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Intramuscular mechanisms of overtraining.
Redox Biology ( IF 11.4 ) Pub Date : 2020-02-26 , DOI: 10.1016/j.redox.2020.101480
Arthur J Cheng 1 , Baptiste Jude 2 , Johanna T Lanner 2
Affiliation  

Strenuous exercise is a potent stimulus to induce beneficial skeletal muscle adaptations, ranging from increased endurance due to mitochondrial biogenesis and angiogenesis, to increased strength from hypertrophy. While exercise is necessary to trigger and stimulate muscle adaptations, the post-exercise recovery period is equally critical in providing sufficient time for metabolic and structural adaptations to occur within skeletal muscle. These cyclical periods between exhausting exercise and recovery form the basis of any effective exercise training prescription to improve muscle endurance and strength. However, imbalance between the fatigue induced from intense training/competitions, and inadequate post-exercise/competition recovery periods can lead to a decline in physical performance. In fact, prolonged periods of this imbalance may eventually lead to extended periods of performance impairment, referred to as the state of overreaching that may progress into overtraining syndrome (OTS). OTS may have devastating implications on an athlete's career and the purpose of this review is to discuss potential underlying mechanisms that may contribute to exercise-induced OTS in skeletal muscle. First, we discuss the conditions that lead to OTS, and their potential contributions to impaired skeletal muscle function. Then we assess the evidence to support or refute the major proposed mechanisms underlying skeletal muscle weakness in OTS: 1) glycogen depletion hypothesis, 2) muscle damage hypothesis, 3) inflammation hypothesis, and 4) the oxidative stress hypothesis. Current data implicates reactive oxygen and nitrogen species (ROS) and inflammatory pathways as the most likely mechanisms contributing to OTS in skeletal muscle. Finally, we allude to potential interventions that can mitigate OTS in skeletal muscle.



中文翻译:

过度训练的肌内机制。

剧烈运动是一种有益的刺激手段,可诱导有益的骨骼肌适应,其作用范围从线粒体生物发生和血管生成引起的耐力增加到肥大引起的力量增强。尽管锻炼是触发和刺激肌肉适应所必需的,但是运动后恢复期对于为骨骼肌内发生代谢和结构适应提供足够的时间同样至关重要。力竭运动和恢复之间的这些周期性周期构成任何有效的运动训练处方的基础,以改善肌肉的耐力和力量。但是,激烈的训练/比赛所引起的疲劳与运动/比赛后恢复时间不足之间的不平衡会导致身体机能下降。事实上,长时间的这种不平衡状态最终可能导致长时间的性能受损,这就是过度锻炼的状态,可能会演变成过度训练综合症(OTS)。OTS可能会对运动员的职业造成毁灭性的影响,而本综述的目的是讨论可能导致运动引起骨骼肌OTS的潜在潜在机制。首先,我们讨论导致OTS的病症及其对骨骼肌功能受损的潜在影响。然后,我们评估支持或驳斥OTS骨骼肌无力的主要提议机制的证据:1)糖原耗竭假说,2)肌肉损伤假说,3)炎症假说和4)氧化应激假说。当前数据暗示活性氧和氮(ROS)和炎症途径是骨骼肌中OTS的最可能机制。最后,我们提到了可能减轻骨骼肌OTS的潜在干预措施。

更新日期:2020-02-26
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