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The effects of oral glutamine supplementation on athletes after prolonged, exhaustive exercise
Abstract
Athletes undergoing intense, prolonged training or participating in endurance races suffer an increased risk of infection due to apparent immunosuppression. Glutamine is an important fuel for some cells of the immune system and may have specific immunostimulatory effects. The plasma glutamine concentration is lower after prolonged, exhaustive exercise: this may contribute to impairment of the immune system at a time when the athlete may be exposed to opportunistic infections. The effects of feeding glutamine was investigated both at rest in sedentary controls and after exhaustive exercise in middle-distance, marathon and ultra-marathon runners, and elite rowers, in training and competition. Questionnaires established the incidence of infection for 7 d after exercise: infection levels were highest in marathon and ultra-marathon runners, and in elite male rowers after intensive training. Plasma glutamine levels were decreased by 20% 1 h after marathon running. A marked increase in numbers of white blood cells occurred immediately after exhaustive exercise, followed by a decrease in the numbers of lymphocytes. The provision of oral glutamine after exercise appeared to have a beneficial effect on the level of subsequent infections. In addition, the ratio of T-helper/T-suppressor cells appeared to be increased in samples from those who received glutamine, compared with placebo.
Author Keywords: athletes; glutamine; exhaustive exercise; infection; oral supplementation; immune system
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Glutamine supplementation in vitro and in vivo, in exercise and in immunodepression.
In situations of stress, such as clinical trauma, starvation or prolonged, strenuous exercise, the concentration of glutamine in the blood is decreased, often substantially. In endurance athletes this decrease occurs concomitantly with relatively transient immunodepression. Glutamine is used as a fuel by some cells of the immune system. Provision of glutamine or a glutamine precursor, such as branched chain amino acids, has been seen to have a beneficial effect on gut function, on morbidity and mortality, and on some aspects of immune cell function in clinical studies. It has also been seen to decrease the self-reported incidence of illness in endurance athletes. So far, there is no firm evidence as to precisely which aspect of the immune system is affected by glutamine feeding during the transient immunodepression that occurs after prolonged, strenuous exercise. However, there is increasing evidence that neutrophils may be implicated. Other aspects of glutamine and glutamine supplementation are also addressed.
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Exercise immunology: nutritional countermeasures.
In contrast to moderate physical activity, prolonged and intensive exertion causes numerous changes in immunity that reflect physiologic stress and suppression, and an increased risk of upper respiratory tract infection. Enzymes in immune cells require the presence of micronutrients, leading to attempts by investigators to alter changes in immunity following heavy exertion through use of nutritional supplements, primarily zinc, dietary fat, vitamin C and other antioxidants, glutamine, and carbohydrate. Except for carbohydrate supplementation, none of these nutrients has emerged as an effective countermeasure to exercise-induced immunosuppression. Data from several studies of endurance athletes suggest that carbohydrate compared to placebo ingestion is associated with an attenuated cortisol, growth hormone, and epinephrine response to heavy exertion, fewer perturbations in blood immune cell counts, lower granulocyte and monocyte phagocytosis and oxidative burst activity, and a diminished pro- and anti-inflammatory cytokine response. Overall, the hormonal and immune responses to carbohydrate compared to placebo ingestion during intensive exercise suggest that physiologic stress and inflammation are diminished, although clinical significance awaits further research.
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Clinical applications of L-glutamine: past, present, and future.
OBJECTIVE: This review will attempt to summarize recent clinical data on glutamine's use. It will present the concept of glutamine as a "drug" or "nutraceutical," given in addition to standard nutrition support. Key references will be discussed, and clinical recommendations with regard to patients who may benefit and dosing are also provided. Recent Findings: Glutamine, traditionally considered a nonessential amino acid, now is considered "conditionally essential" after critical illness, stress, and injury. States of illness or injury can lead to a significant decrease in plasma levels of glutamine, and when this decrease is severe, it has been correlated with increased mortality. Laboratory data have demonstrated numerous benefits of glutamine in experimental models of critical illness, cancer, and cardiac injury. The mechanism of these protective effects includes attenuated proinflammatory cytokine expression, improved gut barrier function, enhanced ability to mount a stress response, improved immune cell function, and decreased mortality. Over the last 10 years, clinical trials of glutamine supplementation in critical illness, surgical stress, and cancer have shown benefit with regard to mortality, length of stay, and infectious morbidity. However, data demonstrating a lack of benefit with glutamine supplementation in some patients have been presented as well. It appears that dose and route of administration clearly influence the benefit observed from glutamine administration, with high-dose parenteral glutamine demonstrating an advantage over low-dose enteral glutamine. SUMMARY: High-dose or parenteral (> 0.25 to 0.30 g/kg/day IV or >or=30 g/day enterally) glutamine appears to demonstrate the greatest potential for benefit in hospitalized patients. No evidence of harm has been observed in studies conducted to date; thus, further clinical trials using glutamine as a pharmacologic supplement to standard nutrition are warranted.
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Outcome of critically ill patients after supplementation with glutamine
Abstract
Glutamine has many important metabolic roles that may protect or promote tissue integrity and enhance the immune system. The normal abundance of glutamine has meant that it has not been considered necessary to include glutamine in traditional parenteral feeds. However low plasma and tissue levels of glutamine (Gln) in the critically ill suggest that demand may exceed endogenous supply. A relative deficiency of glutamine in such patients could compromise recovery, result in prolonged illness, and an increase in late mortality. The few percent of the most critically ill intensive care patients who are unable to tolerate enteral nutrition are especially at risk since they have increased demands for glutamine yet lack an exogenous supply. Such patients undergo considerable skeletal muscle wasting compromising glutamine supply further. In a prospective, randomised double blind clinical study of 84 patients with a high mortality due to multiple organ failure requiring parenteral feeding a significant improvement in six-month survival was observed in the group supplemented with glutamine 24/42 versus isonitrogenous, isoenergetic control 14/42, P = 0.049.
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Glutamine supplementation in cancer patients
Abstract
OBJECTIVES: Three series of studies investigated whether 1) glutamine deficiency occurs in tumor-bearing rats, 2) glutamine supplementation improves protein metabolism during chemotherapy in tumor-bearing rats, and 3) oral glutamine supplement improves systemic immune and gut-barrier function in patients with esophageal cancer receiving radiochemotherapy.
METHODS: In the animal studies, AH109A hepatoma cells or Yoshida sarcoma cells were inoculated into male Donryu rats to induce tumors. Glutamine production was measured by U-14C-glutamine infusion and the conversion of arginine to glutamine was measured by infusion of U-14C-arginine. The effect of glutamine on protein metabolism was investigated by 1-14C-leucine infusion. In the clinical study, 13 patients with esophageal cancer were randomized into two groups, control and glutamine supplemented (30 g/d), for 4 wk.
RESULTS: Glutamine levels in plasma and skeletal muscle were decreased in tumor-bearing rats, although glutamine production and the conversion of arginine to glutamine were increased. Glutamine-supplemented total parenteral nutrition reduced whole-body protein breakdown rate during chemotherapy in tumor-bearing rats. Oral supplementation of glutamine to the patients with esophageal cancer enhanced lymphocyte mitogenic function and reduced permeability of the gut during radiochemotherapy.
CONCLUSIONS: Glutamine depletion in host tissues occurs in tumor-bearing rats. Glutamine supplementation can attenuate loss of protein in the muscle in tumor-bearing animals and protect immune and gut-barrier function during radiochemotherapy in patients with advanced cancer.
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Immunosuppression in undernourished rats: the effect of glutamine supplementation
Abstract
Objective: The aim of our study is to determine the effect of a 30-day-period caloric restriction (CR) upon the immune response of rats and the influence of glutamine upon mononuclear cells proliferation and cytokine production.
Methods: Male albino Wistar rats were submitted to CR receiving an amount of food equivalent to 50% of the mean amount consumed by the control animals. We measured the incorporation of [2-14C]-thymidine by lymphocytes obtained from the spleen and mesenteric lymph nodes, plasma glucose and glutamine concentration, as well as cytokine production by cultivated cells, in the presence of glutamine.
Results: Rats submitted to CR presented reduced body weight (49%) and decreased splenic leukocyte number. CR led to a reduction in the proliferative response of lymphocyte. Spleenocytes from CR animals produced less γ-interferon and interleukins 1, 4 and 10 in 48 h culture than did those from control rats. The same pattern is observed in cells obtained from the mesenteric lymph nodes. The addition of glutamine 2 mM to the culture medium restored spleen and mesenteric lymph node cells’ proliferative response and the production of interleukin 2 by cells obtained from the spleen and from the mesenteric lymph nodes.
Conclusions: The present data reinforce that undernutrition decreases in vitro immune cell function and indicates that, in such circumstances, glutamine supplementation could reverse some of the changes observed in the functionality of cultured immune cells. The presence of the amino acid at physiological concentration, however, reinforces the diversion of the immune response towards a Th1-like response.
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Effects of distance running and subsequent intake of glutamine rich peptide on biomedical parameters of male Japanese athletes
Abstract
Plasma glutamine concentration is considered to be an indicator for immune system, and its kinetics and effects of glutamine supplementation have been widely investigated under various conditions. However most of the investigations were performed using Caucasian subjects and free glutamine as a glutamine source, and there is limited information for Japanese subjects and the efficacy of peptide-bonded glutamine. The purposes of this work were to assess the kinetics of glutamine and other biomedical parameters during and after prolonged exercises and effects of post-exercise administration of glutamine peptide (wheat gluten hydrolysate) in male Japanese athletes. The participants performed a half-marathon and a 45-km running. Glutamine peptide (c.a. 0.2 g Gln/kg bodyweight) was administered after the exercise. Plasma branched chain amino acids (BCAA) decreased after both exercises, while a decrease in glutamine was observed only after 45-km run. Intake of glutamine peptide increased plasma glutamine and BCAA, and decreased Trp/BCAA ratio both after the half marathon and the 45-km run.
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Glutamine is the most versatile of the amino acids. It is not an essential amino acid because it is synthesized in the body from other amino acids: glutamic acid, valine, and isoleucine. However, in certain situations, more glutamine may be needed than can be synthesized. In this case, the amino acid could be termed “conditionally essential.” Glutamine's main store is in the muscle, where it makes up about 50% of the total amino acid pool. In certain situations in which the body is stressed, like surgery, trauma, and high-intensity exercise, muscle glutamine reserves may become depleted. The body cannot make enough in this situation, and this produces a catabolic state. Catabolism involves the breakdown of large molecules (like muscle protein) into smaller molecules to release energy. During the prolonged stress of exercise, glutamine stores in the muscle may be utilized heavily. Depleted muscle glutamine stores will inhibit protein synthesis, and this may cause a catabolic state in the body as well. Glutamine plays a role in maintaining cell volume in the muscle through an interaction with sodium, resulting in an osmotic cell swelling in the skeletal muscle. If cell volume is decreased, then catabolism in the muscle may increase.
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During high intensity exercise, the body increases the levels of glucocorticoids, including cortisol, which increases the rate of muscle protein breakdown. The intake of amino acids has been shown to inhibit muscle protein breakdown while stimulating protein buildup. If athletes break down lean tissue during resistance training and if higher concentrations of amino acids promote tissue synthesis, then athletes may benefit from increasing the amount of amino acids in their diets.
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The branched-chain amino acids (BCAAs), valine, leucine, and isoleucine, are essential in the diet and make up approximately one third of muscle protein. One of the main functions of BCAAs is to be used as a fuel during exercise in order to spare other amino acids. When BCAAs are broken down, the carbon chain residues can be used as an energy substrate. Another function of BCAAs is that they help in protein synthesis. Both valine and isoleucine are used as substrates for glutamine, which is very important to protein anabolism. The third BCAA, leucine, is also believed to have anabolic or anticatabolic effects due to beta-hydroxy beta-methybutyrate, or HMB. HMB is a metabolite of leucine and is believed to help increase ability to build muscle and burn fat in relation to intense exercise. Initial published research with HMB seems to support these claims.
Therefore, in terms of supplementation, if extra BCAAs are consumed, then theoretically, this increases BCAA levels in the blood that will be used as energy first, sparing the BCAAs in the muscles. This would, in turn, decrease protein breakdown during exercise. Several studies completed and underway from this laboratory would support the use of glutamine and BCAA supplementation for those athletes wishing to increase strength and body mass. These nutritional supplements also appear to be safe for long-term use and, when compared with creatine monohydrate use, show similar gains in strength in conjunction with a supervised strength program, while producing greater fat-free mass gains. As with all nutritional supplements, there are individuals who will be responsive to their intake and those who will not, with the athlete's day-to-day nutritional intake playing a determining role in the outcome.
Pearson, David R., McGovern, Bryan. 1999: BRIDGING THE GAP: The ABCs of Glutamine, BCAAs, and HMB. Strength and Conditioning Journal: Vol. 21, No. 4, pp. 66–66.
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ABSTRACT
Twenty-nine (17 men, 12 women) collegiate track and field athletes were randomly divided into a creatine monohydrate (CM, n = 10) group, creatine monohydrate and glutamine (CG, n = 10) group, or placebo (P, n = 9) group. The CM group received 0.3 g creatine;pdkg body mass per day for 1 week, followed by 0.03 g creatine;pdkg body mass per day for 7 weeks. The CG group received the same creatine dosage scheme as the CM group plus 4 g glutamine;pdday1. All 3 treatment groups participated in an identical periodized strength and conditioning program during preseason training. Body composition, vertical jump, and cycle performances were tested before (T1) and after (T2) the 8-week supplementation period. Body mass and lean body mass (LBM) increased at a greater rate for the CM and CG groups, compared with the P treatment. Additionally, the CM and CG groups exhibited significantly greater improvement in initial rate of power production, compared with the placebo treatment. These results suggest CM and CG significantly increase body mass, LBM, and initial rate of power production during multiple cycle ergometer bouts.
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Nutritional supplements have for some time been suggested to enhance athletic performance. However, the vast majority of research studies do not support the ergogenic potential of many nutritional supplements. Glutamine and creatine monohydrate supplementation may be 2 supplements that have substantial ergogenic potential. The ergogenic potential of creatine supplementation has received considerable attention in the scientific literature, but substantially less attention has been directed at glutamine supplementation and its ergogenic effects.
Glutamine supplementation has become increasingly popular in athletic populations (9) as a result of scientific evidence that suggests that ingestion of exogenous glutamine by humans can improve glycogen resynthesis (8, 60) and immune responses (10–12, 46, 49–51) following endurance exercise. The majority of these data support the ingestion of 4- to 5-g doses of pure glutamine (10). Additionally, scientific evidence suggests that glutamine supplementation may have an effect on skeletal muscle protein levels (58).
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Glutamine appears to exert a large effect on muscle protein catabolism and protein synthesis in animal (42, 43) and human models (24). MacLennan et al. (42) have demonstrated that glutamine significantly increases intracellular concentrations of glutamine and protein synthesis in rat models. Additionally, MacLennan et al. (43) have demonstrated that glutamine has an antiproteolytic effect on the noncontractile protein content of rat skeletal muscle. In humans, Hankard et al. (24) report that the infusion of glutamine increases protein synthesis. Increases in muscle protein synthesis or prevention of protein catabolism occur following physiological stress, such as surgery in humans, when glutamine supplementation is employed (23). Vom Dahl and Haussinger (64) suggest that glutamine may exert these anticatabolic effects on muscle protein by mediating increases in cellular volume.
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Glutamine may promote increases in cellular volume and osmolarity as a result of an insulin dependent sodium dependent transport system (1, 2, 26, 34). Haussinger and Lang (25) and Haussinger et al. (27) suggest that increased cellular swelling is an anabolic proliferative signal, which may translate into an increase in muscle mass over time. Antonio and Street (2) suggest that the ergogenic effects of glutamine supplementation may be important for athletes in strength power sports, such as track and field. The protein sparing and synthesis effects of glutamine supplementation may potentially result in improved markers of sports performance (power production, vertical jump performance, or overall muscular strength) as a direct result of increases in muscle mass.
Candow et al. (9) demonstrated that the ingestion of 0.9 g;pdkg1 glutamine during 6 weeks of strength training in a mixed population of active individuals (21 men and 19 women) did not result in significantly greater increases in muscular strength and lean body mass, compared with a placebo treatment. Candow et al. (9) suggested that their findings may have resulted from the short duration of training (6 weeks) and that a longer training period may result in the occurrence of ergogenic effects with glutamine supplementation. Additionally, Candow et al. (9) suggested that the large glutamine dosage used in their investigation may have potentiated the lack of ergogenic effects as a result of an inhibitory effect and that it is possible that a smaller supplementation dosage could stimulate positive ergogenic effects. Finally, Candow et al. (9) suggested that the training stimulus may not have resulted in enough stress and that protocols that employ combinations of training stimuli may produce a larger stressor for the athlete and should be study in conjunction with glutamine supplementation. On the basis of these findings, it is possible that a smaller dosage of glutamine coupled with a longer training program that incorporates more training stimulus could result in increases in lean body mass that may ultimately result in improvements in sports performance.
Similar to glutamine, it has been suggested that increases in lean body mass (16, 35, 38, 39, 47, 55, 61, 62) occur with creatine supplementation, especially when coupled with a structured resistance training program (35, 55). Volek and Kraemer (62) suggested that the increase in lean body mass associated with creatine supplementation results from an increase in cellular swelling as the direct result of a sodium dependent transport mechanism. This cellular swelling mechanism has been suggested to be an anabolic signal that over time results in increases in lean body mass (25, 27). Ziegenfuss et al. (66) have shown that short-term (<5 days) creatine supplementation results in a 2% increase in total body water, 3% increase in intracellular fluid volume, and no effect on extracellular fluid volume. These results suggest that short-term creatine supplementation results in increases in body mass as a result of elevations in fluid retention. Over the long term, it has been suggested that creatine supplementation results in an elevation in body mass and lean body mass as a result of increases in protein synthesis (19, 62). Francaux and Poortmans (19) reported that after 21 days of creatine supplementation that body mass is significantly increased. These increases appear to be partially related to increases in absolute body water content and absolute intracellular compartment water volume. There was no increase seen in the relative body water and intracellular compartment volumes, which led the researchers to conclude that the body mass gains seen following the supplementation protocol were a direct result of protein synthesis. On the basis of the current scientific literature, creatine supplementation appears to result in greater increases in body mass and lean body mass when utilized in conjunction with a resistance training program (16, 63). These increases in body mass and lean body mass may ultimately result increases in overall strength, power, and ability to complete repetitive anaerobic exercise bouts.
When long-term creatine supplementation has been coupled with resistance training it has been shown to enhance peak power production or 1 repetition maximum strength (16, 55, 56), improve vertical jump performance (22, 35, 56), improve single effort sprint performance in sprints lasting 6 to 30 seconds (6, 16, 21), and enhance performance during multiple sprint bouts (35). Kirksey et al. (35) examined the effects of 6 weeks of creatine supplementation coupled with a preseason conditioning program with track athletes (16 men and 20 women). This study reported significant increases in lean body mass, countermovement vertical jump power, peak cycle power, average cycle power, total cycle work, and initial power production during cycling with creatine supplementation. Kirksey et al. (35) suggested that the ergogenic effects occurred as a direct result of the increases in lean body mass seen with the creatine supplementation protocol.
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Currently the popular literature recommends the combination of creatine and glutamine in supplements as a way to increase muscle mass and muscular strength (17). It is often suggested the popular literature that these two supplements act as cell volumizers to enhance the synthesis of muscle mass. Based on the scientific literature, it is hypothetically possible that the combination of creatine and glutamine supplements could result in an increased cellular swelling that could enhance the anabolic signal (25, 27) and result in increased muscle mass and possibly improved performance in strength power athletes. However, the present authors know of no studies that have investigated these hypotheses in athletes. Therefore, the major purpose of this investigation is to elucidate the effects of combining creatine and glutamine supplementation on body mass, lean body mass, and markers of anaerobic performance in track and field athletes who are undergoing a preseason strength and conditioning program. It is our hypothesis that the combination a preseason resistance training program with a glutamine and creatine supplementation regimen would enhance body mass, lean body mass, vertical jump performance, vertical jump power, and multiple bout cycle ergometer performance.
Methods Return to TOC
Experimental Approach to the Problem
A randomized, double-blind research design was utilized in an attempt to assess the effects of creatine monohydrate (CM) supplementation and creatine monohydrate + glutamine (CG) supplementation on body mass, body composition, dynamic explosive strength, and repeated anaerobic cycle ergometer performance. Track and field athletes were selected for the present study based on previous research that suggests that creatine supplementation can significantly alter body mass, explosive strength, and repeated anaerobic performance when coupled with a resistance training protocol in this population (35). All subjects participated in an 8-week preseason strength and conditioning program coupled with supplementation with CM, CG, or a placebo. Supplementation was divided into a 1-week loading phase and a 7-week maintenance phase. Testing was conducted prior to and immediately after the 8 weeks of supplementation.
Subjects
Twenty-nine male (n = 17) and female (n = 12) collegiate track and field athletes (sprinters, jumpers, and throwers) participated in this 8-week supplementation study. A mixed-subject population was selected based on previously published data, which show that men and women both respond to creatine supplementation without gender specific responses (45, 59). Additionally, support for a mixed population design can be found in a recent study looking at creatine supplementation and a mixed population of track athletes undergoing a preseason conditioning program that demonstrated significant ergogenic effects that were manifested as both body mass and performance increases (35). All male subjects were members of the 2001 Southern Conference Indoor Championship Runner-Up Team and the Outdoor Championship Team. All female subjects were members of the 2001 Southern Conference Indoor Championships Team and the Outdoor Championship Runner-Up Team.
All subjects signed informed consent in keeping with American College of Sports Medicine and university guidelines. All subjects agreed to abstain from using any other supplementation (except multivitamins and minerals) during the 7 weeks prior to the investigation. Additionally, none of the subjects included in the investigation was a vegetarian or an anabolic drug user. After the initial testing session, the subjects were randomly assigned to one of three groups. Groups received one of the following treatments: creatine monohydrate (group CM: n = 10, age 19.4 ± 0.3 years, height 175.8 ± 2.5 cm, weight 70.7 ± 3.2 kg); creatine monohydrate and glutamine (group CG: n = 10, age 19.2 ± 0.3 years; height 175.3 ± 2.7 cm; weight 73.5 ± 4.5 kg), or a placebo (potato starch) (group P: n = 9, age 20.1 ± 0.6 years, height 175.0 ± 3.1 cm, weight 72.0 ± 2.7 kg). The three groups were not significantly different based on body mass, height, age, and event. Additionally, there were no statistical differences between the treatment groups for the number of female athletes in each grouping.
Supplementation
The 8-week supplementation period was divided into two phases. The first phase or loading phase required the subjects in the CG group to consume 0.3 g creatine per kilogram body mass per day plus 4 g of glutamine per day for 1 week. The CM group consumed 0.3 g creatine per kilogram body mass per day plus 4 g placebo per day for 1 week. The P group consumed 0.3 g placebo per kg body mass plus an additional 4 g of placebo per day. The second phase (maintenance phase) required the subjects in the CG group to consume 0.03 g creatine per kilogram body mass per day plus 4 g of glutamine for 7 weeks. The CM group also consumed 0.03 g creatine per kilogram body mass per day plus 4 g placebo per day for 7 weeks. The P group consumed 0.03 g placebo per kg body mass plus an additional 4 g of placebo per day for 7 weeks. The creatine supplementation scheme used in the present study is based on the work of Hultman et al. (30). Hultman et al. (30) found that a loading dosage of 0.3 g creatine per kilogram body mass per day for 6 days can significantly elevate muscular stores of creatine. Additionally, it has been reported that after a 6-day loading period, 0.03 g creatine per kilogram body mass per day can maintain muscular stores of creatine at the level achieved in loading (30). The dosage of 4 g;pdd1 glutamine was selected based on the current 4–5 g per day recommendation in the literature exploring glutamine supplementation in low intensity exercise endurance populations (10–12, 46, 49–51).
During the loading phase, subjects were required to report to the Human Performance Laboratory 3 times a day: between 0700 and 1000 hours, at 1500 hours (before practice), and at 1700 hours (immediately after practice) and were observed taking the supplement (22, 35). During the maintenance phase of the study, subjects reported to the laboratory at 1500 hours to receive their supplement. The 4 g of glutamine or placebo was always taken at 1500 hours in both the loading and maintenance phases All supplements were administered in a double-blind fashion and supplied in capsule form to prevent the subjects and researchers from introducing bias into the investigation. Plastic bags containing the supplements were labeled with a subject identification number and supplied to the subjects when they received their treatment (22, 35). On weekends, the subjects were supplied with enough supplements to meet their required dosages. Subjects were required to return the bags with a supplement form, which had their signature, a witness's signature, and the time each dosage was taken (22, 35). Information supplied by Twinlab Inc. (Hauppauge, NY) indicated that the creatine and the glutamine were greater than 90% pure determined by high pressure liquid chromatography methods.
Training Sessions
An 8-week preseason sports specific resistance training program was used to train all of the subjects participating in the present investigation (Table 1 ). The duration of preseason training program was chosen based on previous literature, which has demonstrated significant ergogenic effects when creatine supplementation is utilized during 8 weeks of sport-specific training in elite collegiate athletes (56). There were no differences in the training programs among the three groups. All training sessions were monitored by the research team and track team strength and conditioning coach. Each subject completed a training log, which was collected at the end of each training week. Data from the training logs were analyzed for volume load. Volume load was calculated for each exercise by multiplying repetitions by weight lifted in kilograms (54). Training volume was measured because several authors have suggested that increases in training volume are the main stimuli for the ergogenic effects induced by creatine supplementation (35, 57).
Diet
Three-day diet records (2 weekdays and 1 weekend day) coupled with an interview with our staff dietitian were used during the second, fourth, and sixth weeks of the study. Prior to each data collection, our dietitian discussed portion sizes and diet record techniques with each of the subjects. Three-day diet records were chosen because diet records that last longer than 5 to 6 days appear to cause subjects to alter their eating habits in an attempt to streamline the record-keeping process (41). Data were analyzed by a registered dietitian for total calories and macronutrient content (carbohydrate, protein, and fat) using the Food Processor Plus for Windows, version 6.05 (ESHA Research, Salem, OR) (44). The Food Processor for Plus for Windows was selected based on a recent study, which gave the software package high ratings and reported a low percentage (0.3%) of missing information (40).
Testing Sessions
The subjects were tested on 2 occasions. All tests were performed before the 8-week supplementation period (T1) and at the end (T2) of the study. All variables were measured at T1 and T2.
Subjects reported to the Human Performance Laboratory following an overnight fast and were assessed for body mass, height, and body composition. Body mass was measured to the nearest 0.1 kg on a model 400 Healthometer physician's scale (Continental Scale Corp., Bridgeview IL), and body height was measured to the nearest 0.1 cm with a stadiometer. Body composition (lean body mass and percent fat) was assessed using 2 different methods: a hydrostatic weighing technique and a 7-site skinfold measurement (31, 52). At least 6 underwater weights were measured on each occasion. Three consecutive measures that agreed were used in the data analysis. Residual volume (measured in the same body position by the same tester) was conducted using a multibreath open-circuit nitrogen washout procedure (Cosmed Pulmonary Function Equipment, Rome, Italy). Skinfolds were measured by the same investigator at T1 and T2 and performed using Lange skinfold calipers (Cambridge Scientific Industries, Cambridge, MD). Percent fat was determined using the Siri equation (52). Test-retest reliability for skinfold measures of body composition was R = 0.99, and the reliability of the hydrostatic weighing procedures was found to be R = 0.98.
Static and countermovement vertical jumps were measured with the Vertec (Sports Performance, Columbus, OH) and used to evaluate dynamic explosive strength. Previous research from our laboratory suggests that both static and countermovement vertical jump measures are enhanced with creatine supplementation and serve as an effective measure of dynamic explosive strength (22, 35, 55). All vertical jump methodologies were based on these previous studies.
One week prior to each testing session, all subjects were required to perform a familiarization test consisting of 2 static and 2 countermovement vertical jumps. All subjects were required to perform a standardized warm-up consisting of 1-minute side straddle hops and 2 minutes of light stretching (35). Subjects were then given the opportunity for 1 practice jump. Reach height was then determined with the subjects' feet flat on the ground and arms maximally extended over their heads (35). The last bar of the Vertec, which they could move with their fingertips, was recorded as the reach height. Each subject performed 3 countermovement vertical jumps. During each jump test, the subjects were given a countdown from 3 to 1 and were then instructed to jump on the command “jump” (35). A 1-minute rest was given between each of the jump trials. The depth of knee flexion and arm movements (countermovement) performed by each subject was self-determined. The best value of the three respective jumps was then used for analysis. Following the 3 countermovement vertical jumps, subjects were instructed on proper static vertical jump technique. Briefly, subjects were required to lower to a point at which their upper leg was parallel with the ground. This position was held until the countdown was completed and the jump command was given (35). Three static vertical jumps were performed and the best jump was then used for analysis. The vertical jump displacement was determined by subtracting the reach height from the best jump height achieved during the countermovement and static vertical jump trials. The calculated vertical jump height was then used to determine a power measure (35, 55). The power measure was determined for both the static and countermovement vertical jump with the Lewis formula (55) and Johnson peak and average power equations (32). Vertical jumps were measured T1 and T2 by the same group of testers. Test-retest reliability for the static vertical jump displacement was determined to be R = 0.96, and the test-retest reliability of the countermovement vertical jump displacement was determined to be R = 0.97.
Measurement of power and work was assessed by the use of 5 × 5-second maximum cycle ergometer rides. The present cycle ergometer test was selected based on previous research that suggests that high-intensity repetitive short-duration cycle ergometer bouts are enhanced with creatine supplementation (5, 15, 33, 37). All rides were performed on a Monark cycle ergometer model 868 (Monark-Cresent AB, Barberg, Sweden). Previous research from our laboratory suggests that multiple cycle ergometer rides. One week prior to each testing session all subjects performed a familiarization trial consisting of two 5-second rides. Subjects were required to warm up for 1 minute while pedaling against no resistance (35). The resistance on the ergometer was then set at 0.1 kg;pdkg body mass1. Subject's feet were then taped into the pedals. Once the subject was securely fastened to the ergometer a 2-second burst of pedaling was performed to become familiar with the resistance of the ergometer (35). The Monark cycle ergometer was interfaced with an Apple IIgs (Apple, Cupertino, CA) microcomputer equipped with a Nalandata A2A data acquisition unit and was fitted with electromagnetic switches. The computer was fitted with specifically designed software (Nalan Computer Specialties, Boone, NC) to calculate work and power data (35). Power and work samples were determined each half-pedal revolution with a sample resolution of 4 milliseconds (55). A 50-second recovery period was given between each cycle ride. Values determined by use of the ergometer software included peak power, average peak power, peak power per body mass, average peak power per body mass, average power, and total work. A test-retest reliability of R = 0.98 was determined for both peak and average power on the cycle ergometer. Total and average work on the cycle ergometer was found to have a test-retest reliability of R = 0.97. Additionally, the test-retest reliability of the initial rate of power production was determined to be R = 0.96.
Statistical Analyses
Data were analyzed with a repeated-measures group × trials analysis of variance, with an alpha level of p 0.05. Interactions were tested using paired t-tests and the Holm's sequential Bonferroni method to control for type I errors (29). All values are reported as means ± SEM. Test-retest reliability was assessed with the use of interclass correlations. All statistical analyses were performed with SPSS 10.0 (SPSS, Chicago, IL).
Results Return to TOC
Table 2 depicts the dietary results for the CG, CM, and P treatment groups. Statistical analyses revealed no significant difference between the 2 treatments for kilocalories, carbohydrate, protein, or fat. No significant differences existed within each group from the PRE, MID, and POS measurements.
Body mass and LBM (hydrostatic and skinfolds) increased significantly over time (p < 0.05). A significant interaction showed that both body mass and lean body mass (LBM) (skinfolds) for the CM and CG groups increased more than the P treatment (p < 0.016). However, LBM based on hydrostatic measures did not exhibit a significant interaction. Percent fat and fat mass exhibited no significant changes over time and no interactions (Table 3 ).
The static vertical jump (SVJ) and countermovement vertical jump (CVJ) and tests were used to assess dynamic explosive strength and power. Both CVJ and SVJ displacements increased significantly over time (p < 0.05). However, no significant differences in vertical jump displacement for either CVJ or SVJ existed among the 3 treatment groups. Lewis equation power estimates showed a significant increase over time, but no significant interactions were noted between treatments (Table 4 ).
The peak and average peak cycle power increased significantly from T1 to T2. However, no significant differences existed among the treatment groups. Additionally, when peak and average peak power values were adjusted per kilogram body mass, a significant increase was noted from T1 to T2, with no significance differences among groups. The average power achieved over the 5 rides demonstrated a significant time effect resulting in T2 > T1 and no difference among treatment groups. When average powers were adjusted per kilogram body mass, there was a significant time effect with T2 > T1, with no significant difference existing among treatment groups. A summary of cycle peak and average powers is presented in Table 5 . When examining the peak and average powers generated during the 5 individual rides, there was a significant time effect from T1 to T2 but no significant difference among groups (Figures 1 and 2 ). When looking at the total and average work accomplished over the 5 rides, a significant time effect was noted for all groups, but no significant interactions were noted. Additionally, when looking at total and average work per kilogram body mass, the results for all groups were statistical difference between T1 and T2. No differences existed among treatments (Table 6 ). A significant time effect (p < 0.02) and group-by-time interaction (p < 0.03) was noted for the initial rate data (Figure 3 ), with the CG and CM groups being greater than the P treatment.
When examining the training data, it was determined that no significant differences existed among the CG, CM, and P groups for total volume load and weekly volume load accomplished (Table 7 ).
Discussion Return to TOC
To our knowledge, this is the first study to investigate the effects of combining oral creatine and glutamine supplementation with a preseason strength and conditioning program in an athletic population. We hypothesized that coupling a creatine and glutamine supplementation regime would result in increases in body mass, lean body mass, vertical jump performance, and cycle ergometry performance, compared with a traditional creatine supplementation regimen. However, the results of the present study suggests that the addition of 4 g of glutamine to a creatine supplementation regimen showed minimal effects on body mass, lean body mass, and anaerobic performance, compared with creatine supplementation alone, but both CM and CG treatments resulted in significant increases in LBM, body mass, and initial rate of power production during multiple cycle ergometry bouts, compared with the P treatment. This finding is significant in that glutamine supplementation is very popular among strength power athletes (36) and often suggested to enhance the ergogenic effects of creatine supplementation (17).
In the present study, it was hypothesized that both the CM and CG would result in significantly greater increases in body mass based on consistent findings of a 0.9- to 3.8-kg increase in body mass with creatine supplementation in the scientific literature (3, 4, 13, 16, 19, 20, 35, 38, 39). In the present study, the CM and CG treatments resulted in a significantly greater increase in body mass (CM: +1.7 kg; CG: +2.3 kg) than the P treatment (P: +0.2 kg) over the 8 weeks of supplementation. Generally, the increases in body mass associated with long-term (>8 days) creatine supplementation regimens have been suggested to be a result of increases in protein synthesis (3, 18, 55), which may be manifested as LBM gains. The results of the skinfold data in the present study suggest that both CM and CG supplementation resulted in significant increases in both body mass and LBM when coupled with a strength and conditioning program. These data are in agreement with previously reported research, which suggests that creatine monohydrate increases LBM (22, 55, 63). Based on these findings, CG and CM supplementation regimens have the potential to magnify the body mass and LBM adaptations to a structured strength and conditioning program.
On the basis of the current literature, it was hypothesized that the CG treatment would result in a significantly larger anabolic signal as a result of a larger stimulus by the cellular swelling mechanism (25–27, 64) and result in greater protein synthesis in response to the strength and conditioning program (2). Unexpectedly, the CG treatment group did not experience significantly greater LBM gains, compared with the CM treatment group. However, the CG group experienced a nonstatistically significant absolute body mass increase (CM: +1.7 kg; CG: +2.3 kg) and LBM increase (hydrostatic: CM: +2.4 kg; CG: +2.9 kg; skinfold: CM +2.2 kg; CG: +3 kg), which was greater than that of the CM group. This data might suggest that the addition of 4 g of glutamine to a creatine supplementation regimen is not enough to significantly enhance LBM gains that occur from CM supplementation.
Strength training programs that employ explosive exercises have been shown to result in significant improvements in vertical jump performance (54). Therefore, the significant improvements in both CVJ (CM: +3.8 cm; CG: +3.4 cm; P: +2.5 cm) and SVJ (CM: +2.1 cm; CG: +3.4 cm; P: +1.0 cm) displacements after the 8 weeks of supplementation and training were expected. Several investigations have reported that vertical jump performance can be improved with the combination of a creatine supplementation and a periodized resistance training program (7, 22, 35, 56). However, no difference in the improvement rates of the treatment groups were seen for the SVJ or CVJ performances in the present study, even though all three groups experienced significant gains in jumping performance. Several authors suggest that because vertical jumping tasks takes less than 1 second to complete, it is not likely that the phosphocreatine (PCr) stores are a limiting factor as an energy substrate for this activity (22, 35, 55).
Often the vertical jump performance test is used in an attempt to evaluate power production capabilities (54). Kirksey et al. (35) have reported significant improvements in countermovement vertical jump power outputs in track and field athletes who undertake creatine supplementation protocols in conjunction with a resistance training program. Conversely, Haff et al. (22) have reported that 42 days of creatine supplementation does not alter vertical jump power outputs in track and field athletes. The present study also found no significant differences between the static and countermovement vertical jump power outputs in track and field athletes. However, when looking at the data (Table 4 ) the CG and CM experience nonsignificantly greater gains in CVJ (CM + 8.4%, CG + 7.9%) and SVJ (CM + 6.0%; CG + 7.9%) peak power when compared with the P treatment (CVJ + 4.3%, SVJ + 2.0%). The data of the present study seem to suggest that CM or CG do not favorably alter vertical jump power production capabilities in this population of track athletes.
Repeated anaerobic cycle ergometer tests are another method often used to assess the effects of creatine supplementation on anaerobic power and work capacity because of their ability to stress the phosphagen and glycolytic systems (55). The present study found that 56 days of CM or CG supplementation enhanced the initial rate of power production during 5 × 5-second cycle ergometer performance in track and field athletes. However, there were no significant differences between the CM and CG treatment groups. The results of the present study are similar to those reported by Kirksey et al. (35) for track and field athletes. Kirksey et al (35) reported that 42 days of creatine supplementation results in significant increases in initial rate of power production during 5 sets of 10-second cycle exercise. Additionally, Kirksey et al. (35) demonstrated significant increases in average cycle peak power and cycle average power. However, no differences were seen in the present study among treatment groups for cycle peak power, cycle average power, and total work capacity. The results in the present study are similar to the results reported by Stone et al. (55) for collegiate football players. Because both the present study and the study by Stone et al. (55) used multiple 5-second rides and found no significant increases in cycle ergometer average power production, peak power production, and total work output with creatine, it is possible that the 5 × 5-second test duration was not long enough to significantly stress the phosphagen system.
Hirvonen et al. (28) reported that the PCr concentration is not significantly reduced until the high-intensity effort has been sustained for 5–7 seconds. Because the present cycle ride only lasted 5 seconds, it is likely that only minimal reductions in PCr concentrations were experienced and the recovery time between rides was sufficient enough to restore the ride-induced decrements in PCr. Wootton and Williams (65) have shown that 60 seconds of recovery between multiple cycle rides allows for a maintenance of performance. The present study utilized a 50-second recovery period, and this may partially explain why no differences were seen among the treatment groups. Conversely, Kirksey et al. (35) reported significant increases in cycle performance using 5 × 10-second cycle sprints with 50 seconds of recovery. It is likely that the 10-second ride length explains why Kirksey et al. (35) were able to find significant improvements in cycle performance, but the present study did not.
One limitation to the present study may be the relatively short duration of training (8 weeks). When utilizing trained subjects, it is often difficult to get large alterations in performance over short periods of training (53, 55). However, the present study demonstrates large improvements in vertical jump performance that would suggest that the collegiate athletes tested were not elite. Additionally, the duration of the present study was selected based on several studies, which utilized collegiate athletes (football players and track athletes), lasted 5–8 weeks, and demonstrated that creatine supplementation had significant ergogenic benefits (22, 35, 55, 56). The present study found similar ergogenic benefits as a result of creatine supplementation to those reported in the literature (22, 35, 55, 56).
A second limitation may be the dosage of glutamine selected for use in the present study. Several studies have suggested rather large dosages of glutamine may be need to counteract the fall in muscle protein synthesis and improve nitrogen balance of surgery patients (9, 23, 48). Petersson (48) has suggested that the glutamine dosage may need to be as high as 20 g;pdd1, and Hammarqvist et al. (23) suggest a 0.285 g;pdkg body mass1d1. It is possible that the 4 g dosage selected in the present study was not enough to impact the protein synthesis or protein degradation rates. A larger dosages may be needed when glutamine is consumed orally (9) because approximately 50% of the glutamine absorbed from the gut lumen is metabolized by the gut and lumen (14). However, Candow et al. (9) have found that 45 g·d1 of glutamine supplementation did not enhance muscle protein synthesis and muscular adaptation in response to a resistance training program. Therefore, it is possible that the inclusion of a larger glutamine dosage that ranges between 20–45 g coupled with the creatine supplementation protocol may be needed to magnify the cellular swelling induced anabolic signal for protein synthesis and thus induce greater gains in body mass, LBM, and performance than those reported in the present study.
The mixture of male and female subjects may be an additional limitation of the present study. A mixed-subject population was selected based on previously published data, which show that men and women both respond to creatine supplementation without gender-specific responses (45, 59). Additionally, support for a mixed-population design can be found in 2 recent studies looking at creatine supplementation and a mixed population of track athletes undergoing a preseason conditioning program (22, 35). Both studies demonstrated that creatine can elicit significant ergogenic effects that are manifested as both body mass and performance increases. Based on these studies, the use of a mixed-gender subject population should not significantly alter the ergogenic benefits of either creatine or glutamine.
When looking at the scientific literature it was expected that the CM and CG treatments coupled with a periodized training program would result in significantly greater performance enhancements than those seen in the present study. The lack of difference in performance gains between the treatment groups most likely occurred because of the lack of difference in the volume loads of the treatment groups. Syrotuik et al. (57) have reported that when the training loads and volumes are the same for creatine and placebo treatments, no training advantages occur. This lack of training advantage would then ultimately result in similar alterations in performance among the treatment groups. In the present study, the periodized training programs administered to all the athletes were identical and specified distinct intensities and volumes. After the study it was determined that the total volume load undertaken was not significantly different among the 3 treatment groups. It is very likely that the subjects in the CM and CG treatment groups did not deviate from the prescribed training programs and therefore did not encounter a greater training stimulus. Several authors have suggested that the ergogenic mechanism of creatine is the ability to handle higher training volumes and intensities (35, 57). This phenomenon may partially explain why only marginal performance gains were seen when CM and CG supplementation were undertaken.
The present study seems to suggest that 8 weeks of CM or CG supplementation coupled with an explosive resistance training regimen can lead to positive changes in body composition, body mass, and initial rate of power production during multiple cycle ergometer bouts. At present, the addition of 4 g of glutamine to a CM supplementation protocol does not significantly enhance the benefits of CM supplementation. It is important to note that not all of the mechanisms and ergogenic effects of CM or glutamine are completely understood. More research is required to further understand these mechanisms and effects. Additional research exploring the ergogenic effects and efficacy of glutamine supplementation are needed. Finally, long-term investigations exploring the potential side effects of CM and glutamine supplementation are needed.
Practical Applications Return to TOC
The results of the present study suggest that the CM and CG can have a significant impact on body mass and LBM of track and field athletes who are participating in an 8-week periodized strength training regime. From a practical standpoint, adding 4 g of glutamine to a CM supplementation regimen appears to offer little additional ergogenic effect on body mass or LBM. However, when looking at the trend in the data, it is possible that larger dosages of glutamine may be needed to stimulate the hypothesized increase in body mass and LBM, but this has yet to be substantiated in the scientific literature.
Several investigators have suggested that the main stimulus for improved performance is the ability of creatine to stimulate a situation in which the athlete can train with higher volumes and intensities (35, 57, 63). Based on the present study and data presented by Syrotuik et al. (57), it appears that there is a distinct interaction among training volume, intensity, and the ability of creatine to stimulate improvements in performance. Therefore, athletes who are utilizing CM or CG supplementation in an attempt to improve performance should try to maximize the training stimulus through manipulations of training volume and intensity.
| Lehmkuhl, Mark, Malone, Molly, Justice, Blake, Trone, Greg, Pistilli, Ed, Vinci, Debra, Haff, Erin E., Lon Kilgore, J., Gregory Haff, G. 2003: The Effects of 8 Weeks of Creatine Monohydrate and Glutamine Supplementation on Body Composition and Performance Measures. The Journal of Strength and Conditioning Research: Vol. 17, No. 3, pp. 425–438.
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This finding is significant in that glutamine supplementation is very popular among strength power athletes (36) and often suggested to enhance the ergogenic effects of creatine supplementation (17).
In the present study, it was hypothesized that both the CM and CG would result in significantly greater increases in body mass based on consistent findings of a 0.9- to 3.8-kg increase in body mass with creatine supplementation in the scientific literature (3, 4, 13, 16, 19, 20, 35, 38, 39). In the present study, the CM and CG treatments resulted in a significantly greater increase in body mass (CM: +1.7 kg; CG: +2.3 kg) than the P treatment (P: +0.2 kg) over the 8 weeks of supplementation. Generally, the increases in body mass associated with long-term (>8 days) creatine supplementation regimens have been suggested to be a result of increases in protein synthesis (3, 18, 55), which may be manifested as LBM gains. The results of the skinfold data in the present study suggest that both CM and CG supplementation resulted in significant increases in both body mass and LBM when coupled with a strength and conditioning program. These data are in agreement with previously reported research, which suggests that creatine monohydrate increases LBM (22, 55, 63). Based on these findings, CG and CM supplementation regimens have the potential to magnify the body mass and LBM adaptations to a structured strength and conditioning program.
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Effects of glutamine on whole body and intestinal protein synthesis and on intestinal proteolysis were assessed in humans. Two groups of healthy volunteers received in a random order enteral glutamine (0.8 mmol·kg body wt-1·h-1) compared either to saline or isonitrogenous amino acids. Intravenous [2H5]phenylalanine and [13C]leucine were simultaneously infused. After gas chromatography-mass spectrometry analysis, whole body protein turnover was estimated from traced plasma amino acid fluxes and the fractional synthesis rate (FSR) of gut mucosal protein was calculated from protein and intracellular phenylalanine and leucine enrichments in duodenal biopsies. mRNA levels for ubiquitin, cathepsin D, and m-calpain were analyzed in biopsies by RT-PCR. Glutamine significantly increased mucosal protein FSR compared with saline. Glutamine and amino acids had similar effects on FSR. The mRNA level for ubiquitin was significantly decreased after glutamine infusion compared with saline and amino acids, whereas cathepsin D and m-calpain mRNA levels were not affected. Enteral glutamine stimulates mucosal protein synthesis and may attenuate ubiquitin-dependent proteolysis and thus improve protein balance in human gut.
| Moïse Coëffier, Sophie Claeyssens, Bernadette Hecketsweiler, Alain Lavoinne, Philippe Ducrotté, and Pierre Déchelotte
Enteral glutamine stimulates protein synthesis and decreases ubiquitin mRNA level in human gut mucosa
Am J Physiol Gastrointest Liver Physiol, Jul 2003; 285: G266 - 273. Quote: |
This study used polarized cell line Caco-2 as a model of human enterocytes to determine: 1) whether deprivation of nutrients on the apical (luminal) side of the epithelium (fasting) alters protein synthesis in enterocytes; 2) if so, whether glutamine can attenuate the effects of fasting; and 3) whether the effects of glutamine depend on its route (i.e., apical vs. basolateral) of supply. Caco-2 cells were submitted to nutrient deprivation on the apical side to mimic the effects of fasting, whereas the basolateral side of the epithelium remained exposed to regular medium. Cells were then incubated with [2H3]leucine with or without glutamine, and the fractional synthesis rate (FSR) of total cell protein was determined from [2H3]leucine enrichments in protein-bound and intracellular free leucine measured by gas chromatography/mass spectrometry. A 24-h apical nutrient deprivation (luminal fasting) was associated with a decline in intracellular glutamine, glutamate, and glutathione concentrations (–38, –40, and –40%, respectively), protein FSR (–20%), and a rise in passage of dextran, an index of transepithelial permeability. In fasted cells, basolateral or luminal glutamine supplementation did not alter the glutathione pool, but it restored protein FSR and improved permeability. The effects of glutamine were abolished by 6-diazo-oxo-L-norleucine, an inhibitor of glutaminase, and was mimicked by glutamate. We conclude that in Caco-2 cells, protein synthesis depends on nutrient supply on the apical side, and glutamine regardless of the route of supply corrects some of the deleterious effects of fasting in a model of human enterocytes through its deamidation into glutamate.
| Olivier Le Bacquer, Christian Laboisse, and Dominique Darmaun
Glutamine preserves protein synthesis and paracellular permeability in Caco-2 cells submitted to "luminal fasting"
Am J Physiol Gastrointest Liver Physiol, Jun 2003; 285: G128 - 136. Quote: |
Nuclear, mitochondrial, and plasma membrane events associated with apoptosis were investigated in rat neutrophils cultivated for 3, 24, and 48 h in the absence or presence of glutamine (0.5, 1.0, and 2.0 mM). Condensation of chromatin was reduced after 24 or 48 h of culture in the presence of glutamine compared with its absence as assessed by Hoechst 33342 staining. The level of Escherichia coli phagocytosis in the presence of glutamine was markedly increased compared with the level achieved by cells cultured in the absence of glutamine. Annexin V binding to externalized phosphatidylserine was reduced in the presence of glutamine. Sensitive fluorochrome rhodamine 123, as determined by fluorescence-activated cell sorting and confocal microscopy, was used to monitor loss of the mitochondrial transmembrane potential. In the absence of glutamine, neutrophils exhibited a marked reduction in the uptake of rhodamine 123. In the presence of 1.0 or 2.0 mM glutamine, the uptake of rhodamine was 20 or 38% higher, respectively. Similar effect was found in human neutrophils by measuring DNA fragmentation and mitochondrial transmembrane potential. Therefore, glutamine protects from events associated with triggering and executing apoptosis in both rat and human neutrophils.
| David M. Cohen, Patrick H. Guthrie, Xiaolian Gao, Ryosei Sakai, and Heinrich Taegtmeyer
Glutamine cycling in isolated working rat heart
Am J Physiol Endocrinol Metab, Dec 2003; 285: E1312 - 1316.
Giovanni E. Mann, David L. Yudilevich, and Luis Sobrevia
Regulation of Amino Acid and Glucose Transporters in Endothelial and Smooth Muscle Cells
Physiol Rev, Jan 2003; 83: 183 - 252.
Alberto Bacci, Giulio Sancini, Claudia Verderio, Simona Armano, Elena Pravettoni, Riccardo Fesce, Silvana Franceschetti, and Michela Matteoli
Block of Glutamate-Glutamine Cycle Between Astrocytes and Neurons Inhibits Epileptiform Activity in Hippocampus
J Neurophysiol, Nov 2002; 88: 2302 - 2310.
Barrie P. Bode, Bryan C. Fuchs, Bryan P. Hurley, Jennifer L. Conroy, Julie E. Suetterlin, Kenneth K. Tanabe, David B. Rhoads, Steve F. Abcouwer, and Wiley W. Souba
Molecular and functional analysis of glutamine uptake in human hepatoma and liver-derived cells
Am J Physiol Gastrointest Liver Physiol, Nov 2002; 283: G1062 - 1073.
Natalie His**** and Bente Klarlund Pedersen
Exercise-induced immunodepression- plasma glutamine is not the link
J Appl Physiol, Sep 2002; 93: 813 - 822.
Masafumi Wasa, Hong-Sheng Wang, and Akira Okada
Characterization of L-glutamine transport by a human neuroblastoma cell line
Am J Physiol Cell Physiol, Jun 2002; 282: C1246 - 1253.
Prabhu S. Parimi, Srisatish Devapatla, Lourdes Gruca, Alicia M. O'Brien, Richard W. Hanson, and Satish C. Kalhan
Glutamine and leucine nitrogen kinetics and their relation to urea nitrogen in newborn infants
Am J Physiol Endocrinol Metab, Mar 2002; 282: E618 - 625.
Olivier Le Bacquer, Hassan Nazih, Hervé Blottière, Dominique Meynial-Denis, Christian Laboisse, and Dominique Darmaun
Effects of glutamine deprivation on protein synthesis in a model of human enterocytes in culture
Am J Physiol Gastrointest Liver Physiol, Dec 2001; 281: G1340 - 1347. Quote: |
To assess the effect of glutamine availability on rates of protein synthesis in human enterocytes, Caco-2 cells were grown until differentiation and then submitted to glutamine deprivation produced by exposure to glutamine-free medium or methionine sulfoximine [L-S-[3-amino-3-carboxypropyl]-S-methylsulfoximine (MSO)], a glutamine synthetase inhibitor. Cells were then incubated with 2H3-labeled leucine with or without glutamine, and the fractional synthesis rate (FSR) of total cell protein was determined from 2H3-labeled enrichments in protein-bound and intracellular free leucine measured by gas chromatography-mass spectrometry. Both protein FSR (28 ± 1.5%/day) and intracellular glutamine concentration (6.1 ± 0.6 µmol/g protein) remained unaltered when cells were grown in glutamine-free medium. In contrast, MSO treatment resulted in a dramatic reduction in protein synthesis (4.6 ± 0.6 vs. 20.2 ± 0.8%/day, P < 0.01). Supplementation with 0.5-2 mM glutamine for 4 h after MSO incubation, but not with glycine nor glutamate, restored protein FSR to control values (24 ± 1%/day). These results demonstrate that in Caco-2 cells, 1) de novo glutamine synthesis is highly active, since it can maintain intracellular glutamine pool during glutamine deprivation, 2) inhibition of glutamine synthesis is associated with reduced protein synthesis, and 3) when glutamine synthesis is depressed, exogenous glutamine restores normal intestinal FSR. Due to the limitations intrinsic to the use of a cell line as an experimental model, the physiological relevance of these findings for the human intestine in vivo remains to be determined.
| Karen Krzywkowski, Emil Wolsk Petersen, Kenneth Ostrowski, Jens Halkjær Kristensen, Julio Boza, and Bente Klarlund Pedersen
Effect of glutamine supplementation on exercise-induced changes in lymphocyte function
Am J Physiol Cell Physiol, Oct 2001; 281: C1259 - 1265.
Anthony Blikslager, Elaine Hunt, Richard Guerrant, Marc Rhoads, and Robert Argenzio
Glutamine transporter in crypts compensates for loss of villus absorption in bovine cryptosporidiosis
Am J Physiol Gastrointest Liver Physiol, Sep 2001; 281: G645 - 653
Julio J. Boza, Martial Dangin, Denis Moënnoz, Franck Montigon, Jacques Vuichoud, Andrée Jarret, Etienne Pouteau, Gerard Gremaud, Sylviane Oguey-Araymon, Didier Courtois, Alfred Woupeyi, Paul-André Finot, and Olivier Ballèvre
Free and protein-bound glutamine have identical splanchnic extraction in healthy human volunteers
Am J Physiol Gastrointest Liver Physiol, Jul 2001; 281: G267 - 274.
Tomas Welbourne and Itzhak Nissim
Regulation of mitochondrial glutamine/glutamate metabolism by glutamate transport: studies with 15N
Am J Physiol Cell Physiol, May 2001; 280: C1151 - 1159.
Shama Ahmad, Carl W. White, Ling-Yi Chang, Barbara K. Schneider, and Corrie B. Allen
Glutamine protects mitochondrial structure and function in oxygen toxicity
Am J Physiol Lung Cell Mol Physiol, Apr 2001; 280: L779 - 791
B. Mittendorfer, E. Volpi, and R. R. Wolfe
Whole body and skeletal muscle glutamine metabolism in healthy subjects
Am J Physiol Endocrinol Metab, Feb 2001; 280: E323 - 333. Quote: |
We measured glutamine kinetics using L-[5-15N]glutamine and L-[ring-2H5]phenylalanine infusions in healthy subjects in the postabsorptive state and during ingestion of an amino acid mixture that included glutamine, alone or with additional glucose. Ingestion of the amino acid mixture increased arterial glutamine concentrations by ~20% (not by 30%; P < 0.05), irrespective of the presence or absence of glucose. Muscle free glutamine concentrations remained unchanged during ingestion of amino acids alone but decreased from 21.0 ± 1.0 to 16.4 ± 1.6 mmol/l (P < 0.05) during simultaneous ingestion of glucose due to a decrease in intramuscular release from protein breakdown and glutamine synthesis (0.82 ± 0.10 vs. 0.59 ± 0.06 µmol · 100 ml leg1 · min1; P < 0.05). In both protocols, muscle glutamine inward and outward transport and muscle glutamine utilization for protein synthesis increased during amino acid ingestion; leg glutamine net balance remained unchanged. In summary, ingestion of an amino acid mixture that includes glutamine increases glutamine availability and uptake by skeletal muscle in healthy subjects without causing an increase in the intramuscular free glutamine pool. Simultaneous ingestion of glucose diminishes the intramuscular glutamine concentration despite increased glutamine availability in the blood due to decreased glutamine production.
| Régis G. Hankard, Morey W. Haymond, and Dominique Darmaun
Role of glucose in the regulation of glutamine metabolism in health and in type 1 insulin-dependent diabetes
Am J Physiol Endocrinol Metab, Sep 2000; 279: E608 - 613. Quote: |
To determine the effect of glucose availability on glutamine metabolism, glutamine kinetics were assessed under conditions of hyperglycemia resulting from 1) intravenous infusion of 7.5% dextrose in healthy adults and 2) insulin deficiency in young adults with insulin-dependent diabetes mellitus (IDDM). Eight healthy adults and five young adults with IDDM were studied in the postabsorptive state by use of a primed continuous infusion of D-[U-14C]glucose, L-[5,5,5-2H3]leucine, and L-[3,4-13C]glutamine. Whether resulting from insulin deficiency or dextrose infusion, the rise in plasma glucose was associated with increased glucose turnover (23.5 ± 0.7 vs. 12.9 ± 0.3 µmol · kg1 · min1, P < 0.01 and 20.9 ± 2.5 vs. 12.8 ± 0.4 µmol · kg1 · min1, P = 0.03, in health and IDDM, respectively). In both cases, high blood glucose failed to alter glutamine appearance rate (Ra) into plasma [298 ± 9 vs. 312 ± 14 µmol · kg1 · h1, not significant (NS) and 309 ± 23 vs 296 ± 26 µmol · kg1 · h1, NS, in health and IDDM, respectively] and the estimated fraction of glutamine Ra arising from de novo synthesis (210 ± 7 vs. 217 ± 10 µmol · kg1 · h1, NS and 210 ± 16 vs. 207 ± 21 µmol · kg1 · h1, NS, in health and IDDM, respectively). When compared with the euglycemic day, the apparent contribution of glucose to glutamine carbon skeleton increased when high plasma glucose resulted from intravenous dextrose infusion in healthy volunteers (10 ± 0.8 vs. 4.8 ± 0.3%, P < 0.01) but failed to do so when hyperglycemia resulted from insulin deficiency in IDDM. We conclude that 1) the contribution of glucose to the estimated rate of glutamine de novo synthesis does not increase when elevation of plasma glucose results from insulin deficiency, and 2) the transfer of carbon from glucose to glutamine may depend on insulin availability.
| Gianni Biolo, Fulvio Iscra, Alessandra Bosutti, Gabriele Toigo, Beniamino Ciocchi, Onelio Geatti, Antonino Gullo, and Gianfranco Guarnieri
Growth hormone decreases muscle glutamine production and stimulates protein synthesis in hypercatabolic patients
Am J Physiol Endocrinol Metab, Aug 2000; 279: E323 - 332.
Michelle Timmerman, Cecilia Teng, Randall B. Wilkening, Paul Fennessey, Frederick C. Battaglia, and Giacomo Meschia
Effect of dexamethasone on fetal hepatic glutamine-glutamate exchange
Am J Physiol Endocrinol Metab, May 2000; 278: E839 - 845.
M. Abely, P. Dallet, M. Boisset, and J. F. Desjeux
Effect of cholera toxin on glutamine metabolism and transport in rabbit ileum
Am J Physiol Gastrointest Liver Physiol, May 2000; 278: G789 - 796.
Toshiki Okada, Yukinaga Watanabe, Saul W. Brusilow, Richard J. Traystman, and Raymond C. Koehler
Interaction of glutamine and arginine on cerebrovascular reactivity to hypercapnia
Am J Physiol Heart Circ Physiol, May 2000; 278: H1577 - 1584.
M. Haisch, N. K. Fukagawa, and D. E. Matthews
Oxidation of glutamine by the splanchnic bed in humans
Am J Physiol Endocrinol Metab, Apr 2000; 278: E593 - 602.
Timothy M. Pawlik, Rüdiger Lohmann, Wiley W. Souba, and Barrie P. Bode
Hepatic glutamine transporter activation in burn injury: role of amino acids and phosphatidylinositol-3-kinase
Am J Physiol Gastrointest Liver Physiol, Apr 2000; 278: G532 - 541.
N. C. Jackson, P. V. Carroll, D. L. Russell-Jones, P. H. Sönksen, D. F. Treacher, and A. M. Umpleby
Effects of glutamine supplementation, GH, and IGF-I on glutamine metabolism in critically ill patients
Am J Physiol Endocrinol Metab, Feb 2000; 278: E226 - 233. |
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