Tissue damage, myocardial injury and recruitment of mature and banded neutrophils after high-intensity endurance exercise

Abstract

Neutrophils are key players in inflammatory responses that are modulated by cytokines/chemokines and damage associated molecular patterns (DAMPs). Exercise induces acute neutrophilia, but little is known regarding recruitment of neutrophil subsets (banded (CD16dim/CD62Lbright) and hypersegmented (CD16bright/CD62Ldim) cells) and its relation with the liberation of markers of tissue damage. The aim of this study was to investigate the neutrophil compartment in response to a single bout of high-intensity endurance exercise and the association with tissue damage, cortisol and myocardial injury. Blood samples were prospectively collected from 35 athletes participating in a long-distance trail-run (before, directly after, and 24 h after exercise) for biomedical analysis. The neutrophil compartment was directly analyzed in the field by automated, mobile, flow cytometry. Linear regression analyses were performed for neutrophil (subset) counts vs markers of tissue damage (CK, LDH, and AST), cortisol and markers of cardiac injury. Neutrophilia was present directly after exercise, with the appearance of banded and hypersegmented neutrophils. This was accompanied by increased levels of markers of tissue damage, cortisol and cardiac troponins. Increased cortisol levels showed a positive correlation with the increase in cell counts of both banded and mature neutrophils. This correlation was not found for hypersegmented neutrophils. No relations were found between the neutrophil (subsets) and markers of tissue damage or cardiac troponins. This study demonstrates the recruitment of 3 distinct neutrophil subsets following a single bout of high-intensity endurance exercise. These results indicate an association between neutrophil recruitment after exercise and cortisol levels, rather than tissue damage or cardiac injury.