Exercise and hypoxia: effects on leukocytes and interleukin-6-shared mechanisms?

Stress-induced immunological reactions to exercise have stimulated much research into stress immunology and neuroimmunology. It has been suggested that exercise can be employed as a model of temporary immunosuppression, which occurs during physical stress, such as hypoxia. Acute exercise and acute hypoxia mediate in principle identical effects on circulating lymphocyte and neutrophil numbers. Thus, during exercise and hypoxia, lymphocytes are recruited to the blood. After the stress, the number of lymphocytes declines after the stress, whereas the neutrophil number continues to increase. When exercise is performed during hypoxia, the exercise-induced immune changes are pronounced. There is some evidence that the exercise- and hypoxia-induced changes in leukocyte subpopulations are mediated by neuroendocrinological factors such as catecholamines, growth hormone, and cortisol. In contrast, although exercise, as well as hypoxia, is associated with increased plasma levels of IL-6, the mechanisms are not likely to be the same. Thus, during exercise, contracting skeletal muscles are the main source of IL-6 production, whereas the source of IL-6 during hypoxia has not been demonstrated. The increased level of adrenaline contributes to the enormous increase in plasma IL-6 only to a minor degree during strenuous exercise. However, the only modest increase in IL-6 during hypoxia may be linked to hormonal changes, whereas the prolonged increase in IL-6 during chronic hypoxia is likely to be multifactorial.