短跑训练神经肌肉功能重塑再生机制和科学监控研究进展

Research Progress of Mechanism and Monitoring of Neuromuscular Function Remodeling and Regeneration in Sprint Training

目的:神经肌肉系统将训练刺激转换为长期适应性变化的能力是短跑运动训练可塑性的重要生物学基础。本文拟对短跑训练诱发神经肌肉功能重塑和代谢适应性变化相关分子机制和最新研究方法进行系统分析探讨。方法:采用最新文献研究和前瞻性分析相结合的方法,本文对短跑训练神经肌肉功能重塑及适应性代谢变化的关键影响因素进行分类整理和归纳分析,并对代谢组学应用于短跑训练机体适应性变化及疲劳发生的有效监控和干预进行研究展望。结果:脑源性神经营养因子(BDNF)等运动因子能够以旁分泌方式在调控肌肉卫星干细胞分化和神经肌肉系统功能重塑发挥关键作用;Ca^(2+)离子通路及p53/PGC-1α、AMPK、p38MAPK等线粒体生物发生和能量代谢调节的关键分子是介导短跑训练通过表观遗传变化诱导运动表现提升和能量代谢稳态调控网络的重要靶点。根据专项特点有针对性地进行整合间歇训练、速度力量训练和连续循环训练的高强度功能性训练(HIFT),以均衡方式对神经肌肉及心血管多系统产生整体训练负荷刺激,能够更有效诱发BDNF表达和分泌,激活表观遗传学关键通路,在提高短跑训练生理适应性(氧利用率及能量代谢)及神经系统可塑性方面均产生了积极效应,对于神经肌肉功能及控制能力和运动损伤预防等短跑训练的主要限制性因素具有潜在改善作用。而基于液相色谱串接质谱联用(LC-MS/MS)等的非靶向代谢组学技术通过对关键性差异代谢物和相关分子通路系统性分析,为短跑训练中科学监控能量稳态调控以及神经肌肉功能恢复和再生提供了有效途径。结论:运动可促进肌肉等组织以自分泌、旁分泌和/或内分泌方式,通过肌肉—器官交互作用(cross-talk)产生运动生理学效应,发挥调控神经肌肉功能重塑、提高运动认知和适应性、改善线粒体能量代谢稳态等作用。随着基于运动诱发表观遗传学基因靶点和关键代谢物变化的组学分析技术发展,能够更全面、灵敏、系统地反映运动训练过程中机体整体代谢适应性变化及规律,进而对科学化监控和运动疲劳有效预防和干预提供依据和技术支撑。

OBJECTIVE:The ability of the neuromuseular system to convert training stimuli into long-term adaptive changes is an important biological basis for the plasticity of sprinting training.This paper aims t systematically analyze and discuss the molecular mechanism and the latest rescarch methods of sprint training induced neuromuscular functional remnodeling and met abolie adaptation.METHODS:Through the combination of the latest literature research and prospective analysis,the key factors aecting the remodeling of neuromuscular function and adaptive metabolic changes in sprinting training were classfed,summarized and analyzed,and the effective monitoring and intervention of the application of metabolomics to the adaptive changos and fatigue in sprinting training were prospected.RESULTS:Brain-derived neurotrophic factor(BDNF)and other motor factors could play a key role in regulating the diferentiation of muscle stellite stem cells and the functional renodeling of neuromuscular system.The Ca^(2+)pathway,p53/PGC-1a,AMPK,p38MAPK and other key molecules in mitochondrial biogenesis and energy metabolism regulation are important targets for the epigenetic changes in sprint training to induce the improvement of athletic performance and the homeostasis regulation network.of energy metabolism.High-intensity functional training integrating the HIFT of interval training,speed strength training and continwous circuit training can stimulate the overall training load on the neuromuscular and cardiowascular multiple systems in a bal anced way,which can more ffectively induce the expression and secretion of BDNF and the key epigenetic adaptions,thus exerting a positive ffct on improving the physiological adptability(oxygen utilization and energy metabolism)and the plasticity of the nervous system in sprint training,and has a potential effet on the main limiting factors of sprint training,such as neuromuscular function and control ability and sports injury prevention.Non-targeted metabolomics technologics based on liquid chromatography tandem mass spectrometry(IC-MS/MS)provide an ffective approach for scientifie monitoring of energy homeostasis regulation and neuromuscular function reovery and regeneration in sprint training through systematic analysis of key differential metabolites and related molecular pat hways.CONCLUSIONS:Exercise can promote muscle and other tissues to produce exercise physiological efects through muscle-organ interaction(cross-talk)in an autocrine,paracrine and/or endocrine way,and play a role in regulating neuromuscular function remodeling,improving exercise cognition and adaptability,and improwing mi tochondial energy metabolism homeostasis.With the development of omics analysis technology based on the changes of exreise-induced epigenetic gene targets and key metabolites,it can more comprehensively,sensitively and systematically reflect the changos and rules of the overall metabolic adaptability of the body during exercise trai ning,thus providing basis and techrical support for scientific monitoring and efctive prevention and intervention of exercise fatigue.