Can high-intensity training protect against exercise-induced oxidation of sarcoplasmic reticulum Ca^<2+>-ATPase?
高强度训练能否防止运动引起的肌浆网Ca^2-ATP酶氧化?
基本信息
- 批准号:16500419
- 负责人:
- 金额:$ 2.43万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2004
- 资助国家:日本
- 起止时间:2004 至 2006
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
The cytosolic free Ca^<2+> concentration ([Ca^<2+>]_f) plays a central role in muscle contraction and relaxation. In skeletal muscle, the regulation of [Ca^<2+>]f is accomplished primarily by the kinetics of Ca^<2+> release and uptake by the sarcoplasmic reticulum (SR). Although the fatigue process involves multiple factors and mechanisms, recent evidence implies that functional impairment of the SR is a major contributor to muscle fatigue. We previously observed that a loss of SR function may be attributed, at least partly, to protein oxidation by reactive oxygen species, generation of which is elevated during muscle contraction. However, no published data presently exists that examines whether high-intensity training could protect against deteriorating SR Ca^<2+>2+-ATPase activity and oxidation of Ca^<2+>-ATPase with acute exercise. The purpose of this study was to investigate the influence of high-intensity training and/or a single bout exercise on SR function and oxidation of Ca^<2+>-ATPase.Our in vitro measures on the superficial region of the vastus lateralis revealed that 8 weeks of running training elicited an increase in SR Ca^<2+>-uptake rate without concomitant changes in SR Ca^<2+>-ATPase activity and Ca^<2+>-release rate. These results implicate training-induced decreases in Ca^<2+> efflux from the SR lumen. Despite the extension of the run time to exhaustion, no differences existed in exhaustive exercise-induced reductions in SR Ca^<2+>-uptake ability and increases in carbonyls contained in Ca^<2+>-ATPase between trained and untrained muscles. These findings suggest that high-intensity training might protect Ca^<2+>-ATPase enzyme against oxidative modification that occurs during vigorous muscle contraction.
胞质游离CA^<2+>浓度([Ca^<2+>] _ f)在肌肉收缩和放松中起着核心作用。在骨骼肌中,[Ca^<2+>] F的调节主要是通过肌浆网(SR)的Ca^<2+>释放和吸收的动力学来完成的。尽管疲劳过程涉及多种因素和机制,但最近的证据表明,SR的功能障碍是肌肉疲劳的主要因素。我们先前观察到,至少部分地将SR功能的丧失归因于活性氧的蛋白质氧化,在肌肉收缩期间,其产生的产生升高。但是,目前尚无公开的数据来检查高强度训练是否可以防止Sr Ca^<2+> 2+-ATPase活性和急性运动中Ca^<2+> - ATPase的氧化。这项研究的目的是研究高强度训练和/或单个回合练习对Ca^<2+> - ATPase的氧化和氧化的影响 速度。这些结果暗示训练引起的SR腔中的Ca^<2+>外排的降低。尽管运行时间延长了疲惫的时间,但在详尽的锻炼引起的Sr Ca^<2+> - 吸收能力的降低中,ca^<2+> - ATPase中包含的羰基的增加,在受过训练的肌肉和未经训练的肌肉之间含有差异。这些发现表明,高强度训练可能会保护CA^<2+> - ATPase酶免受剧烈肌肉收缩期间发生的氧化修饰。
项目成果
期刊论文数量(7)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Depressed sarcoplasmic reticulum Ca^<2+>-ATPase activity following high-intensity exercise-The oxidation of protein and the muscle fiber type-
高强度运动后肌浆网Ca^<2>-ATP酶活性降低-蛋白质的氧化和肌纤维类型-
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Matsunaga;S.
- 通讯作者:S.
Effects of high-intensity training and acute exercise on in vitro function of rat sarcoplasmic reticulum
- DOI:10.1007/s00421-006-0381-8
- 发表时间:2007-01
- 期刊:
- 影响因子:3
- 作者:S. Matsunaga;Takashi Yamada;T. Mishima;M. Sakamoto;Minako Sugiyama;M. Wada
- 通讯作者:S. Matsunaga;Takashi Yamada;T. Mishima;M. Sakamoto;Minako Sugiyama;M. Wada
高強度運動による筋小胞体Ca^<2+>-ATPase活性の減退-タンパク質の酸化と筋線維タイプ-
高强度运动导致肌浆网Ca^2+-ATP酶活性降低 - 蛋白质氧化和肌纤维类型 -
- DOI:
- 发表时间:2007
- 期刊:
- 影响因子:0
- 作者:中村敏雄;山本徳郎;他;Tokuro Yamamoto et al.;松永 智
- 通讯作者:松永 智
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MATSUNAGA Satoshi其他文献
MATSUNAGA Satoshi的其他文献
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24750138 - 财政年份:2012
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$ 2.43万 - 项目类别:
Grant-in-Aid for Young Scientists (B)
Does the sarcoplasmic reticulum function contribute to the decline of muscle contractile force following eccentric contraction ?
肌浆网功能是否会导致离心收缩后肌肉收缩力的下降?
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21500634 - 财政年份:2009
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$ 2.43万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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