Strenuous, acute exercise suppresses polymorphonuclear leukocyte respiratory burst under adherence to surface-adherent platelets in men.

Interaction between polymorphonuclear leukocyte (PMN) and platelets is important in the pathogenesis of thrombosis and inflammation. This study investigates how strenuous, acute exercise affects PMN oxidative burst activity under adherence to surface-adherent platelets. Thirty sedentary healthy men exercised strenuously (up to maximal oxygen consumption) on a bicycle ergometer. Before and immediately after exercise, the kinetics of oxidant production, phosphorylation of various protein kinase C (PKC) isoforms, and translocation of p47(phox) in PMNs under adherence to surface-adherent platelets were measured using fluorescence microscopy combined with computerized image analysis. Analytical results can be summarized as follows: (i) either treating the platelet with P-selectin (CD62P) and glycoprotein IIb/IIIa (CD41) antibodies or treating the PMN with beta 2-integrin (CD18) and Mac-1 (CD11b) anti-bodies and PKC zeta pseudosubstrate effectively inhibits platelet-promoted oxidant production of PMN; (ii) PMNs adhesion to surface-adherent platelets is associated with a higher amount of phospho-PKC zeta and a larger ratio of membrane to cytosolic p47(phox) than suspended PMNs; (iii) strenuous, acute exercise decreases platelet-promoted oxidant production of PMN and is accompanied by suppressed phosphorylation of PKC zeta, translocation of p47(phox), and inhibition of PKC zeta pseudosubstrate to oxidant production; (iv) no significant changes occur in PKC alpha/beta II and delta phosphorylation of adherent PMNs following this exercise. Therefore, we conclude that strenuous, acute exercise suppresses platelet-promoted oxidative burst of PMN, possibly by reducing phosphorylation of PKC zeta and translocation of the cytosolic p47(phox) to the plasma membrane, thus inhibiting the assembly and activation of NADPH oxidase in PMN.