Reactive oxygen species promote endurance exercise-induced adaptations in skeletal muscles.

IF 9.7 1区 医学 Q1 HOSPITALITY, LEISURE, SPORT & TOURISM
Journal of Sport and Health Science Pub Date : 2024-11-01 Epub Date: 2024-05-07 DOI:10.1016/j.jshs.2024.05.001
Scott K Powers, Zsolt Radak, Li Li Ji, Malcolm Jackson
{"title":"Reactive oxygen species promote endurance exercise-induced adaptations in skeletal muscles.","authors":"Scott K Powers, Zsolt Radak, Li Li Ji, Malcolm Jackson","doi":"10.1016/j.jshs.2024.05.001","DOIUrl":null,"url":null,"abstract":"<p><p>The discovery that contracting skeletal muscle generates reactive oxygen species (ROS) was first reported over 40 years ago. The prevailing view in the 1980s was that exercise-induced ROS production promotes oxidation of proteins and lipids resulting in muscle damage. However, a paradigm shift occurred in the 1990s as growing research revealed that ROS are signaling molecules, capable of activating transcriptional activators/coactivators and promoting exercise-induced muscle adaptation. Growing evidence supports the notion that reduction-oxidation (redox) signaling pathways play an important role in the muscle remodeling that occurs in response to endurance exercise training. This review examines the specific role that redox signaling plays in this endurance exercise-induced skeletal muscle adaptation. We begin with a discussion of the primary sites of ROS production in contracting muscle fibers followed by a summary of the antioxidant enzymes involved in the regulation of ROS levels in the cell. We then discuss which redox-sensitive signaling pathways promote endurance exercise-induced muscle adaptation and debate the strength of the evidence supporting the notion that redox signaling plays an essential role in muscle adaptation to endurance exercise training. In hopes of stimulating future research, we highlight several important unanswered questions in this field.</p>","PeriodicalId":48897,"journal":{"name":"Journal of Sport and Health Science","volume":" ","pages":"780-792"},"PeriodicalIF":9.7000,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11336304/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Sport and Health Science","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.jshs.2024.05.001","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/5/7 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"HOSPITALITY, LEISURE, SPORT & TOURISM","Score":null,"Total":0}
引用次数: 0

Abstract

The discovery that contracting skeletal muscle generates reactive oxygen species (ROS) was first reported over 40 years ago. The prevailing view in the 1980s was that exercise-induced ROS production promotes oxidation of proteins and lipids resulting in muscle damage. However, a paradigm shift occurred in the 1990s as growing research revealed that ROS are signaling molecules, capable of activating transcriptional activators/coactivators and promoting exercise-induced muscle adaptation. Growing evidence supports the notion that reduction-oxidation (redox) signaling pathways play an important role in the muscle remodeling that occurs in response to endurance exercise training. This review examines the specific role that redox signaling plays in this endurance exercise-induced skeletal muscle adaptation. We begin with a discussion of the primary sites of ROS production in contracting muscle fibers followed by a summary of the antioxidant enzymes involved in the regulation of ROS levels in the cell. We then discuss which redox-sensitive signaling pathways promote endurance exercise-induced muscle adaptation and debate the strength of the evidence supporting the notion that redox signaling plays an essential role in muscle adaptation to endurance exercise training. In hopes of stimulating future research, we highlight several important unanswered questions in this field.

Abstract Image

活性氧促进骨骼肌在耐力运动中的适应。
40 多年前,人们首次发现收缩的骨骼肌会产生活性氧(ROS)。20 世纪 80 年代的主流观点认为,运动诱发的 ROS 会促进蛋白质和脂质氧化,从而导致肌肉损伤。然而,随着越来越多的研究发现,ROS 是一种信号分子,能够激活转录激活因子/共激活因子,并促进运动诱导的肌肉适应,因此在 20 世纪 90 年代发生了范式转变。越来越多的证据表明,还原-氧化(氧化还原)信号通路在耐力运动训练所引起的肌肉重塑过程中发挥着重要作用。本综述探讨了氧化还原信号在这种耐力运动诱导的骨骼肌适应中发挥的具体作用。我们首先讨论了收缩肌纤维中产生 ROS 的主要部位,然后总结了参与调节细胞中 ROS 水平的抗氧化酶。然后,我们讨论了哪些对氧化还原反应敏感的信号传导途径可促进耐力运动引起的肌肉适应,并就支持氧化还原反应信号传导在肌肉适应耐力运动训练中发挥重要作用这一观点的证据的强度进行了辩论。为了激励未来的研究,我们强调了这一领域的几个重要未解之谜。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
18.30
自引率
1.70%
发文量
101
审稿时长
22 weeks
期刊介绍: The Journal of Sport and Health Science (JSHS) is an international, multidisciplinary journal that aims to advance the fields of sport, exercise, physical activity, and health sciences. Published by Elsevier B.V. on behalf of Shanghai University of Sport, JSHS is dedicated to promoting original and impactful research, as well as topical reviews, editorials, opinions, and commentary papers. With a focus on physical and mental health, injury and disease prevention, traditional Chinese exercise, and human performance, JSHS offers a platform for scholars and researchers to share their findings and contribute to the advancement of these fields. Our journal is peer-reviewed, ensuring that all published works meet the highest academic standards. Supported by a carefully selected international editorial board, JSHS upholds impeccable integrity and provides an efficient publication platform. We invite submissions from scholars and researchers worldwide, and we are committed to disseminating insightful and influential research in the field of sport and health science.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信