Platelet Activation Favours NOX2-Mediated Muscle Damage in Elite Athletes: The Role of Cocoa-Derived Polyphenols

Abstract

Mechanisms of exercise-induced muscle injury with etiopathogenesis and its consequences have been described; however, the impact of different intensities of exercise on the mechanisms of muscular injury development is not well understood. The aim of this study was to exploit the relationship between platelet activation, oxidative stress and muscular injuries induced by physical exercise in elite football players compared to amateur athletes. Oxidant/antioxidant status, platelet activation and markers of muscle damage were evaluated in 23 elite football players and 23 amateur athletes. Compared to amateurs, elite football players showed lower antioxidant capacity and higher oxidative stress paralleled by increased platelet activation and muscle damage markers. Simple linear regression analysis showed that sNOX2-dp and H2O2, sCD40L and PDGF-bb were associated with a significant increase in muscle damage biomarkers. In vitro studies also showed that plasma obtained from elite athletes increased oxidative stress and muscle damage in human skeletal muscle myoblasts cell line compared to amateurs’ plasma, an effect blunted by the NOX2 inhibitor or by the cell treatment with cocoa-derived polyphenols. These results indicate that platelet activation increased muscular injuries induced by oxidative stress. Moreover, NOX2 inhibition and polyphenol extracts treatment positively modulates redox status and reduce exercise-induced muscular injury.

Natural Activators of Autophagy Reduce Oxidative Stress and Muscle Injury Biomarkers in Endurance Athletes: A Pilot Study

“…A previous study demonstrated that polyphenol-rich nutrient supplementation with dark chocolate positively modulated redox status and reduced exercise-induced muscular injury biomarkers in elite football athletes [ 30 ]. Moreover, in vitro studies support the positive effect of cocoa-derived polyphenols, as skeletal muscle myoblast cell lines treated with polyphenol extracts displayed decreased oxidative stress and muscle injury biomarker levels [ 5 ].…”

“…These changes were coincident with increased levels of biomarkers of muscle injury such as LDH, CK, and myoglobin [ 30 ]. Moreover, elite football players compared to amateurs displayed increased concentrations of dopamine, which plays a key role in favoring platelet activation and in promoting NOX2-mediated oxidative stress, ultimately favoring muscle injury [ 5 ].…”

“…In these mice, completely abolished ROS production was observed after an acute moderate-intensity treadmill exercise [ 4 ]. Moreover, our group demonstrated that elite athletes who practiced highly intensive sports displayed higher levels of NOX2, paralleled by a significant reduction in antioxidant capacity activation, compared to amateur athletes [ 5 ]. These data support the role of NOX2 as a major source of ROS generation during exercise.…”

New light on changes in the number and function of blood platelets stimulated by cocoa and its products

“…Another recent paper by D’Amico et al (2022) studied the relationship between blood platelet activation, oxidative stress and muscular injuries stimulated by physical exercise, as well as the role of cocoa-derived phenolic compounds, in elite athletes. Their results suggest that the cocoa-derived phenolic compounds: catechin and epicatechin significantly reduce oxidative stress and muscle injury in supernatants of human skeletal muscle myoblast cell cultures treated with plasma.…”

Polyphenol Supplementation and Antioxidant Status in Athletes: A Narrative Review

“…The oxidative burst is mediated by NADPH oxidase, which produces O 2 - and H 2 O 2 [ 77 ], and these products achieve their cytotoxic effects due to reactions with other antimicrobial systems to generate ROS [ 67 , 78 ]. In skeletal muscle cells in culture, two primary NADPH oxidase isoforms (NOX2 and NOX4) [ 79 ] were found to be the main sources of ROS [ 80 , 81 ]. Thus, the role of NADPH oxidase-derived ROS is important in pathogen-mediated and sterile inflammation (i.e., without pathogen involvement).…”