Abstract des Autors

Exercise-induced changes of immunological parameters are closely related to hormonal responses and metabolic changes. Exercise leads to an activation of the sympathetic nervous system and is consecutively followed by a mobilization of leukocytes from the marginal into the circulating blood pool. The extent of demargination is dependent on exercise intensities and the individual anaerobic threshold represents a physiological breakpoint. Increasing cortisol levels are followed by a neutrocytosis due to a recruitment of cells from the bone marrow. At the same time homing of lymphocytes into tissues is responsible for the lymphocytopenia. Natural killer cells increase most during exercise and may decrease by 50% compared to pre-exercise counts. Duration of exercise is more important for these effects than intensity. Reports about the impact of exercise on proliferative responses of T- and B-lymphocytes as well as cytotoxicity of natural killer cells are contradictory. Monocytes are activated slightly and play a central role in the exercise-induced acute-phase-response. Oxidative burst activity of neutrophils is suppressed by intensive aerobic exercise and anaerobic training sessions, but enhanced after moderate bouts of exercise. In summary, exercise is capable to modulate innate immunity. This modulation is physiological. Type, intensity and duration of exercise are important variables. Adaptive immunity does not seem to be influenced as much as innate immune functions. In comparison to changes of cell counts - as an indicator of impaired cell trafficking - modulations of immune functions are relatively small. In healthy individuals exercise does not induce pathological responses of the immune system. Also, there is no immunosuppression comparable with classical immune defects. One important question for the sports medical practice cannot yet be answered. This question deals with the impact of exercise on the immune system and other organs like the heart during common infections to prevent athletes i.e. from myocarditis. Verf.-Referat