论文标题
能量代谢改变的代谢组措施介导炎症性miRNA与大学足球运动员的运动控制的关系
Metabolomic measures of altered energy metabolism mediate the relationship of inflammatory miRNAs to motor control in collegiate football athletes
论文作者
论文摘要
最近的研究表明,短期和长期接触运动的暴露可能会产生有害的神经系统作用。在本研究中,代谢组分析与炎症miRNA定量,计算行为,虚拟现实(VR)测试运动控制以及头部碰撞事件监测,以探索整个大学球员对人类行为的跨性能和碰撞影响。我们将基于置换的统计数据与中介分析集成在一起,以测试miRNA,代谢物和VR任务性能之间的复杂,定向关系。在季前赛(n = 6)(n = 6)和整个季节(n = 8)中发现了14个显着介体(代谢物=介体; miRNA =自变量=因变量),SOBEL P值小于或等于0.05,并且在或超过50%的总效应。大多数调解发现涉及长到中链脂肪酸(2-Hg,8-Hoa,UND,甲苯二甲酸酯,甲虫和七生)。同时,在季后赛相对于季前赛时,发现TCA代谢产物明显下降。 HAE与季节中的代谢组措施和miRNA水平有关。总之,这些观察结果表明,慢性HAE诱导的神经炎症(作为升高的miRNA的证据)和线粒体功能障碍(如FAS和TCA代谢物异常所观察到的),从而产生了神经学功能的细微变化(如运动不良的运动控制行为所观察到的微妙变化)。这些发现表明,线粒体代谢的转变,远离线粒体功能,与其他被分类为线粒体疾病的疾病一致,这表明接触体育和潜在的治疗干预措施中的HAES基础机制具有合理的机制。
Recent research has shown there can be detrimental neurological effects of short- and long-term exposure to contact sports. In the present study, metabolomic profiling was combined with inflammatory miRNA quantification, computational behavior with virtual reality (VR) testing of motor control, and head collision event monitoring to explore trans-omic and collision effects on human behavior across a season of players on a collegiate American football team. We integrated permutation-based statistics with mediation analyses to test complex, directional relationships between miRNAs, metabolites, and VR task performance. Fourteen significant mediations (metabolite = mediator; miRNA = independent variable; VR score = dependent variable) were discovered at preseason (N=6) and across season (N=8) with Sobel p-values less than or equal to 0.05 and with total effects at or exceeding 50%. The majority of mediation findings involved long to medium chain fatty acids (2-HG, 8-HOA, UND, sebacate, suberate, and heptanoate). In parallel, TCA metabolites were found to be significantly decreased at postseason relative to preseason. HAEs were associated with metabolomic measures and miRNA levels across-season. Together, these observations suggest a state of chronic HAE-induced neuroinflammation (as evidence by elevated miRNAs) and mitochondrial dysfunction (as observed by abnormal FAs and TCA metabolites) that together produce subtle changes in neurological function (as observed by impaired motor control behavior). These findings point to a shift in mitochondrial metabolism, away from mitochondria function, consistent with other illnesses classified as mitochondrial disorders, suggesting a plausible mechanism underlying HAEs in contact sports and potential avenue for treatment intervention.