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1 Copenhagen Muscle Research Centre and Department of Infectious Diseases, and 2 Department of Orthopedic Medicine and Rehabilitation, Rigshospitalet, 2200 Copenhagen N, Denmark; and 3 Nestlé Research Center CH100, Lausanne, Switzerland
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 O2 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
+ and
CD3+TCR
+ 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.
training; physical activity; immunology; natural killer cells
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