Neuroendocrine mediators in the modulation of phagocytosis by exercise: physiological implications.

Neuroendocrine mediation of the effects of exercise on macrophage and neutrophil phagocytosis, the organism's first line of defense against external aggression, is reviewed. Exercise modulates the immune system via the actions of "stress hormones". Although stress had long been regarded as generally immunosuppressive, it is now accepted that this is not always true. Indeed exercise-induced stress stimulates the "phagocytic process" of phagocytes. One of the new physiological interpretations emerging from recent studies is that the general stimulation of phagocytosis and other innate mechanisms during strenuous physical activity may counterbalance the decreased lymphoid activity, preventing the entry and survival of microorganisms in situations where the specific responses are depressed. In some cases this behaviour is also medicated by "stress hormones", unlike in lymphocytes in which glucocorticoids and catecholamines both are immunosuppressive. The mediatory role of glucocorticoids in macrophages may also differ between the non-specific functions, like chemotaxis and phagocytosis, and the more specific ones, like antigen-presentation. Neutrophils and monocytes may be stimulated by catecholamines or sympathetic signals, and variations in phagocytosis and catecholamines have been proposed as a good "neuroimmuno-endocrinological marker" in athletes. Other hormones (prolactin, GH, endorphins, thyroid hormones) in general also contribute to the effects of exercise-stress on phagocytosis. This review focuses on a physiological interpretation of the immune response to exercise which differs markedly from the classical immunosuppression-centered view. More studies on in vivo variations of stress hormones during exercise are needed.