1) Hum. Sport Exerc. Vol. 7, No. 4, pp.770-782, 2012

Hakimi M, Mohamadi MA, Ghaderi Z.

The effects of glutamine supplementation on performance and hormonal responses in non-athlete male students during eight week resistance training..



The aim of this study was to determine the effects of glutamine supplementation on performance, and hormonal changes during an 8-week resistance training program in non athlete male students. Thirty healthy non athlete male (age 21.25 ± 1.6 years, height 173.2 ± 3.2 cm, body mass 72.8 ± 2.8 kg, VO2max 43.48± 2.38 ml·kg-1·min-1) were randomly divided into a glutamine supplementation (GL) group (n=15), and a placebo (PL) group (n=15). Each group was given either glutamine or a placebo in a double blind manner to be taken orally for eight weeks (0.35 g/kg/day). GL and PL groups performed the same weight training program 3 days, each week for 8 weeks. The training consisted of 3 sets of 8 repetitions, and the initial weight was 80% of the pre-1RM. Subjects were tested for performance and blood hormone concentrations before and after the 8-week period. Both groups increased their performance however the GL group showed significantly greater increases in upper and lower body strength, explosive muscular power, blood testosterone, GH and IGF-1 when compared to the PL group; however, cortisol concentrations were significantly more reduced in GL group when compared to the PL group. It can, therefore, be concluded that within 8 weeks glutamine supplementation during resistance training was found to increase performance (explosive muscular power, muscle strength) and improved body composition (increased body mass, fat-free mass and reduced body fat).


2) Nutrition. 2015 Jan;31(1):119-26.

Effect of glutamine supplementation on cardiovascular risk factors in patients with type 2 diabetes.

Mansour A1Mohajeri-Tehrani MR2Qorbani M3Heshmat R4Larijani B5Hosseini S6.



The aim of this study was to assess clinical relevance of long-term oral glutamine supplementation on lipid profile and inflammatory and metabolic factors in patients with diabetes.


Sixty-six patients with type 2 diabetes between the ages of 18 and 65 y were randomized to receive glutamine 30 g/d (10 g powder, three times a day) or placebo, in a double-blind, placebo-controlled trial during a 6-wk treatment period. Fifty-three patients completed the trial. Independent samples t test and analysis of covariance were used.


After a 6-wk treatment period, a significant difference was observed between the two groups in body fat mass (P = 0.01) and percentage of body fat (P = 0.008). Moreover, a significant reduction in waist circumference (P < 0.001) and a tendency for an increase in fat-free mass (P = 0.03), with no change in body weight and body mass index (BMI) was found. Enhancement in body fat-free mass was mainly attributed to trunk (P = 0.03). There was a downward trend in systolic blood pressure (P = 0.005) but not diastolic. Fasting blood glucose (mmol/L) concentration significantly decreased after the 6-wk intervention (P = 0.04). Mean hemoglobin A1c was significantly different between the groups at week 6 (P = 0.04). No significant difference was detected for fasting insulin, homeostasis model assessment for insulin resistance and quantitative insulin sensitivity index between groups (P > 0.05). No significant difference was observed between groups in total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol and triglyceride. No treatment effect on C-reactive protein was found (P = 0.44).


We demonstrated that the 6-wk supplementation with 30 g/d glutamine markedly improved some cardiovascular risk factors, as well as body composition, in patients with type 2 diabetes. Future glutamine dose-response studies are warranted in these areas.


3) Am J Clin Nutr. 1995 May;61(5):1058-61.

Increased plasma bicarbonate and growth hormone after an oral glutamine load.

Welbourne TC1.


An oral glutamine load was administered to nine healthy subjects to determine the effect on plasma glutamine, bicarbonate, and circulating growth hormone concentrations. Two grams glutamine were dissolved in a cola drink and ingested over a 20-min period 45 min after a light breakfast. Forearm venous blood samples were obtained at zero time and at 30-min intervals for 90 min and compared with time controls obtained 1 wk earlier. Eight of nine subjects responded to the oral glutamine load with an increase in plasma glutamine at 30 and 60 min before returning to the control value at 90 min. Ninety minutes after the glutamine administration load both plasma bicarbonate concentration and circulating plasma growth hormone concentration were elevated. These findings demonstrate that a surprisingly small oral glutamine load is capable of elevating alkaline reserves as well as plasma growth hormone.


4) Int J Sport Nutr Exerc Metab. 2015 Oct;25(5):417-26.

The Influence of Oral L-Glutamine Supplementation on Muscle Strength Recovery and Soreness Following Unilateral Knee Extension Eccentric Exercise.

Legault Z1Bagnall NKimmerly DS.



The study aimed to examine the effects that L-glutamine supplementation has on quadriceps muscle strength and soreness ratings following eccentric exercise. It was hypothesized that glutamine ingestion would quicken the recovery rate of peak force production and decrease muscle soreness ratings over a 72-hr recovery period. Sixteen healthy participants (8♀/8♂; 22 ± 4 years) volunteered in a double-blind, randomized, placebo-controlled crossover study. Supplement conditions consisted of isoenergetic placebo (maltodextrin, 0.6 g·kg-1·day-1) and L-glutamine (0.3 g·kg-1·day-1 + 0.3 g·kg-1·day-1 maltodextrin) ingestion once per day over 72 hr. Knee extensor peak torque at 0°, 30°, and 180° per second and muscle soreness were measured before, immediately following, 24, 48, and 72 hr posteccentric exercise. Eccentric exercise consisted of 8 sets (10 repetitions/set) of unilateral knee extension at 125% maximum concentric force with 2-min rest intervals. L-glutamine resulted in greater relative peak torque at 180°/sec both immediately after (71 ± 8% vs. 66 ± 9%), and 72 hr (91 ± 8% vs. 86 ± 7%) postexercise (all, p < .01). In men, L-glutamine produced greater (p < .01) peak torques at 30°/ sec postexercise. Men also produced greater normalized peak torques at 30°/sec (Nm/kg) in the L-glutamine condition than women (all, p < .05). In the entire sample, L-glutamine resulted in lower soreness ratings at 24 (2.8 ± 1.2 vs. 3.4 ± 1.2), 48 (2.6 ± 1.4 vs. 3.9 ± 1.2), and 72 (1.7 ± 1.2 vs. 2.9 ± 1.3) hr postexercise (p < .01). 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.


5) Int J Clin Pharmacol Ther. 2015 May;53(5):372-6.

Glutamine supplementation and immune function during heavy load training.

Song QHXu RMZhang QHShen GQMa MZhao XPGuo YHWang Y.



Athletes with heavy training loads are prone to infectious illnesses, suggesting that their training may suppress immune function. This study sought to determine whether supplementation with the amino acid glutamine, which supports immune health, alters immune function in athletes during heavy load training. 24 athletes were randomly assigned to either an experimental group (n = 12) or a control group (n = 12). Athletes exercised using heavy training loads for 6 weeks. Athletes in the experimental group took 10 g glutamine orally once a day beginning 3 weeks after initial testing, while athletes in the control group were given a placebo. Immune function was assessed by measuring the following immunity markers: CD4⁺ and CD8⁺ T cell counts, serum IgA, IgG, and IgM levels, and natural killer (NK) cell activity both before and after the completion of training. The percentages of circulating CD8⁺ T cells were significantly different before (39.13 ± 5.87%) and after (26.63 ± 3.95%) training in the experimental group (p < 0.05). Although CD8⁺ T cell percentages in the control group were similar before (38.57 ± 5.79%) and after (37.21 ± 5.58%) training, the post-training CD8⁺ T cell percentages were significantly different between the two groups (p < 0.05). The ratios of CD4⁺/CD8⁺ cells in the experimental group were significantly different before (0.91 ± 0.14) and after (1.39 ± 0.19) training (p < 0.05). The CD4⁺/CD8⁺ ratios in the control group were similar before (0.93 Â ± 0.15) and after (0.83 ± 0.11) training, but the post-training CD4⁺T/CD8⁺ T cell ratio was higher in the experimental group than in the control group (p < 0.05). NK cell activity was also significantly different between the two groups after training (experimental, 25.21 ± 3.12 vs. control, 20.21 ± 2.59; p < 0.05). However, no differences were observed in serum IgA, IgG, or IgM levels. Thus, glutamine supplementation may be able to restore immune function and reduce the immunosuppressive effects of heavy-load training.


6) J Appl Physiol . 1999 Jun;86(6):1770-7.

Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise.

Bowtell JL1Gelly KJackman MLPatel ASimeoni MRennie MJ.



The purpose of this study was to determine the efficacy of glutamine in promoting whole body carbohydrate storage and muscle glycogen resynthesis during recovery from exhaustive exercise. Postabsorptive subjects completed a glycogen-depleting exercise protocol, then consumed 330 ml of one of three drinks, 18.5% (wt/vol) glucose polymer solution, 8 g glutamine in 330 ml glucose polymer solution, or 8 g glutamine in 330 ml placebo, and also received a primed constant infusion of [1-13C]glucose for 2 h. Plasma glutamine concentration was increased after consumption of the glutamine drinks (0.7-1.1 mM, P < 0.05). In the second hour of recovery, whole body nonoxidative glucose disposal was increased by 25% after consumption of glutamine in addition to the glucose polymer (4.48 +/- 0.61 vs. 3.59 +/- 0.18 mmol/kg, P < 0.05). Oral glutamine alone promoted storage of muscle glycogen to an extent similar to oral glucose polymer. Ingestion of glutamine and glucose polymer together promoted the storage of carbohydrate outside of skeletal muscle, the most feasible site being the liver.


7) Nutrition. 1996 Nov-Dec;12(11-12 Suppl):S78-81.

Glutamine: an essential amino acid for the gut.

van der Hulst RR1von Meyenfeldt MFSoeters PB.



Glutamine is a non-essential amino acid which is produced in sufficient amount by the healthy human body. From experimental work it is known that glutamine is an important nutrient for rapidly dividing cells such as cells from the immune system and the gut. During several conditions a lack of glutamine may occur. This will result in functional disturbances of the immune system and/or the gut. Glutamine is produced mainly by the muscle tissue. A decrease in muscle mass during nutritional depletion may result in decreased glutamine production capacity. Furthermore during critical illness, there is an increased demand for glutamine probably as a result of an increased utilization by the immune system. In addition, patients receiving standard parenteral nutrition do not receive glutamine, until recently, commercial parenteral nutrition did not contain glutamine because of instability of this amino acid during prolonged storage. One of the important functions of the gut is to prevent migration of bacteria and/or toxins from the gut lumen into the systemic circulation. A lack of glutamine may result in deterioration of this intestinal barrier. Supplementation of glutamine to certain patients could be essential. The relation between glutamine and the gut in several situations (nutritional depletion, critical illness, parenteral nutrition) is discussed in this paper.


8) Neuron Glia Biol. 2010 Nov;6(4):263-76.

Roles of glutamine in neurotransmission.

Albrecht J1Sidoryk-Węgrzynowicz MZielińska MAschner M.



Glutamine (Gln) is found abundantly in the central nervous system (CNS) where it participates in a variety of metabolic pathways. Its major role in the brain is that of a precursor of the neurotransmitter amino acids: the excitatory amino acids, glutamate (Glu) and aspartate (Asp), and the inhibitory amino acid, γ-amino butyric acid (GABA). The precursor-product relationship between Gln and Glu/GABA in the brain relates to the intercellular compartmentalization of the Gln/Glu(GABA) cycle (GGC). Gln is synthesized from Glu and ammonia in astrocytes, in a reaction catalyzed by Gln synthetase (GS), which, in the CNS, is almost exclusively located in astrocytes (Martinez-Hernandez et al., 1977). Newly synthesized Gln is transferred to neurons and hydrolyzed by phosphate-activated glutaminase (PAG) to give rise to Glu, a portion of which may be decarboxylated to GABA or transaminated to Asp. There is a rich body of evidence which indicates that a significant proportion of the Glu, Asp and GABA derived from Gln feed the synaptic, neurotransmitter pools of the amino acids. Depolarization-induced-, calcium- and PAG activity-dependent releases of Gln-derived Glu, GABA and Asp have been observed in CNS preparations in vitro and in the brain in situ. Immunocytochemical studies in brain slices have documented Gln transfer from astrocytes to neurons as well as the location of Gln-derived Glu, GABA and Asp in the synaptic terminals. Patch-clamp studies in brain slices and astrocyte/neuron co-cultures have provided functional evidence that uninterrupted Gln synthesis in astrocytes and its transport to neurons, as mediated by specific carriers, promotes glutamatergic and GABA-ergic transmission. Gln entry into the neuronal compartment is facilitated by its abundance in the extracellular spaces relative to other amino acids. Gln also appears to affect neurotransmission directly by interacting with the NMDA class of Glu receptors. Transmission may also be modulated by alterations in cell membrane polarity related to the electrogenic nature of Gln transport or to uncoupled ion conductances in the neuronal or glial cell membranes elicited by Gln transporters. In addition, Gln appears to modulate the synthesis of the gaseous messenger, nitric oxide (NO), by controlling the supply to the cells of its precursor, arginine. Disturbances of Gln metabolism and/or transport contribute to changes in Glu-ergic or GABA-ergic transmission associated with different pathological conditions of the brain, which are best recognized in epilepsy, hepatic encephalopathy and manganese encephalopathy.