As a precursor to glutathione (together with cysteine and glycine), L-GIn can assist in ameliorating the oxidation that occurs during metabolic stress. Glutathione protects epithelial cell membranes from damage, and its depletion can negatively affect gut barrier function and result in severe degeneration of colonic and jejunal epithelial cells (lantomasi 1994, Ziegler et al 1999). In animal studies it has also been shown to inhibit fatty acid oxidation, resulting in a reduction in body weight and alleviation of hyperglycaemia and hyperinsulinaemia in mice fed a high-fat diet (Opara et al 1996).
As L-GIn is stored primarily in skeletal muscles and becomes conditionally essential under conditions of metabolic stress, the anticatabolic/anabolic properties of supplemented L-GIn are likely due to a sparing effect on skeletal muscle stores.
Following strenuous exercise, glutamine levels are depleted by approximately 20%, resulting in immunodepression (Castell 2003, Castell & Newsholme 1997, Rogero et al 2002). As a result supplemental L-GIn may be of benefit in athletes to prevent the deleterious effects of glutamine depletion associated with 'over-training syndrome'. Evidence supporting a direct ergogenic effect is currently lacking.
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