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Exercise-induced immunodepression- plasma glutamine is not the link.
Hiscock N, Pedersen BK.
Copenhagen Muscle Research Centre and Department of Infectious Diseases, Rigshospitalet, University of Copenhagen, DK-2100 Copenhagen, Denmark.
The amino acid glutamine is known to be important for the function of some immune cells in vitro. It has been proposed that the decrease in plasma glutamine concentration in relation to catabolic conditions, including prolonged, exhaustive exercise, results in a lack of glutamine for these cells and may be responsible for the transient immunodepression commonly observed after acute, exhaustive exercise. It has been unclear, however, whether the magnitude of the observed decrease in plasma glutamine concentration would be great enough to compromise the function of immune cells. In fact, intracellular glutamine concentration may not be compromised when plasma levels are decreased postexercise. In addition, a number of recent intervention studies with glutamine feeding demonstrate that, although the plasma concentration of glutamine is kept constant during and after acute, strenuous exercise, glutamine supplementation does not abolish the postexercise decrease in in vitro cellular immunity, including low lymphocyte number, impaired lymphocyte proliferation, impaired natural killer and lymphokine-activated killer cell activity, as well as low production rate and concentration of salivary IgA. It is concluded that, although the glutamine hypothesis may explain immunodepression related to other stressful conditions such as trauma and burn, plasma glutamine concentration is not likely to play a mechanistic role in exercise-induced immunodepression.
PMID: 12183472 [PubMed - indexed for MEDLINE]
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Albo:
Effect of glutamine supplementation on exercise-induced changes in lymphocyte function.
Krzywkowski K, Petersen EW, Ostrowski K, Kristensen JH, Boza J, Pedersen BK.
Copenhagen Muscle Research Centre and Department of Infectious Diseases, Rigshospitalet, 2200 Copenhagen N, Denmark.
The purpose of this study was to investigate the possible role of glutamine in exercise-induced impairment of lymphocyte function. Ten male athletes participated in a randomized, placebo-controlled, double-blind crossover study. Each athlete performed bicycle exercise for 2 h at 75% of maximum O(2) consumption on 2 separate days. Glutamine or placebo supplements were given orally during and up to 2 h postexercise. The trial induced postexercise neutrocytosis that lasted at least 2 h. The total lymphocyte count increased by the end of exercise due to increase of both CD3(+)TCR alpha beta(+) and CD3(+)TCR gamma delta(+) T cells as well as CD3(-)CD16(+)CD56(+) natural killer (NK) cells. Concentrations of CD8(+) and CD4(+) T cells lacking CD28 and CD95 on their surface increased more than those of cells expressing these receptors. Within the CD4(+) cells, only CD45RA(-) memory cells, but not CD45RA(+) naive cells, increased in response to exercise. Most lymphocyte subpopulations decreased 2 h after exercise. Glutamine supplementation abolished the postexercise decline in plasma glutamine concentration but had no effect on lymphocyte trafficking, NK and lymphokine-activated killer cell activities, T cell proliferation, catecholamines, growth hormone, insulin, or glucose. Neutrocytosis was less pronounced in the glutamine-supplemented group, but it is unlikely that this finding is of any clinical significance. This study does not support the idea that glutamine plays a mechanistic role in exercise-induced immune changes.
PMID: 11546663 [PubMed - indexed for MEDLINE]
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Natomiast badania w których suplementacja glutaminą wypada korzystnie - przeprowadzane są na myszach...