Marathon Race Affects Neutrophil Surface Molecules: Role of Inflammatory Mediators

Abstract

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.

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1. Effect of the marathon race on muscle damage markers and CRP.

The plasma was separated before, immediately after, 24 h after, and 72 h after the marathon race. The plasma activities of LDH (A), CK (C), CK-MB (D), and plasma levels of CRP (B) were determined. The values presented are the mean ± SEM of 23 runners.a p<0.001 vs before the marathon race, b p<0.0001 vs immediately after the marathon race, and c p<0.01 vs 24 h after the marathon race.

Fig 2. Effect of the marathon race on plasma cytokines.

Plasma concentrations of IL-6 (A), IL-8 (B) IL-10 (C), IL-12 (D), and TNF-alpha (E) were determined using cytometric bead array. The values presented are the mean ± SEM of 23 runners.ap<0.05 vs before the marathon race, bp<0.05vs immediately after the marathon race, and c p<0.05 vs 24 h after the marathon race.

Fig 3. Effect of the marathon race on hematological parameters.

Total leukocyte number (A), neutrophil number (B), hematocrit (C), and hemoglobin (D) were determined before, immediately after, 24 h, and 72 h after the marathon race. The values presented are the mean ± SEM of 23 runners.ap<0.05 vs before the marathon race, bp<0.05 vs immediately after the marathon race, and cp<0.05 vs 24 h after the marathon race.

Fig 4. Effect of the marathon race on neutrophil surface molecules and DNA fragmentation.

Neutrophils were separated after blood collection before, immediately after, 24 h after, and 72 h after the marathon race. Expression of ICAM-1 (A), TNFR1 receptor (B), L-selectin (C), and Fas receptor (D), and % of cells with DNA fragmentation (D) were determined. The fluorescence was determined by flow cytometry (BD Accuri cytometer). The values presented are the mean ± SEM of 21 runners. a p<0.05 vs before the marathon race, b p<0.05 vs immediately after the marathon race, and cp<0.05 vs 24 h after the marathon race.

Fig 5. Model on the temporal dynamics of the cytokine’s responses to the marathon race.