Mechanisms of eccentric contraction-induced muscle damage and nutritional supplementations for mitigating it.

IF 1.7 3区 生物学 Q4 CELL BIOLOGY
Keita Kanzaki, Daiki Watanabe, Jiayu Shi, Masanobu Wada
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引用次数: 3

Abstract

Eccentric contraction (ECC) often results in large and long-lasting force deficits accompanied by muscle soreness, primarily due to muscle damage. In this sense, exercises that involve ECC are less desirable. Paradoxically, exercise training that includes a substantial eccentric phase leads to a more powerful activation of the genes responsible for skeletal muscle remodeling (e.g., hypertrophy) than other types of training that emphasize a concentric or isometric phase. Therefore, effective strategies that lessen ECC-induced muscle damage will be of interest and importance to many individuals. The purpose of this brief review is to highlight the published literature on the effects of ECC and/or nutritional supplementations on proteins, lipids, metabolic and ionic changes, and enzyme activities in skeletal muscles subjected to an acute bout of ECC. First, we discuss the potential mechanisms by which ECC causes muscle damage. Previous findings implicate a Ca2+ overload-oxidative modification pathway as one possible mechanism contributing to muscle damage. Thereafter, the efficacy of two nutritional supplementations, i.e., L-arginine and antioxidant, is discussed because L-arginine and antioxidant would be expected to ameliorate the adverse effects of Ca2+ overload and oxidative modification, respectively. Of these, L-arginine ingestion before ECC seems likely to be the effective strategy for mitigating ECC-related proteolysis. More studies are needed to establish the effectiveness of antioxidant ingestion. The application of effective strategies against muscle damage may contribute to improvements in health and fitness, muscle function, and sports performance.

Abstract Image

偏心收缩引起的肌肉损伤的机制和营养补充减轻它。
偏心收缩(ECC)经常导致大而持久的力量不足,并伴有肌肉酸痛,主要是由于肌肉损伤。从这个意义上说,涉及ECC的练习不太可取。矛盾的是,包含大量偏心阶段的运动训练比其他类型的强调同心或等距阶段的训练更能激活负责骨骼肌重塑(如肥厚)的基因。因此,减轻ecc引起的肌肉损伤的有效策略将对许多人感兴趣和重要。这篇简短的综述的目的是重点介绍ECC和/或营养补充对急性ECC发作时骨骼肌中蛋白质、脂质、代谢和离子变化以及酶活性的影响。首先,我们讨论了ECC引起肌肉损伤的潜在机制。先前的研究结果暗示Ca2+超载氧化修饰途径可能是导致肌肉损伤的一种机制。随后,讨论了两种营养补充剂的功效,即l -精氨酸和抗氧化剂,因为l -精氨酸和抗氧化剂分别有望改善Ca2+超载和氧化修饰的不利影响。其中,在ECC之前摄入l -精氨酸似乎可能是减轻ECC相关蛋白水解的有效策略。需要更多的研究来确定抗氧化剂摄入的有效性。针对肌肉损伤的有效策略的应用可能有助于改善健康和健身,肌肉功能和运动表现。
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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.
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