Glutamine is an non-essential amino acid produced in all tissues of the body. However the liver and skeletal muscles are the most important sites of synthesis quantitatively. The role of glutamine in physiological regulation of both skeletal muscle protein and glycogen stores is well reported but the mechanisms are not entirely clear. During times of catabolism, the skeletal muscle stores of glutamine fall, and during times of anabolism, these pools can increase in size. However, the cause and effect of this relationship may be complex. Depletion of muscle glutamine stores are associated with reductions in plasma levels, and this may compromise the immune system as glutamine is the prefered fuel substrate for macrophages and lymphocytes. During times of glutamine depletion from skeletal muscle, supplements of L-glutamine are able to increase plasma levels, and uptake to skeletal muscle subsequently increases. As stores of glutamine increase glycogen synthesis and protein synthesis rates also increase.
High levels of muscle glutamine may stimulate the activity of glycogen synthases phosphatases and this in turn may dephosphorylate glycogen synthase, one of the main glycogen synthesising enzymes. Dephosphorylation of glycogen synthase increases its activity and this increases the rate of glycogen synthesis. In addition, glutamine is a glucogenic amino acid. Deamination of its two nitrogen groups allows the carbon skeleton of glutamine to feed into the gluconeogenic pathway and in this way glutamine can act as a substrate for the production of new glucose. This new glucose can then either be converted to glycogen, if the pathway is present in the skeletal muscle, or pass from the cells into the blood to maintain plasma levels of blood glucose, in the case of the liver. In this way glutamine is pivotal in maintaining muscle and liver glycogen as well as plasma levels of blood glucose, and depletion of glutamine pools may interfere with the homeostatic balance of these systems.
Oral L-glutamine appears effective at increasing skeletal muscle glycogen synthesis rates. For example, in one study1, researchers deplete the glycogen stores of healthy subject through exhaustive exercise. Following the exercise, which involved cycling at mixed workloads, the subjects consumed either 330 mL of an 18.5 % glucose polymer drink, 8 grams of L-glutamine in 330 mL water or 8 grams of L-glutamine in an 18.5 % glucose polymer drink, just before undergoing a radiolabelled glucose infusion for 2 hours. The researchers used the radiolabeled glucose to assess the rates of glucose disposal, which would include both oxidation and glycogen storage. Both L-glutamine containing drinks increase plasma glutamine concentrations significantly and in the subsequent 2 hours, whole body glycogen synthesis rates increased 25 % in both glutamine treatments. The glucose and glutamine drink also promoted the storage of glycogen outside of skeletal muscle, most likely in the liver.
Dr Robert Barrington’s Nutritional Recommendation: Around 8 grams of L-glutamine appear to be as effective at stimulating glucose disposal and subsequently glycogen synthesis rates. This may relate to the ability of glutamine to directly regulate the dephosphorylation enzymes that control glycogen synthesis as well as through an ability of the alpha-keto acid of glutamine (its deaminated carbon skeleton) to act as a precursor to glucose through the gluconeogenic pathway. Oral L-glutamine is safe and readily mixed with water and can easily be mixed into post workout nutrition drinks in order to take advantage of these beneficial effects. The ability of glutamine to regulate glycogen synthesis and glucose production may explain the reports that oral L-glutamine is able to decrease sugar cravings. If sugar cravings are caused by either low glycogen levels or low plasma concentrations of glucose, glutamine may be able to increase both of these pools of glucose and thus switch of appetite stimulatory signals from the hypothalamus.
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