Marathon Race Affects Neutrophil Surface Molecules: Role of Inflammatory Mediators
Neutrophil Extracellular Traps
Creatine kinase
DOI:
10.1371/journal.pone.0166687
Publication Date:
2016-12-02T13:27:14Z
AUTHORS (18)
ABSTRACT
The fatigue induced by marathon races was observed in terms of inflammatory and immunological outcomes. Neutrophil survival activation are essential for inflammation resolution contributes directly to the pathogenesis many infectious conditions. aim this study investigate effect on surface molecules related neutrophil adhesion extrinsic apoptosis pathway its association with markers. We evaluated 23 trained male runners at São Paulo International Marathon 2013. following components were measured: hematological mediators, muscle damage markers, function. race an increased leukocyte counts; creatine kinase (CK), lactate dehydrogenase (LDH), CK-MB, interleukin (IL)-6, IL-10, IL-8 levels. C-reactive protein (CRP), IL-12, tumor necrosis factor (TNF)-α plasma concentrations significantly higher 24 h 72 after race. Hemoglobin hematocrit levels decreased also intercellular molecule-1 (ICAM-1) expression decreasedTNF receptor-1 (TNFR1) immediately DNA fragmentation L-selectin Fas receptor expressions recovery period, indicating a possible slow rolling phase delayed apoptosis. racing affects neutrophils course inflammation, supporting "open-window" post-exercise hypothesis.
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