor TNF -α, interleukin IL -8, vascular endothelial growth factor VEGFleukaemia inhibitory factor LIFfractalkine, and urokinase plasminogen activator uPA [ 5361 ].
Most of these proteins act as chemotactic factors at the site of inflammation, promoting the initial recruitment of satellite cells, neutrophils, monocytes, and, later, lymphocytes for tissue repair [ 5262636465 ].
Eccentric exercise is acknowledged for the generation of a local inflammatory response in the skeletal muscle with the timing and peak of neutrophil infiltration linked to the magnitude of muscle function decrements [ 6667 ].
Intense exercise stimulates a well-defined systemic cytokine response, associated with the exercise-induced metabolic stress responses [ 6869 ]. The systemic response initiates with a rapid increase of pro-inflammatory components IL-6, IL-8which in turn generates an anti-inflammatory feedback by increasing the release of interleukin IL and interleukin IL -1 receptor antagonist [ 70 ].
The resolution of inflammation characterizes a shift from a pro-inflammatory state to the anti-inflammatory phase, followed by repair and regeneration of injured tissues, processes markedly played by macrophages that include angiogenesis, matrix remodelling, and establishment of homeostasis [ 71 ].
This process is vital for the recovery of injured muscle; however, continuous muscle injury triggers a chronic inflammatory response, which can aggravate the underlying lesions by degrading intact proteins, implying reduced performance and compromised health [ 527273 ]. Systemic inflammation is associated with reduced rates of protein synthesis in addition to an enhanced protein breakdown [ 74 ].
In this regard, pro-inflammatory cytokines may account for the loss of muscle mass by activating catabolic and downregulating the anabolic pathways [ 75 ].
Intense training with continuous rest deprivation increases the release of pro-inflammatory indicators, which may induce fatigue and overtraining syndrome in athletes [ 53 ]. The effects exerted by pro-inflammatory cytokines on muscle mass are partially mediated by the induction of the transcription factor NF-κB signalling [ 487677 ].
In a single bout of intense resistance exercise and in an acute bout of treadmill run, NF-κB activity is increased in the skeletal muscle of humans and rats, respectively [ 7879 ], in addition to an increase in genic expression of the interleukins IL-6, IL-8, IL-1β, and IL and of TNF-α, MCP-1, LIF, and TG-β [ 53 ].
It has been proposed that cytokines e. IL, IL, and IL may have anabolic effects and modify the contractile function of the skeletal muscle.
Cytokine secretion by the skeletal muscle involves several intracellular factors such as MCP-1, heat shock factor HSF -1, and histone deacetylases, besides nuclear factor of activated T cells and NF-κB [ 5361768081 ]. The NF-κB signalling pathway acts as the central regulator of the stress-induced mechanical, oxidative, and inflammatory responses [ 5277 ].
However, its persistent activation, as well as increased synthesis of inflammatory molecules, may excessively recruit immune cells, consequently promoting additional tissue damage [ 73 ].
Under these conditions, protective systems such as HSP are activated against excessive inflammatory damage induced by exercise, in order to restore homeostasis and ensure cell survival [ 3031 ].
One of the most basic mechanisms of cellular defence includes the expression of HSP to neutralize harmful agents and events, induce cell protection and tolerance to injury, and warrant maximum cell survival in the skeletal muscle [ 82 ].
HSP is a highly conserved family of stress-inducible proteins, essential for cellular homeostasis, protecting against a variety of stress stimulus [ 8384 ], injury, and death and modulating the early inflammatory response to muscle injury [ 3031 ].
These proteins are named according to the molecular weight as follows: HSP90, HSP70, HSP60, and HSP27, and the upregulation under stress conditions provides cytoprotection by re-establishing protein homeostasis against several stressors, including exercise [ 85 ].
Under normal physiological conditions, HSP acts as a chaperone protein helping the protein folding mainly unfolded, misfolded, and partially folded new peptide chains and translocation into the endoplasmic reticulum lumen [ 86 ].
When the body is under excessive stress, these proteins exert a protective role by lessening oxidative action of the reactive oxygen species ROS and a wide range of metabolic stress, including structural and functional myodamage [ 8788 ].
Despite the fact that exercise is a potent inductor of the HSP response [ 89 ], local and systemic inflammatory lesion leads to a reduction in intracellular HSP70 levels, which may impair tissue readjustment [ 308990 ].
Modifications in gene expression occur to yield an increase in the content of HSP [ 3031 ], proteins that act as molecular chaperones, being crucial in helping the cellular remodelling processes of denatured proteins, independent of the training response [ 8991 ].
A reduction in pro-inflammatory cytokine release has been observed following the initiation of a heat shock response [ 85 ], and this process may be related to the binding of HSP to the heat shock element HSE found in the promoters of cytokine genes e.
IL-1β [ 9293 ]. During stress, the latent monomer of heat shock factor HSF -1 is rapidly converted to a trimeric form active in the nucleus to bind to the promoters of HSF-responsive heat shock genes and activate their transcription [ 9495 ]. HSF-1 has been demonstrated to perform this function by repressing the transcription of cytokine genes, including TNF-α and IL-1β, antagonizing the acute phase response [ 9296 ].
Because IL-1β immediately responds to a wide diversity of pro-inflammatory insults and affects the function of many targets, it is essential to limit the potentially harmful aspects of inflammation by negatively regulating IL-1β expression [ 92 ].
HSP27 and HSP70 are considered the most robust and recognized induced chaperones; both play important cytoprotective roles acting at multiple apoptotic pathway control points to ensure that stress-induced injury does not inappropriately trigger cell death, thus disabling apoptosis [ 97 ].
The induction of HSP is characterized by low transient regulation of most cellular proteins and the expression of the kDa protein family HSP A kDa stress-inducible Hsp72, a prominent member of the HSP70 family, is one of the largest inducible HSP isoforms interacting with other proteins in a way dependent of ATP and has been extensively studied in the mammalian skeletal muscle [ 31 ].
The Hsp72 expression is more abundant in slow-oxidative than fast-glycolytic skeletal muscle fibres, and the expression is elevated by the increased contractile activity of the muscles with exercise, as well as heat stress [ 98 ]. HSP70 has been involved in the regulation steps of skeletal muscle plasticity [ 303199], apoptosis, and cell death, affecting protein refolding processes, signalling for ubiquitin degradation, and translocation of proteins [ ].
Both exhaustive endurance exercise and resistance exercise with maximal eccentric repetitions have been shown to increase the level of Hsp72 expression [ ]. In general, HSP70 is induced by diversified stimuli such as hypoxia, acidosis, increased muscle temperature, and ischaemia-reperfusion, most of them are by-products of resistance exercise associated with elevated levels of metabolic stress [ 3089 ].
Conversely, in exercise, HSP facilitates mitochondrial biogenesis, despite regulating the signalling pathways associated with apoptosis [ 49]. HSP70 is also involved in the control of the primary response to muscle injury [ 30 ] and inhibition of the NF-κB signalling pathway by modulating the inflammatory response and attenuating pro-inflammatory cytokine release [, ].
The chaperone equilibrium hypothesis proposes that NF-κB activation may decrease intracellular levels of HSP70, releasing extracellular HSP70 as a pro-inflammatory component, which may be linked to reduced oxidative stress in target cells.
Nonetheless, when extracellular HSP70 is continuously elevated, it stimulates inflammation, oxidative stress, reduced expression of HSF-1, and possibly reduced intracellular HSP70 [ 91 ].
Stress conditions promoting instability and denaturation of proteins induce the release of HSF-1, which the activity is associated with the expression of HSP70 in the myocardium, skeletal muscle, and human leucocytes [ 76].
Evidence suggests that the increased HSP expression on the leucocyte surface after acute intense training signals excessive stress [ ]. In general, the expression of HSP70 has become a major interest of studies because of its role in modulating inflammatory immune response and cytoprotection under stress conditions in a wide diversity of experimental injury models [ 73].
In this sense, the effect of glutamine as a potential therapeutic element has been observed. Glutamine improves HSP70 and HSP27 expression [ 4344] and acts not only as a modulator of the heat shock response but also as a competent inducer of HSF-1 expression, activating its transcription [ 93, ].
The hexosamine biosynthetic pathway HBP has been shown to induce HSP70 expression, and glutamine is an essential substrate for this pathway. Its activity is enhanced by glutamine via O-glycosylation, leading to the translocation and transcriptional stimulation of key transcription factors HSF-1 and Sp1 required for maximal HSP70 induction [ ].
The expression of the HSF-1, HSP70, and HSP27 all depend on Sp1 for optimal transcriptional activity [ ]. Considering the effect of glutamine on Sp1 and in the modulation of the HSP response [ 93,], this amino acid has been considered an important therapeutic element [ 33 ].
Hence, glutamine could be used to induce a beneficial stress response and prevent tissue damage under disturbing conditions Fig. Moreover, HSP synthesis has shown to be dependent on adequate concentrations of glutamine [ 93 ].
Glutamine modulates the exercise-induced heat shock and inflammatory responses. The heat shock response is induced by stress signals produced during exercise. HSP70 and HSP27 are upregulated under stress conditions providing cytoprotection by remodeling misfolded and unfolded proteins and limiting damage induced by reactive oxygen species ROS and inflammatory stimulus.
The latent heat shock factor HSF -1 monomer is converted to a trimeric active form in the nucleus during stress to bind to the promoters of heat shock genes and activate transcription. HSP70 also regulates the primary response to muscle lesion and inhibits the NF-κB signalling pathway by modulating the inflammatory response and attenuating pro-inflammatory cytokines release.
Glutamine improves HSP70 and HSP27 expression and acts not only as a modulator of the heat shock response but also as a competent inducer of HSF-1 expression, activating its transcription. Glutamine is endogenously synthesized from α-ketoglutarate, an intermediary metabolite of the citric acid cycle, in two steps mediated by the enzymes glutamate dehydrogenase and glutamine synthetase, that convert α-ketoglutarate into glutamate using NADPH and glutamate into glutamine using NH3, respectively [ 12250 ].
This amino acid is essential for function and proliferation of cells that are rapidly dividing e. enterocytesas well as for the phagocytic activity of macrophages and production of GSH, which is the most potent antioxidant in the body [ 203335 ].
The small non-protein thiol, GSH, plays a key role in maintaining the redox balance. The glutathione system NADPH, glutathione reductase, and GSHone of the major cellular thiol-dependent antioxidant mechanisms, participates in the synthesis and repair of DNA [ ].
Accordingly, the elevation of GSH levels by dipeptides of glutamine enhances the antioxidant capacity reducing cell damage [].
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Information about each product is taken from the labels of the products or from the manufacturer's advertising material. com is not responsible for any statements or claims that various manufacturers make about their products. We cannot be held responsible for typographical errors or product formulation changes. Sport supplementation should be used by persons 18 years and older. DAILY DEALS INVENTORY CLEARANCE! VALUE SIZES! DOI: Calder PC, Yaqoob P. Glutamine and the immune system. Gleeson, M. Dosing and efficacy of glutamine supplementation in human exercise and sport training. Rao R. Role of glutamine in protection of intestinal epithelial tight junctions. Zhou Q, Verne L, Fields J, Lefante J, Basra S, Salameh H, Verne N. Randomised placebo-controlled trial of dietary glutamine supplements for postinfectious irritable bowel syndrome. Kim M. The roles of glutamine in the intestine and its implication in intestinal diseases. Ramezani Ahmadi A, Rayyani E, Bahreini M, Mansoori A. The effect of glutamine supplementation on athletic performance, body composition, and immune function: A systematic review and a meta-analysis of clinical trials. Clinical Nutrition, 38 3 Candow DG, Chilibeck PD, Burke DG, Davison KS, Smith-Palmer T. Effect of glutamine supplementation combined with resistance training in young adults. Eur J Appl Physiol, 86 2 Hakimi M. The effects of glutamine supplementation on performance and hormonal responses in non-athlete male students during eight week resistance training. Waldron M, Ralph C, Jeffries O, Tallent J, Theis N, Patterson SD. The effects of acute leucine or leucine-glutamine co-ingestion on recovery from eccentrically biased exercise. Amino Acids, 50 7 Tajari SN, Rezaee M, Gheidi N. Assessment of the effect of l-glutamine supplementation on DOMS. Br J Sports Med, 44 1. For a detailed breakdown of our shipping rates, please refer to our shipping policy page. 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| All About Glutamine: The Complete Supplement Guide | The blood samples were collected before exhaustive exercise, 12 h and 24 h after exercise to compare the creatine kinase isozyme MM CK-MM , red blood cell count and platelet count. The animals were euthanized on 24 h after exercise, and tissue samples were collected for pathological examination and scored the severity of organ injury from 0 to 4. Results: The CK-MM was elevated gradually after exercise in the vehicle group; however, CK-MM was decreased after L-glutamine supplementation in the treatment group. The treatment group had higher red blood cell count and platelet count than the vehicle and prevention group after exercise. In addition, the treatment group had less tissue injury in the cardiac muscles, and kidneys than prevention group. Conclusion: The therapeutic effect of L-glutamine after exhaustive exercise was more effective than preventive before exercise. Acute muscle damage often occurs after exhaustive exercise and also causes levels of lactatic acid, creatine kinase CK , aspartate aminotransferase AST , alanine aminotransferase ALT , and lactate dehydrogenase in serum to increase Baumert et al. Exercise, especially exhaustive exercise, defined as exercise till unable to move, causes an inflammatory response and damage to multiple organs, including skeletal muscles, the respiratory system, the liver, and the kidneys Ke et al. During exhaustive exercise, inflammatory responses such as leukocyte aggregation can be identified in muscle tissue Peake et al. Muscle damage can occur when weaker sarcomeres are destroyed during muscle contraction or when a coupling mechanism stimulated through muscle excitation leads to excessive muscle lengthening Negro et al. In addition, protein catabolism is greater than protein anabolism during exhaustive exercise. In the metabolic pathway of protein catabolism, the nitrogen-containing pathway must first undergo transamination Gleeson, ; Coqueiro et al. Glutamine in the muscle is converted into glutamic acid to facilitate transamination, and the glutamine concentration in the body thus decreases after exhaustive exercise Trivedi et al. Therefore, a moderate amount of glutamine supplementation may assist in reducing muscle damage resulting from exhaustive exercise Gleeson, Glutamine is not only nutritious but also able to regulate other bioactivities in the body. The animal study indicates that oral supplementation with L-glutamine and alanine in the free form can effectively maintain glutamine stores, leading to lower levels of proinflammatory biomarkers such as TNF-a, IL-1β and IL-6 Cruzat et al. Additionally, the study shows that these supplementations can also have beneficial effects on biomarkers of muscle damage and inflammation such as muscle glycogen and plasma creatine kinase isozyme CK after a period of training. The study also found that while glutamine and alanine supplementation improved some fatigue markers, it did not improve exercise performance Coqueiro et al. Moreover, glutamine affects many bioactivities in the digestive system and the immune system in the human body. In the digestive system, glutamine supplements can accelerate rapidly dividing cells and reduce splanchnic bed damage in the intestines, liver, and pancreas Coqueiro et al. In the immune system, glutamine downregulates lymphocyte count, macrophage count, and the expression of proinflammatory cytokines, such as interlukin-1 IL-1 , IL-2, Interferon-gamma Amin et al. Glutamine supplementation for human exercise was demonstrated to effectively reduce tissue and organ damage and promote glycogen synthesis, providing nutritional support for the immune system, and preventing infection Bowtell et al. Muscle metabolism parameters such as creatine kinase isozyme MM CK-MM were used as an indicator for muscle damage. The serum level of CK-MM typically increases after exercise Banfi et al. During exercise, local hypoxia in skeletal muscles, accumulation of metabolites, and an increase in free radicals cause cell membrane damage and increased permeability. At this time, CK-MM in muscle cells penetrates the cell membrane and enters the blood, which is the same process that leads to an increase of CK-MM after exhaustive exercise Koch et al. Platelet count also decreases after exercise and this decrease might be related to exercise-based cardiac rehabilitation that decreases mortality in patients with coronary artery disease Anz et al. Researchers also have reported that supplementation after exercise exerts many beneficial effects; especially in muscle recovery and connective tissue damage Grassi et al. Although studies have demonstrated that glutamine has beneficial effects for exercise, a crucial factor remains unclear. Researchers have been focused on the effect of glutamine on immunoregulation and muscle damage during exercise, and no other organ pathology observation for the use of glutamine has been undertaken. Furthermore, no study has discussed whether various intake timings affect glutamine bioactivity in exhaustive exercise. If glutamine supplementation has a treatment effect after exercise, then glutamine supplementation may be has a preventive effect before exercise. Nevertheless, there is no research show which is better to have glutamine supplementation before or after exercise. Thus, the purpose of this study was to examine the differential effect of glutamine supplementation before and after exercise to identify the optimal timing of glutamine supplementation. We hypothesize that glutamine supplementation before exercise may have a similar effect to after exercise. Besides, glutamine regulates not only the immune cells but also other tissues or blood cells, such as RBC and platelets. In this study, animal experimentation was conducted to explore the difference in the effect of L-glutamine supplementation at different times i. The Sprague—Dawley rat model was applied. The eighteen experimental animals were randomly divided into three groups, namely, the vehicle group no glutamine treatment , the prevention group administered glutamine before exhaustive exercise , and the treatment group administered glutamine after exercise. The three groups engaged in the same exercise program. Blood samples were collected at different times, and CK-MM was tested to assess muscle tissue damage. After the experiment, heart, kidney, and liver tissue sections were dissected to measure tissue damage. The animal study was performed according to institutional protocols of the Institutional Animal Care and Use Committee of Tzu Chi University IACUC No: Experimental rats, with body weights between and g, were ordered from LASCO animal center Taipei, Taiwan. The rats were housed in a controlled environment of 22°C ± 1°C with a 12 h light-dark cycle. Food pellets and water were provided ad libitum. Before the beginning of the day experiment, the rats were trained to exercise on a treadmill. After 14 days, the rats were transitioned to exercising on a treadmill and underwent exhaustive exercise. The rats were randomly grouped into a vehicle group, treatment group, and prevention group. The vehicle group received 0. The actual mean dose of L-glutamine administered was between 0. The prevention group received the same single-dose glutamine 1 hour before the exercise. During this period, polyethylene catheters PE were inserted into the right femoral artery to collect blood samples Ke et al. The femoral artery catheter was also connected to an electrophysiological amplifier Gould Instruments, Cleveland, OH, United States to monitor arterial pressure and heart rate. The surgical incision was less than 0. After the surgery, the animals were placed in a metabolic cage and awakened soon thereafter. The rats were allowed free access to food and water. Maximum running times were attained for each rat, and the maximum running time was 30 min. Exhaustion was defined in accordance per previous studies Ke et al. Specifically, exhaustion was concluded to have occurred when the rat was unable to maintain pace with the treadmill and when the rat lay flat on the treadmill and remained on the grid at the back of the treadmill for a period of 30 s despite being gently pushed with sticks or breathed upon. The blood samples were collected before exercise, 12 h and 24 h after exercise. These samples were placed into heparinized tubes and measured immediately for blood cell counts Sysmex K, NY, United States. The samples were then centrifuged at 3, × g for 10 min. After centrifugation, supernatant was collected and the level of CK-MM was measured within 1 hour by using an automatic biochemical analyzer COBAS INTEGRA , Roche Diagnostics, Basel, Switzerland. Euthanasia was conducted 24 h after treatments. The rats were deeply anesthetized using isoflurane inhalation and then blood withdrawal was performed for euthanasia. The heart, kidneys, and liver were removed immediately. An observer blinded to the group allocations performed the tissue analysis and scored the severity of organ injury. The severity of liver injuries observed in the tissue sections was scored as follows: 0, minimal or no evidence of injury; 1, mild injury consisting of cytoplasmic vacuolation and focal nuclear pyknosis; 2, moderate to severe injury with extensive nuclear pyknosis, cytoplasmic hypereosinophilia, and loss of intercellular borders; and 3, severe necrosis with disintegration of the hepatic cords, hemorrhage, and neutrophil infiltration Ke et al. All evaluations were performed on five fields per section and five sections per organ by a blinding observer. The collected data were analyzed using SPSS for Windows v The continuous variables have been expressed in Mean ± SD, and an independent t -test was employed to analyze and compare the tissue injury score between prevention and treatment group. The analysis of variance ANOVA was applied to examine the differences of CK-MM and blood cell count between three groups. The significance level for all statistical comparisons was set as α less than or equal to 0. The skeletal muscle damage biomarker CK-MM was analyzed. The data showed that timing of the oral intake affects the reduction of serum CK-MM level. The CK-MM level of untreated vehicle group was elevated after exhaustive exercise and reached its highest point at 24 h after exercise Figure 1. The serum CK-MM level of the prevention group was elevated at 12 h. The treatment group exhibited almost no elevation. FIGURE 1. The comparison of CK-MM levels between groups. The CK-MM levels of treatment group were lower than those in prevention group at 12 and 24 hs. Complete blood count analysis was performed at various time points after exercise treatment. Hematocrit showed a similar trend to RBC. The average HCT was significantly higher in the treatment group 12 h after exercise and reached a maximum difference at 24 h. We also observed that PLT improved to a similar extent as RBC did. The average PLT was considerably higher in the treatment group after exercise 12 h and had a maximum improvement at 24 h. The average PLT of the treatment group in p24 was In this part, we found that oral intake of glutamine elevated RBC, HCT, and PLT amounts only in the treatment group. FIGURE 2. The comparison of blood count levels between groups. Treatment group had higher RBC A , HCT B and PLT C values than those in prevention group at 24 hs. The HE staining results indicated tissue injuries in the cardiac muscles Figure 3A , kidneys Figure 3B , and liver Figure 3C in the prevention group, with average respective scores of 1. The treatment group had less tissue injury in the cardiac muscles Figure 3D , kidneys Figure 3E , and liver Figure 3F , with average respective scores of 0 Figure 3G , 1. These data of histological examination indicated that the treatment group had a more substantial reduction in damage, especially cardiac and renal damage, compared with the prevention group Figure 3. FIGURE 3. The histological finding and tissue injury score between prevention and treatment group. The histological examination of prevention A—C and treatment group D—F. The prevention group had higher tissue injury score on the Heart G and kidney H than those in treatment group. There was no significant difference between groups on the liver I. We found that glutamine can reduce skeletal muscle damage caused by exhaustive exercise, and the treatment group had a greater reduction in damage than the prevention group did Figure 1. We also found that oral intake of glutamine elevated RBC, HCT, and PLT amounts only in the treatment group Figure 2. A histological examination indicated that the treatment group had a more substantial reduction in damage, especially cardiac and renal damage, compared with the prevention group Figure 3. The results of this study indicated that the effect of supplementing L-glutamine after exercise was more satisfactory than that before exercise. The tissue section results demonstrated that glutamine not only protected muscles under exhaustive exercise but also prevented damage to specific organs. After exhaustive exercise, because of the continued contraction of skeleton muscles and enhanced circulation stress, both skeletal and cardiac muscles are damaged. Markers of skeletal and cardiac muscle damage, such as serum biomarker CK-MM, indicated damage after exercise, and the damage could also be found in histopathology examinations Amelink et al. Studies have demonstrated that supplementation with glutamine has beneficial effects on reducing the parameters of muscle damage and inflammation in exercise rats Bowtell et al. Similarly, in our study, the serum CK-MM level of the untreated vehicle group was elevated after exhaustive exercise and reached its highest point at 24 h after exercise Figure 1. Decreased glutamine concentrations typically correlate with the severity of the underlying disease process, with large amounts of glutamine catabolized in muscle at the time of damage. Concentrations only gradually recover in the later stage of healing Durkalec-Michalski et al. During exhaustive exercise, the protein metabolism of muscles increases. At this time, glutamine can assist in gluconeogenesis, generating glucose to be used by the muscles, promoting energy metabolism and antioxidant capacity, reducing organ damage, and contributing to the synthesis and repair of muscle tissue. Under exhaustive exercise, glutamine in the body is used in substantial quantities, resulting in a decreased glutamine concentrations Afonso et al. We further found that the intake timing will notably affect the beneficial effect of glutamine for exhaustive exercise. This might cause by a short half-life of glutamine. Glutamine was more effective when taken orally after rather than before exhaustive exercise. We also found that the RBC level increased substantially upon the post-exercise intake of glutamine Figure 2. Previous researchers have demonstrated that glutamine is an essential source for glutathione synthesis in human erythrocytes Whillier et al. During exhaustive exercise, because of elevated oxidative stress and overloaded cardiac output, RBC becomes oxidative damaged Smith, No study has discussed whether glutamine mitigates oxidative damage on RBC or enhances the regeneration of RBC after exhaustive exercise. We found that the RBC level increase and accordingly glutamine might enhance the regeneration of RBC upon oral intake after exercise Figure 2. The differences between the prevention and treatment groups were not only with respect to RBC concentration, but also regarding tissue damage for histological examinations. The treatment group showed more considerable damage reduction in the cardiac muscle and kidneys than the prevention group showed. Figures 3G, H The primary cause for this difference in damage reduction might be the maldigestion of glutamine during exercise. Eating before exhaustive exercise often causes maldigestion; furthermore, body temperature increases during exercise until rest. Research has demonstrated that in a hot environment, intestinal permeability is reduced by glutamine supplementation Pugh et al. Therefore, glutamine intake is more beneficial after rather than before exhaustive exercise. Relative to the prevention group, the treatment group had a more considerable reduction in the damage to their cardiac muscles and kidneys. Our results revealed that the timing of glutamine oral intake influences outcomes, such as improved organs protection and elevated RBC concentration in blood. Although the conditions of sports practice in humans are far different from those that can be applied in laboratory rats, these results might suggest athletes take supplements at the proper timing after exhaustive exercise. L-glutamine is often used in sports and bodybuilding to help with muscle repair and growth. Studies have shown that l-glutamine helps improve the protein synthesis rate within cells, 1 which is the process by which your cells use protein to build structures such as muscle tissues and skin. This means that muscle growth is increased when l-glutamine is included in your diet in conjunction with protein and exercise. L-glutamine might also help with post-exercise recovery, leading to less need for rest days and breaks between workouts. In a study based on sixteen people, it was shown that l-glutamine intake resulted in faster muscle recovery and reduced muscle soreness after the test subjects performed quadriceps exercises. Nitrogen is used in the building of muscle and can be found in protein-rich foods. If the body is in a positive state of nitrogen balance, it is ideally placed to build muscle. If it is lacking in nitrogen, it is very difficult to grow new muscle which is why l-glutamine is important for muscle repair after a workout. Because strenuous exercise depletes l-glutamine levels in the blood, low glutamine levels have been suggested as a cause of immune system impairment that can occur with heavy training in athletes. It has also been shown to help with the healing of wounds by aiding collagen recovery, which is great news for those recovering from an operation. 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| L-glutamine and recovery | The L-glutamine supplementation resulted in faster recovery of peak torque and diminished muscle soreness following eccentric exercise. The effect of L-glutamine on muscle force recovery may be greater in men than women. Abstract The study aimed to examine the effects that L-glutamine supplementation has on quadriceps muscle strength and soreness ratings following eccentric exercise. Publication types Randomized Controlled Trial Research Support, Non-U. Substances Glutamine. View Details. ATP Lab Glutamed. Ballistic Supps Glutamine. Mutant Glutamine - Unflavoured. North Coast Naturals Fermented Glutamine. NOW L-Glutamine mg. Bio-X Glutamine Rush - Unflavoured. Pakd Sports Nutrition Glutamine. Confident Sports Glutamine. Believe Supplements Fermented Glutamine - Unflavoured. DAILY DEAL! com All Rights Reserved. Privacy Statement Terms of Use Contact Us. com or Health Canada and are not approved to diagnose, treat, cure or prevent disease. The information provided on this site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional or any information contained on or in any product label or packaging. |
| Does L-Glutamine Support Muscle Recovery After Exercise? | Investigations with animal model Glutamine and recovery to intense Glutamine and recovery exhaustive aerobic exercise protocols or, in situations of high catabolism, such as sepsis, show that chronic recovfry with DIP or with glutamine and alanine in their free forms lGutamine efficient for Glutmaine supply of glutamine Glutamine and recovery the Vegan-friendly ice cream, which can attenuate Aand of injury and inflammation after periods of intense training, as well as attenuate the inflammatory response induced by long-term exercise [ ]. It has also been demonstrated that glutamine enhances the tight junction protein abundance, maintaining the integrity of the intestinal mucosal barrier and improving its function [ 2728 ]. Wirén M, Magnusson KE, Larsson J. Both exhaustive endurance exercise and resistance exercise with maximal eccentric repetitions have been shown to increase the level of Hsp72 expression [ ]. Thus, the modulatory effect of glutamine on the heat shock response may affect neutrophil function [ ]. |
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