Bk. Pedersen et al., EXERCISE-INDUCED IMMUNOMODULATION - POSSIBLE ROLES OF NEUROENDOCRINE AND METABOLIC FACTORS, International journal of sports medicine, 18, 1997, pp. 2-7
Acute muscular exercise induces an increased neutrophil count concomit
ant with recruitment of natural killer (NK), B and T cells to the bloo
d as reflected by an elevation in the total lymphocyte count. Meanwhil
e, following intense exercise of long duration the lymphocyte count de
clines, non-MHC-restricted cytotoxicity is suppressed, but the neutrop
hil concentration increases. In relation to eccentric exercise involvi
ng muscle damage, the plasma concentrations of interleukin-1, interleu
kin-6 and the tumor necrosis factor are elevated. In this review we wi
ll propose a model based on the possible roles that stress hormones pl
ay in mediating the exercise-related immunological changes: adrenaline
and to a lesser degree noradrenaline are responsible for the immediat
e effects of exercise on lymphocyte subpopulations and cytotoxic activ
ities. The increase in catecholamines and growth hormone mediate the a
cute effects of exercise on neutrophils, whereas cortisol may be respo
nsible for maintaining lymphopenia and neutrocytosis after exercise of
long duration. Lastly, the role of beta-endorphin is less clear, but
the cytokine response is closely related to muscle damage and stress h
ormones do not seem to be directly involved in the elevated cytokine l
evel. Other possible mechanisms of exercise-induced immunomodulation m
ay include the so-called glutamine hypothesis, which is based on the f
act that skeletal muscle is an important source of glutamine productio
n and that lymphocytes are dependent on glutamine for optimal growth.
Furthermore, physiological changes during exercise, e.g. increased bod
y temperature a nd decreased oxygen saturation may also in theory cont
ribute to the exercise-induced immunological changes.