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Marathon Race Affects Neutrophil Surface Molecules: Role of Inflammatory Mediators

2016; Public Library of Science; Volume: 11; Issue: 12 Linguagem: Inglês

10.1371/journal.pone.0166687

1932-6203

Vinícius Coneglian Santos, Ana Sierra, Rodrigo Oliveira, Kim Guimarães Caçula, César Miguel Momesso, Fábio Takeo Sato, Maysa Braga Barros Silva, Heloisa Helena de Oliveira, Maria Elizabeth Pereira Passos, Diego Ribeiro de Souza, Olivia Santos Gondim, Marino Benetti, Adriana Cristina Levada‐Pires, Nabil Ghorayeb, Maria Augusta Peduti Dal ́Molin Kiss, Renata Gorjão, Tânia Cristina Pithon‐Curi, Maria Fernanda Cury‐Boaventura,

High Altitude and Hypoxia

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