08-04-2005, 05:23 PM
I took the liberaty of colleting a few recent studies on glutamine.
Piattoly et al. (2004) examined the influence of Glutamine on time to exhaustion and power before and after a prolonged bout of exercise. All participants performed All participants performed a Graded Exercise Test and two Wingate tests on a cycle ergometer after a period of rest to assess Peak Power, Mean Power, and Fatigue Index. Results found that glutamine had a positive effect on these performance variables. They concluded that, “Participants in the Glutamine group increased time to exhaustion following 6 days of supplementation, and appeared to recover from exhaustive exercise earlier than the placebo group.”
Medicine & Science in Sports & Exercise: Volume 36(5) Supplement May 2004 p S127
L-Glutamine Supplementation: Effects on Recovery from Exercise
Piattoly, Tavis; Welsch, Michael A.
Here is a quote from:
Medicine & Science in Sports & Exercise: Volume 32(7) Supplement July 2000 pp S377-S388
Glutamine and arginine: immunonutrients for improved health
FIELD, CATHERINE J.; JOHNSON, IAN; PRATT, VERA C.
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The acute effects of intense aerobic and anaerobic exercise on immune parameters are well established (54). Although the total number of leukocytes in peripheral circulation increases with acute exercise, transient immunosuppression occurs, as indicated by changes in the CD4/CD8 ratio and the ability of lymphocytes to respond in various ways to immune challenges (41). The immune response to an acute bout of exercise is influenced by both the duration and intensity of the exercise (54). These factors should always be considered when reviewing literature that examines the role of supplemental gln in athletes. Additionally, the functional significance of exercise-induced immunomodulation to infection risk is not clear. It has been reported that the incidence of infections in sedentary individuals can be decreased by moderate, regular exercise but athletes undergoing repeated physical stress (such as that occurs in prolonged training or endurance sports) appear to suffer an increased incidence of infections (23,54,77,92,93,100,116).
Estimates of the biochemical origins of plasma gln in healthy individuals have suggested that approximately 40% of gln comes from protein and the remaining 60% from de novo synthesis (from other amino acids and carbon intermediates, found primarily in muscle (51)). Therefore, muscle (the protein and de novo synthesis source) serves as a labile store of fuel for activated lymphocytes (89). Indeed in severely stressed states, providing gln can maintain muscle gln concentrations (140). Thus, it is logical to predict that providing gln will improve or at least maintain muscle gln concentrations in athletes. Recently, it was suggested (91) that the high demand for gln by the immune system during exercise may contribute to the observed increase in amino acid catabolism with exercise (53). Additionally, it is hypothesized that over-training may reduce the release of gln from muscle, thus contributing to lower plasma gln concentrations reported in athletes diagnosed with the over-training syndrome (99). Epinephrine and cortisol, at physiological levels (that occur during exercise), alter the rate of protein degradation in skeletal muscle, inhibit gln release from muscle (60), and suppress immune function (19). With exhaustive prolonged exercise, there is a decrease in muscle gln levels in both the rat (53) and in man (104). After athletic injury this decrease may be even more magnified as the acute effects of glucagon, adrenaline and cortisol stimulate the net efflux of gln from muscle (105). Abnormal eating patterns, in some athletes, could also contribute to a gln debt, as muscle amino acid concentrations and oxidation rates are depressed in protein deficient states (82). In any of these situations, acute decreases in muscle gln concentrations would reduce the rate of muscle protein synthesis and potentially limit gln availability to the immune system. By using this evidence and data that exercise, particularly intense prolonged exercise, limits gln availability to immune cells, gln supplementation has been recommended by several research groups for athletes who undergo intense exercise programs (25,116).
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Krieger et al. (2003) examine the effects of chronic glutamine supplementation on sIgA concentration and output during an overreaching program. Participants consisted of runners who exercised twice-daily using interval training for 9-9.5 days, followed by 5-7 days of recovery. Participants ingested glutamine or a placebo 4 times a day for 14 days. Results found that glutamine supplementation attenuated the decline in nasal IgA with training. They concluded taht “Chronic glutamine supplementation during strenuous training may attenuate changes in nasal IgA output.”
There is also a large amount of evidence that glutamine can immensely assist myofibril hydration, which is imperative. You stated you wanted some full texts, so here are some quotes from one:
Effect of glutamine on water and sodium absorption in human jejunum at baseline and during PGE1-induced secretion
Moďse Coëffier, Bernadette Hecketsweiler, Philippe Hecketsweiler, and Pierre Déchelotte
J Appl Physiol 98: 2163-2168, 2005. First published January 20, 2005;
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Glutamine, a major fuel for enterocytes, stimulates water and sodium absorption in animal models of secretory diarrhea, but data in humans are still limited. The aim of this study was to investigate the effect of glutamine on jejunal absorption during hypersecretion in humans. In six healthy adults, the effects of glutamine on jejunal absorption were assessed with a triple-lumen tube on two occasions, at baseline and during PGE1-induced hypersecretion (0.1 µg•kg–1•min–1) in a random order. Isoosmolar solutions containing polyethylene glycol 4000 as nonabsorbable marker were infused in the jejunum at 10 ml/min over 1-h periods: saline (sodium chloride 308 mmol/l), glucose-mannitol 45:45 mM, glucose 90 mM, alanine-glucose 45:45 mM, glutamine-glucose 45:45 mM, and glutamine 90 mM. Net absorptive and secretory fluxes were measured at steady state. At baseline, glutamine- and alanine-containing solutions induced a threefold increase of water and sodium absorption (P < 0.05); 90 mM glutamine stimulated water absorption more than 90 mM glucose (3.6 ± 0.6 vs. 1.9 ± 0.3 ml•min–1•30 cm–1, P < 0.05). PGE1-induced hypersecretion was reduced (P < 0.05) by solutions of alanine-glucose, glutamine-glucose, and glutamine 90 mM (P < 0.05) and reversed to absorption by alanine-glucose and glutamine-glucose. Glutamine and alanine absorption was nearly complete and was not influenced by PGE1. In conclusion, glutamine stimulates water and electrolyte absorption in human jejunum, even during experimental hypersecretion. In addition to the metabolic effects of glutamine, these results support the evaluation of glutamine-containing solutions for the rehydration and the nutritional support of patients with secretory diarrhea.
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ORAL REHYDRATION THERAPY, the main way of treating dehydration due to diarrhea, is based on the cotransport of sodium with glucose (14), which is maintained in acute secretory diarrhea of diverse etiologies (e.g., Cryptosporidium parvum, cholera toxin) (30). Despite its efficacy, improvements of the glucose-based oral rehydration solution (ORS) are needed, both to enhance its efficacy and reduce the stool output and to provide a more adequate nutritional support to patients often malnourished in developing countries (25). Improvement of glucose-ORS could be achieved either by low osmolality of solutions (16, 40) or by addition of amino acids promoting intestinal transport (7).
Indeed, neutral amino acids and dipeptides are cotransported with Na+ in the intestine by carriers that are different from the glucose-galactose carrier and may thus be added to the glucose-sodium ORS. Glutamine has been identified as a potential candidate to supplement or replace glucose in ORS (7, 23, 34). It was reported that L-glutamine stimulates sodium intestinal absorption in animals by a distinct and additive mechanism to that of glucose (29) and that this promising effect was maintained to some extent in animals with experimental diarrhea (33, 37). In addition, glutamine supports the metabolism of intestinal epithelial cells both as a major fuel and as a precursor for nucleic acid synthesis (39). Finally, glutamine is a major nitrogen carrier in vivo and plays a key role in the regulation of intestinal protein turnover (9) and lipolysis (12).
We previously reported the characteristics of L-glutamine absorption in human jejunum (12). In the present study performed in healthy subjects, the effect of L-glutamine on water and electrolyte jejunal absorption was assessed by means of an intestinal infusion method and was compared with the effects of glucose and alanine, at baseline and during an experimentally induced hypersecretion achieved by intrajejunal infusion of PGE1.
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The present study demonstrates that glutamine is able to promote absorption more potently than glucose and that both substrates may be used in an additive way. Moreover, the stimulating effect of glutamine is maintained during an experimental stimulation of secretion mimicking a secretory diarrhea.
The intestinal infusion technique is an established method to assess water and electrolyte transport in human intestine and the effects of specific substrates, both in healthy humans (14, 15, 20) and diarrheic patients (4, 28, 41). The triple-lumen tube method used in this study is more accurate than the double-lumen tube to measure segmental fluxes (4, 27). The intrinsic limitation of the intestinal infusion technique comes from the limited length of intestine under study, which does not allow a definite extrapolation of data on the full length of intestine. However, the jejunum is a major site for intestinal absorption, and most of nutrients are absorbed up to 75% over 50 cm of jejunum (42); more specifically, glutamine is absorbed almost 70% over 30 cm jejunum (12); thus the present study on 30 cm already gives a reasonable estimate of the major part of glutamine-related water and electrolyte absorption. Hypersecretion induced by PGE1 was chosen because infusion of PGE1 in human jejunum induces a reproducible pattern of water and electrolyte secretion, which resembles much that of cholera (4, 26). Moreover, intestinal hypersecretion induced by cholera enterotoxin may be mediated in part by an increased local production of prostaglandins (2, 41). The infusion rate of PGE1 used in this study (0.1 µg•kg–1•min–1) was selected to induce a marked hypersecretion, yet without saturation of secretory pathways (38). The resulting water secretion (Fig. 2) was in the medium range of that reported in the jejunum of cholera patients (4).
The effects of glutamine on water and electrolyte absorption have been well established in experimental models. Indeed, glutamine stimulates sodium and water absorption in rabbit (1, 19, 29, 37), bovine (5, 10), porcine (2, 32, 33), or rat small intestine (24) under basal conditions and during hypersecretion. In these models, hypersecretion was induced by cholera toxin (1, 24, 37), cryptosporidiosis (2, 5, 10), rotavirus (33), or enteropathogenic Escherichia coli (29). In cholera-infected humans, glutamine in the presence of glucose reduced net water and sodium secretion to the same degree as glucose alone (41). Nevertheless, the effects of glutamine alone were not tested (41). In infants with acute noncholera diarrhea, a glutamine-enriched ORS did not provide any additional therapeutic advantage over the standard ORS, possibly because the total osmolarity of this experimental ORS was too high (34). Indeed, hypoosmolar solutions could be more efficient (17).
In the present study, the 90 mM glutamine solution stimulated sodium and water segmental absorption more potently than the 90 mM glucose solution in baseline. Because coupling ratios between sodium and both solutes are similar, this could be explained in part by a higher segmental absorption of glutamine compared with glucose (Table 3). In vitro studies with Ussing chambers have suggested that glutamine stimulates to a variable extent both electrogenic sodium absorption and electroneutral NaCl absorption (1, 29, 32). These two components of sodium transport cannot be distinguished in vivo. However, the superiority of glutamine over glucose could come in part from its ability to promote chloride absorption and consequently electroneutral NaCl absorption, whereas glucose effect is limited to the electrogenic glucose-sodium cotransport. In hypersecretion-induced conditions, gln:glc and gln90 increased water and sodium absorption compared with saline, whereas glc90 did not significantly affect fluxes. With the glutamine-glucose solution, the net water and sodium absorptive fluxes were about twofold those observed with glucose. This result confirms in vitro experiments (13, 29, 31) showing that glutamine and glucose have additive effects on sodium absorption, which reflects the existence of separate sodium-solute cocarriers for glucose and glutamine at the apical membrane of enterocytes (31), with no competitive effect of glucose on glutamine intestinal absorption (13).
The alanine-glucose ORS also stimulated water and sodium absorption, which is in accordance with previous data (24, 41). The effects of alanine-glucose and glutamine-glucose solutions on sodium absorption were almost identical, suggesting that at the tested amino acid concentration (45 mM), sodium absorption results mainly from a solute-sodium cotransport of similar capacities. It has been suggested in some experiments that alanine and glutamine may be transported by the same carrier in rat enterocytes (6), but other studies indicate that glutamine transport may be carried by several distinct Na+-dependent (A, N, Y+) and Na+-independent (L) transport systems, whereas alanine is transported mainly by the Na+-dependent ASC system (31). During a secretory diarrhea induced by cholera toxin in rats (24), an experimental ORS containing the dipeptide alanyl-glutamine was more effective than a glutamine-containing ORS on water and sodium absorption; this could be explained by a stronger effect of the dipeptide on sodium absorption compared with any constitutive single amino acid (31), by the additive effects of alanine and glutamine generated by the intraluminal hydrolysis of the dipeptide, or by the effect of a proton/dipeptide cotransport (11). Alanyl-glutamine containing ORS have not been evaluated in humans.
In the present study, an apparent stoichiometric ratio of about 1:1 for sodium-glucose and glutamine-glucose cotransport has been estimated, which is in accordance with classical experiments in rabbit ileum but probably underestimates the true absorptive glutamine:sodium ratio; other studies have suggested that a ratio of 2:1 was closer to the actual transepithelial influxes (3, 5, 13, 20, 29). Indeed, glutamine transport across intestinal brush-border membrane is only partly sodium dependent (36). Thus the actual Na+-glutamine coupling ratio is probably higher than 1.2:1 at baseline and than 1.7:1 at the hypersecretory state, because of an enhanced paracellular Na+ efflux (33).
Finally, glutamine was almost completely absorbed along the 45-cm-long jejunal segment. This confirms our previous observations that, in this range of infusion rate (27 and 54 mmol/h), glutamine absorption is ~70% over 30 cm jejunum (12). The estimated Km for glutamine absorption in human jejunum is 2.3 mmol/min, i.e., 139 mmol/h (12); thus even the highest infusion rate in the present study is far from saturating glutamine absorption. Interestingly, glutamine absorption was not affected by experimental hypersecretion (Table 3); this is in accordance with experimental studies showing maintained glucose (8) or glycine (21) absorption during cholera and with the clinical observations that glucose- or amino acid-linked sodium absorption is maintained in cholera patients (4, 28). Glucose and alanine were also almost completely absorbed, even during PGE1 infusion; only a very high PGE1 infusion rate decreased glucose absorption ~25% in other studies (26).
In conclusion, glutamine promotes sodium absorption in human jejunum both at baseline and during hypersecretion, an effect that is additive to that of glucose. Moreover, glutamine absorption is maintained during hypersecretion. Thus, in addition to its beneficial effect on intestinal fluid and electrolyte transport, glutamine could be efficiently administered to diarrheic patients via the enteral route, as a specific component of the nutritional therapy of associated malnutrition.
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Here is a quote from my article:
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Glutamine has been shown to enhance cellular hydration, which is absolutely vital to athletic performance . SY Low et al. tested the connection between glutamine transport, and cellular hydration . He induced glutamine uptake into rat myotubes at osmolalities of 170, 320 or 430 mosmol. Glutamine at 320 mosmol increased cell volume by 36%. When insulin was administrated, it additionally enhanced cell volume by 22%, and glutamine transport by 40%. They noted that the effects of both glutamine and insulin were additive to cell volume. At 170 mosmol there was also a huge increase in cell volume and glutamine transport. At 430 mosmol, however, cell volume and glutamine transport was diminished. These benefits were attributed to an increase in the Na(+)-dependent glutamine transport system.
To elaborate on this, glutamine uses a sodium transport system, which results in osmotic cellular swelling. This is vital for post-workout oral rehydration! To test this hypothesis, Rhoads et al. gave 30 mmol/L of glutamine to his participants . It was shown that glutamine stimulated large amounts of electrogenic and electro neutral NaCl absorption rates. This would likewise result in a major increase in cellular water absorption. They concluded that glutamine is an effective method of oral re-hydration. Such knowledge can be applied to several scenarios, most importantly, post-workout nutrition. Moreover, using patients with diarrhea, Van Loon et al. tested several oral rehydration solutions . He utilized 3 groups: glucose, sodium (group 1), sodium, glucose, and glutamine (group 2), or alanine, glucose, and salt (group 3). The glutamine, sodium, glucose group was the most proficient one, showing a significant reduction in water and sodium secretion, while increasing fluid absorption.
Another experiment by Islam S et al. showed glutamine, in his words, is “superior to glucose in stimulating water and electrolyte absorption .” Bold talk for a one-eyed fat man! Oops; excuse me, been watching to many John Wayne movies, but I digress. Islam did, however, back his words up with results. He applied 50 mM of L-glutamine (group 1) and 50 mM D-glucose (group 2) to electrolyte water solutions. He found that the absorption of water (P = 0.000), sodium (P = 0.002), potassium (P = 0.001), and chloride (P = 0.003) from the glutamine electrolyte solution was much greater than from the glucose electrolyte solution in the ileum. He concluded that, “L-glutamine may be a useful component to be tested in oral re-hydration solutions.” Now, considering that glucose greatly benefits oral re-hydration, especially when accompanied with sodium, due to the Glucose/Sodium co transport system [134, 80, 81, 82, 83], this gives immense support to glutamine supplementation post-exercise. And when you take into account Van Loon’s findings, you see that taking both glucose and glutamine will give you the best of both worlds.
These findings are of the utmost importance to post-workout nutrition. For more on the anabolism of cellular swelling, refer to, Effect of Plasma Volume on Myofibril Hydration, Nutrient Delivery, and Athletic Performance. Lastly, to understand the sodium transport systems mentioned above, you will want to read, Sodium - A comprehensive Analysis.
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The amount of research on this is quote extensive, and has found that in basal and in dehydrated states, glutamine can assist hydration, making it an excellent supplement post exercise.
Lagranha et al. (2005) investigated the effect of a single bout of intensive exercise on rat neutrophil function and the possible effect of glutamine supplementation. This was building of their previous study, which showed the “protective effect of glutamine on neutrophil apoptosis induced by acute exercise.” Results found that glutamine supplementation, sigifigantly increased phagocytosis; further, the decrease nitric oxide production induced by exercise was abolished and production of reactive oxygen species was raised. They concluded that “Glutamine supplementation presents a significant effect on neutrophil function including changes induced by exercise. “
The effect of glutamine supplementation on the function of neutrophils from exercised rats.
Lagranha CJ, de Lima TM, Senna SM, Doi SQ, Curi R, Pithon-Curi TC.
Cell Biochem Funct. 2005 Mar-Apr;23(2):101-7.
Iwa****a1*, et al. (2005) investigated the interaction of glutamine availability and glucose homeostasis during and after exercise. You said you wanted full texts, so here is there intro:
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Glutamine is one of the most abundant free amino acids found in the body,
playing a central metabolic role during many important biological processes, such as
immune function (15), neurological activity (19), and the development and maintenance
of gastrointestinal integrity (15). The skeletal muscle glutamine pool is significantly
reduced under several types of metabolic stress (15), providing a basis for glutamine to
be referred to as a “conditionally essential” amino acid.
Whether glutamine availability is limiting during and after the stress of exercise is
not uniformly clear. This may partially be due to differences in study design, including
the length and intensity of exercise, or the fact that some investigators report values for
blood and some for muscle and a glutamine concentration gradient exists between blood
and muscle. Circulating glutamine has been demonstrated to increase with exercise (4).
However, others have shown that muscle glutamine progressively decreases with exercise
in swimming rats (10), circulating glutamine decreases in running dogs (13), and the net
loss of glutamine from muscle is greater with exercise in both dogs (35) and humans (12).
After exercise, however, the majority of data suggest that glutamine availability is
reduced, particularly after strenuous exercise (13). This has led to the hypothesis that
reduced circulating glutamine may be an indicator of exercise stress and overtraining (21,
Even less is known about the role glutamine availability plays in exercise-related
metabolism. Recent studies have suggested important interactions between glutamine
and carbohydrate homeostasis (3, 5, 20, 23, 30). Glutamine carbon has potential to enter
the Krebs cycle through -ketoglutarate, thereby providing carbon for gluconeogenesis
(1). Glutamine has also been shown to interact with glucose utilization, stimulating
whole body glucose utilization and hindlimb glucose uptake during hyperinsulinemiceuglycemia
in post-absorptive dogs (5).
Exercise elevates whole body glucose utilization to meet fuel demands in both
exercising and non-exercising tissues (14, 31, 33). On the other hand, the liver responds
to exercise by increasing glucose production to meet these increased demands for glucose
(31, 33). After exercise, glucose production and utilization initially remain elevated and
insulin sensitivity is enhanced to facilitate glycogen replenishment in the liver and
skeletal muscle tissues (22, 26, 28). Although glutamine appears to interact with glucose
production and utilization, it has not been elucidated whether glutamine influences
glucose production and utilization during and after exercise. Furthermore, while there is
considerable commercial interest in using glutamine as an ergogenic aid, few studies
have investigated the interactions of glutamine with glucose metabolism during and after
exercise (7, 32).
Therefore, the following study was conducted to test the hypotheses that 1)
increased glutamine availability would further stimulate glucose production and
utilization during exercise and 2) increased glutamine availability after exercise would
enhance glucose production and insulin-mediated glucose utilization. Therefore, to
investigate the interactions between glutamine availability and glucose metabolism
during and after exercise, isotope dilution and organ balance techniques were used in
exercising multicatheterized dogs. The exercise period represents the influence of
glutamine during a situation when both glucose production and utilization are stimulated.
In the post-exercise period, a hyperinsulinemic-euglycemic clamp technique was used to
represent a condition similar to post-exercise carbohydrate supplementation, when
accelerated glycogen repletion is beneficial, but glucose production is blunted by insulin.
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I discuss this benefit of glutamine extensively min my article—take a look.
Anyway, here was there experiment.
Participants received a glutamine or salin solution. Results found that “GLN increased glucose utilization by 16% compared to salin after exercise (p<0.05). Furthermore, net hindlimb glucose uptake in the post-exercise period was increased ~2- fold versus basal with GLN (p<0.05), but not with salin. Net hepatic uptake of glutamine during the post-exercise period was three-fold greater for GLN than salin (p<0.05).” They concluded that “n conclusion, glutamine availability modulates glucose homeostasis during and after exercise, which may have implications for post-exercise recovery.”
However, this study was on dogs, but similar results have been seen in both canines and humans.
The Impact of Glutamine Supplementation on Glucose Homeostasis During and After Exercise
Soh Iwa****a1*, Phillip Williams2, Kareem Jabbour2, Takeo Ueda3, Hisamine Kobayashi3, Shawn Baier1, and Paul J Flakoll4 J Appl Physiol (July 21, 2005).
You will notice almost all of these studies aer around 2005, and some even got released in July! Glutamine is getting more and more support each day.
You will notice almost all of these studies are around 2005, and some even got released in July! Glutamine is getting more and more support each day.
Concerning contradictory studies. What must be understood is that humans are noisy (which means variable, in motor terms). This leads to conflicting results in almost any investigations on any topic; including well established sups such as Creatine. Further, methodologies often skew the results because they are poorly designed, and or do not investigate enough variables.
For instance, I have yet to see on study on exercise that is even near to the amount of volume of my workouts. I have seen studies do bench press three times a week, 3 sets per workout, and then conclude glutamine supplementation is worthless during exercise! I us more glutamine in a week just from making my food lol. /forum/images/graemlins/tongue.gif
Further, studies have found that carbs play an important role in sparing glutamine. This is intuitive, as carbohydrates spare proteins, and glutamine is no exception For instance, Blanchard et al. (2001) investigated the relationship between muscle glutamine, muscle glycogen, and plasma glutamine concentrations over 3 d of high-intensity exercise during which dietary carbohydrate (CHO) intake varied. Five endurance-trained men completed two exercise trials in randomized order, over a 14-d period. Each trial required subjects to perform 50 min of high-intensity continuous and interval exercise on three consecutive days while consuming a diet that provided 45% of the energy as CHO or a diet in which CHO provided 70% of the total energy. Results found that plasma glutamine concentration was significantly higher during the 70% CHO exercise trial when compared with the 45% CHO trial (P < 0.05). This suggests again, that during dieting situations, in which carbohydrates are often extremely low, supplementing with glutamine may be of immense benefit.
The influence of diet and exercise on muscle and plasma glutamine concentrations.
Medicine & Science in Sports & Exercise. 33(1):69-74, January 2001.
BLANCHARD, MICHELLE A.; JORDAN, GREGORY; DESBROW, BENJAMIN; MACKINNON, LAUREL T.; JENKINS, DAVID G.
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As well as being influenced by exercise, plasma glutamine levels may also vary with changes in dietary intake (4,5,9,14,16). Gleeson et al. (4) investigated the relationship between carbohydrate (CHO) intake, plasma glutamine, and circulating lymphocytes; subjects exercised twice for 60 min at 70% maximal oxygen uptake (O2max): once after consumption of a normal diet and once after 3 d on either a high (75%) or low (4%) CHO diet. Exercise after the low CHO diet resulted in lower postexercise plasma glutamine concentration when compared with the high CHO diet. In addition, circulating lymphocyte counts were lower after exercise on the low CHO diet.
Zanker et al. (16) examined several variables including changes in plasma glutamine concentration in response to 60 min of running after an exercise and diet regime intended to deplete muscle glycogen. Subjects performed two trials: both involved two exhaustive exercise bouts separated by 14 h of dietary manipulation. In one trial, subjects were fed an 80% CHO meal, whereas in the other they fasted. Post- exercise increases in plasma glutamine concentration were observed after exercise in the fed group, though no changes were noted in the fasted group. Although muscle glycogen was not measured, the authors suggested that increased glycogen availability after the high CHO meal had stimulated glutamine synthesis and release from skeletal muscle. However, they also suggested that a greater stress on amino acid metabolism, rather than a reduced release of glutamine from glycogen-depleted skeletal muscle may have been primarily responsible for the postexercise decline in plasma glutamine. This was supported by the fact that there was no apparent decrease in plasma glutamine in the glycogen-depleted state, but rather an increase in plasma glutamine in the fed state. Their data indicate that glutamine release from muscle was similar under both conditions and that the observed increase in plasma glutamine in the fed state was due to some other factor.
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So from my studies, there is a multitude of evidences which support supplementation of glutamine for hard-core athletes. And present studies continue to support this notion. Are there contradictor studies? Certainly, but perhaps with better methodologies, such as an increased workload, and long term studies, more participants, etc. the findings will be more consistent.
And there are more studies I could have shown. But I think this makes an adequate argument for glutamine, in addition to my article, and numerous other posts on the topic.
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