Exercise and lymphocyte functions

Although exercise induces an increase in the absolute number of leukocytes and changes the lymphocyte subpopulation profile, the functional impact of exercise on immune effectors is equivocal. While there have been an increasing number of investigations in this area, the results are difficult to compare because of variations in protocol methodology, the confounding of exercise effects by circadian hormone patterns, and the heterogeneity in exercise capacity among subjects. These limitations notwithstanding, a number of general patterns emerge regarding exercise and lymphocyte responses.

The most well-characterized lymphocyte response to exercise is that of the cellular proliferation response to mitogens and antigens in vitro. The ability of lymphocytes to proliferate to classical T cell mitogens (phytohemagglutinin (PHA), concanav-alin A (con A)) is decreased immediately after exercise but returns to baseline levels within 24 h; the proliferative response to B cell mitogens (lipopoly-saccharides, LPS) or mixed T-B cell mitogens (pokeweed mitogen, PWM) increases post-exercise. These proliferative changes do not appear to reflect altered function or activation of individual lymphocytes but are rather due to concurrent numerical changes in lymphocyte subsets. Natural killer (NK) cell (i.e. CD56+/CD16 + ) function is markedly affected by exercise above 60% V02max; in vitro cytolvsis of 51Cr-labeled tumor cells is suppressed after intense exercise which is due to decreased numbers of NK cells in blood and prostaglandin-mediated suppression. The influence of a single bout of exercise on modulating antibody synthesis is minimal. In trained athletes, high-intensity endurance exercise is associated with a decrease in salivary IgA levels after exercise; levels of secretory IgA in nasal washings remain unchanged. In contrast, basal levels of serum IgG, IgM and IgA, and the capacity to produce antibody to tetanus toxoid antigen is not compromised by exercise.

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