Department of Movement, Human and Health Sciences, University of Rome "Foro Italico", 00135 Rome, Italy.
Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome, 04100 Latina, Italy.
Nutrients. 2022 Apr 8;14(8):1558. doi: 10.3390/nu14081558.
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 HO, 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.
运动引起的肌肉损伤的机制及其发病机制已经描述过;然而,不同强度的运动对肌肉损伤发展机制的影响尚不清楚。本研究旨在探讨与精英足球运动员和业余运动员相比,血小板激活、氧化应激与运动引起的肌肉损伤之间的关系。评估了 23 名精英足球运动员和 23 名业余运动员的氧化应激/抗氧化状态、血小板激活和肌肉损伤标志物。与业余运动员相比,精英足球运动员的抗氧化能力较低,氧化应激水平较高,同时血小板激活和肌肉损伤标志物增加。简单线性回归分析显示,sNOX2-dp 和 HO、sCD40L 和 PDGF-bb 与肌肉损伤生物标志物的显著增加相关。体外研究还表明,与业余运动员的血浆相比,来自精英运动员的血浆可增加人骨骼肌成肌细胞系的氧化应激和肌肉损伤,而 NOX2 抑制剂或用可可衍生的多酚处理细胞可减轻这种作用。这些结果表明,血小板激活增加了氧化应激引起的肌肉损伤。此外,NOX2 抑制和多酚提取物处理可正向调节氧化还原状态并减少运动引起的肌肉损伤。