The effect of antioxidants on sarcoplasmic reticulum function during muscle fatigue

抗氧化剂对肌肉疲劳时肌浆网功能的影响

• 批准号: 13680030
• 负责人: WADA Masanobu
• 金额: $ 2.11万
• 依托单位: Hiroshima University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13680030/
• 关键词: sarcoplasmic reticulum; fatigue; antioxidant; reactive oxygen species; calcium pump; oxidation; カルシウム; 筋収縮; 運動; 酸化; Ca^<2+>取り込み速度; Ca^<2+>放出速度

The purpose of the first experiment was to examine a cause of exercise-induced decreases in Ca^<2+>-sequestering capacity by sarcoplasmic reticulum (SR) using the superficial portions of the gastrocnemius and vastus lateralis muscles of the rat after treadmill running to exhaustion. Exercise led to 16% and 34% decreases in SR Ca^<2+>-ATPase activity and Ca^<2+> uptake rate, respectively. The carbonyl group content in SR Ca^<2+>-ATPase protein was increased by 127%. In the second experiment, the hypothesis was tested that N-acetylcysteine (NAC) that is one of antioxidants may influence diaphragmic fatigue by modulating SR Ca^<2+> handling capacity. In the absence or presence of NAG, rat diaphragm was electrically stimulated with titanic trains (350 msec) delivered at 0.5 train/sec for various durations. At 60 sec after the onset of stimulation and beyond, force developed by NAC-treated muscle was significantly greater that that of non-treated muscle. In muscles where force was reduced to 50-80% of the initial level, treatment of NAG inhibited reductions in SR function. These results suggest that oxidation of SR Ca^<2+> -ATPase protein may account for decreases in Ca^<2+> -sequestering capacity by the SR and that antioxidant-induced inhibition of a decline in SR function may be responsible, at least partly, for a delay of the rate of fatigue development in the middle phase of muscular fatigue.

第一个实验的目的是使用跑台运动至力竭后的大鼠腓肠肌和股外侧肌的浅表部分，研究运动诱导的肌浆网（SR）的Ca^2+螯合能力降低的原因。运动导致肌浆网Ca^<2+>-ATP酶活性和Ca^<2+>摄取率分别下降16%和34%。SR Ca^<2+>-ATP酶的羰基含量增加了127%.实验二验证了抗氧化剂N-乙酰半胱氨酸（NAC）可能通过调节肌浆网Ca^2+处理能力而影响运动性疲劳的假设。在NAG存在或不存在的情况下，用以0.5串/秒的速度递送的Titanic串（350毫秒）电刺激大鼠膈肌不同的持续时间。在刺激开始后60秒及以后，由NAC处理的肌肉产生的力显著大于未处理的肌肉。在肌肉的力量减少到50-80%的初始水平，治疗NAG抑制SR功能的减少。这些结果表明，肌浆网Ca^<2+> -ATP酶蛋白的氧化可能是肌浆网Ca^<2+> -螯合能力降低的原因，抗氧化剂诱导的抑制肌浆网功能下降可能是肌疲劳中期疲劳发展速度延迟的部分原因。

项目成果

和田正信ほか: "筋小胞体の構造および筋活動に伴うその機能の変化"体育学研究. 46・5. 443-459 (2001)

和田正信等：“肌浆网的结构及其与肌肉活动相关的功能变化”《体育研究》46・5（2001）。

Satoshi Matsunaga: "Oxidation of SR Ca^<2+>-ATPase induced by high-intensity exercise"Pflugers Archives. 446. 334-399 (2003)

Satoshi Matsunaga：“高强度运动诱导的SR Ca^2-ATP酶的氧化”Pflugers Archives。

Satoshi, Matsunaga: "Oxidation of sarcoplasmic reticulum Ca^<2+>-ATPase induced by high-intensity exercise"Pflugers Archives. 394-399 (2003)

Satoshi，Matsunaga：“高强度运动诱导的肌浆网C​​a^2-ATP酶的氧化”Pflugers档案。

三島隆章ほか: "H-acetylcysteineが筋疲労時の横隔膜筋小胞体に及ぼす影響"広島体育学研究. 29. 27-34 (2003)

Takaaki Mishima等：“肌肉疲劳时H-乙酰半胱氨酸对膈肌浆网的影响”广岛体育研究29. 27-34（2003）。

三島隆章: "N-acetylcysteineが筋疲労時の横隔膜筋小胞体に及ぼす影響"広島体育学研究. 29. 27-34 (2003)

Takaaki Mishima：“肌肉疲劳时N-乙酰半胱氨酸对膈肌浆网的影响”广岛体育研究29. 27-34（2003）。