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离心肌肉收缩增强了大鼠快肌中与titin 僵硬相关的收缩特性。

Eccentric muscle contraction potentiates titin stiffness-related contractile properties in rat fast-twitch muscles.

机构信息

Graduate School of Integrated Arts and Sciences, Hiroshima University, Hiroshima, Japan.

Graduate School of Humanities and Social Sciences, Hiroshima University, Hiroshima, Japan.

出版信息

J Appl Physiol (1985). 2022 Sep 1;133(3):710-720. doi: 10.1152/japplphysiol.00327.2022. Epub 2022 Aug 18.

Abstract

This study was conducted to examine the effects of an acute bout of eccentric muscle contraction (ECC) on titin stiffness-related contractile properties in rat fast-twitch skeletal muscles. Intact gastrocnemius muscles were electrically stimulated in situ to undergo 200 repeated ECCs. Immediately after the cessation of the stimulation, the superficial regions of the muscles were dissected and subjected to biochemical and skinned fiber analyses. Small heat shock protein αB-crystallin in the muscle fraction enriched for myofibrillar proteins was increased by ECC. ECC resulted in an increase in the titin-based passive force. Protein kinase A-treatment decreased the passive force only in ECC-subjected but not in rested fibers. ECC decreased the maximum Ca-activated force at a sarcomere length (SL) of 2.4 μm and had no effect on myofibrillar-Ca sensitivity at 2.6-μm SL. In both rested and ECC-subjected fibers, these two variables were higher at 3.0-μm SL than at 2.4- or 2.6-μm SL. The differences in the two variables between the short and long SLs were greater in ECC-subjected than in rested fibers. These results indicate that an acute bout of ECC potentiates titin-based passive force, maximum active force at long SLs, and length-dependent activation and suggest that this potentiation may resist muscle fatigue in the muscles of the exercising body. It remains unclear whether eccentric contraction of skeletal muscle affects titin stiffness-related contractile properties. Here, we provide evidence that an acute bout of eccentric contraction can potentiate titin-based passive force, maximum active force at long sarcomere lengths, and length-dependent activation. This potentiation may resist muscle fatigue in the muscles of the exercising body.

摘要

这项研究旨在探讨急性离心肌肉收缩(ECC)对大鼠快肌纤维中与肌联蛋白僵硬相关的收缩特性的影响。在原位用电刺激完整的腓肠肌进行 200 次重复的 ECC。刺激停止后,立即解剖肌肉的浅层区域,并进行生化和去皮纤维分析。富含肌原纤维蛋白的肌肉部分中小热休克蛋白αB-晶体蛋白增加。ECC 导致基于肌联蛋白的被动力增加。蛋白激酶 A 处理仅降低 ECC 处理过的纤维的被动力,而不降低休息纤维的被动力。ECC 降低了在肌节长度(SL)为 2.4μm 时的最大 Ca 激活力,并且对 2.6μm SL 时的肌原纤维-Ca 敏感性没有影响。在休息和 ECC 处理过的纤维中,这两个变量在 SL 为 3.0μm 时均高于在 2.4μm 或 2.6μm SL 时的值。在短和长 SL 之间,这两个变量的差异在 ECC 处理过的纤维中大于在休息纤维中。这些结果表明,急性 ECC 可以增强基于肌联蛋白的被动力、长肌节长度时的最大主动力以及长度依赖性激活,这表明这种增强可能抵抗运动身体肌肉的疲劳。目前尚不清楚骨骼肌肉的离心收缩是否会影响与肌联蛋白僵硬相关的收缩特性。在这里,我们提供的证据表明,急性离心收缩可以增强基于肌联蛋白的被动力、长肌节长度时的最大主动力和长度依赖性激活。这种增强可能抵抗运动身体肌肉的疲劳。

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