Purpose: Intense exercise bouts are associated with a reduction of immune function and increased susceptibility to infections. Neutrophils act as a first line of defense to eliminate infectious agents and are also involved in muscle tissue inflammatory response to exercise. Intensive exercise suppresses several neutrophil functions including chemotaxis. The study investigates the pathophysiological mechanisms of impaired chemotaxis after submaximal aerobic exercise.
Methods: Twenty-three healthy physically active adult males were tested before and 24 h after 30 min of treadmill running at 75% V˙O2max. N-formyl-Met-Leu-Phe (fMLP)-stimulated neutrophil migration, polarization, adherence, expression of adhesion molecules (CD11b/CD18), and chemotactic receptor (C5aR) were assessed preexercise and postexercise.
Results: Neutrophil chemotaxis and polarization were found to be impaired 24 h postexercise. Adherence was impaired 24 h postexercise as well, but the expression of the adhesion molecule CD11b/CD18 was not affected. Further, the availability of the C5aR was found to be unaffected 24 h postaerobic exercise.
Conclusions: The pathophysiological mechanism of the impaired chemotaxis is likely related to the impaired postexercise neutrophil adherence and polarization but not to changes in the chemotactic receptor availability.