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Strenuous, acute exercise affects reciprocal modulation of platelet and polymorphonuclear leukocyte activities under shear flow in men
Author(s) -
Wang JS.,
Chow SE.,
Chen JK.
Publication year - 2003
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1046/j.1538-7836.2003.00350.x
Subject(s) - platelet , platelet activation , medicine , endocrinology , nitric oxide , chemistry
Summary.  Vigorous exercise transiently increases the risk of primary cardiac arrest. The reciprocal modulation of platelet and polymorphonuclear leukocyte (PMN) activities is important in the pathogenesis of thrombosis. This study investigates how strenuous, acute exercise affects platelet–PMN reciprocal modulation by closely examining 18 sedentary men who exercised strenuously on a bicycle ergometer. Shear‐induced platelet activation, PMN interaction with surface‐adherent platelets under shear flow, and PMN‐dependent inhibition of platelet activation were measured both before and immediately after exercise. Analytical results can be summarized as follows: (i) shear‐induced platelet adhesion on fibronectin‐coated surface as well as ADP‐induced release of platelet soluble P‐selectin release and elevation of [Ca 2+ ] i significantly increases after strenuous exercise; (ii) strenuous exercise is associated with higher velocity and percentage of rolling PMNs and lower numbers of PMNs remaining bound to surface‐adherent platelets under shear flow than at rest; (iii) PMN‐dependent inhibition of platelet [Ca 2+ ] i elevation and soluble P‐selectin release after strenuous exercise is much greater than that at rest; and (iv) strenuous exercise increases PMN‐derived nitric oxide metabolite level and reduces oxidized low‐density lipoprotein‐promoted interaction between platelets and PMNs. Therefore, we conclude that platelet activity may be sensitized by strenuous exercise. However, strenuous exercise can also simultaneously enhance the antiplatelet effect of PMNs. The finding provides a new insight into the negative feedback of PMNs against exercise‐evoked platelet‐related thrombotic risk.

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