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MgADP 激活有助于在分离的骨骼肌肌原纤维快速拉伸过程中增强力量。

MgADP activation contributes to force enhancement during fast stretch of isolated skeletal myofibrils.

作者信息

Minozzo Fábio C, Altman David, Rassier Dilson E

机构信息

Department of Kinesiology and Physical Education, McGill University, Canada.

Department of Physics, Willamette University, Salem, OR, USA.

出版信息

Biochem Biophys Res Commun. 2015 Aug 7;463(4):1129-34. doi: 10.1016/j.bbrc.2015.06.070. Epub 2015 Jun 19.

Abstract

BACKGROUND

When an activated muscle is rapidly stretched, force rises and peaks while muscle lengthens. The peak force is normally called critical-force (Pc). The mechanism behind this increase in force is not well understood, but it has been associated with crossbridges operating in different states.

METHODS

Myofibrils were attached between a cantilever and a micro-needle, and activated with Ca(2+) or MgADP. During activation, the myofibrils were stretched by 3% SLo at 10 SLo·s(-1). A crossbridge model was developed to better understand the effects of MgADP in myofibrils activation.

RESULTS

Despite a similar stretch magnitude, MgADP activation produced a higher Pc (1.37 ± 0.07 P/Po) than Ca(2+) activation (Pc = 1.23 ± 0.03 P/Po). These results suggest that myofibrils activated with MgADP become stiffer than myofibrils activated with Ca(2+).

CONCLUSIONS

MgADP induces a fraction of crossbridges to form a "rigor-like" state that precedes ADP release, and that may not contribute to isometric forces. Such interpretation was strengthened by the results obtained with the developed crossbridge model, which showed that MgADP bias crossbridges into the rigor-like state. This state would be crucial to initiate a cooperative activation of crossbridges and actin, and to resist to unbinding from actin when the myofibrils are stretched.

SIGNIFICANCE

Our results suggest a new mechanism contributing for force output during stretch, which underlies basic mechanisms of muscle contraction.

摘要

背景

当一块被激活的肌肉快速拉伸时,力量会在肌肉伸长时上升并达到峰值。这个峰值力量通常被称为临界力(Pc)。力量增加背后的机制尚未完全理解,但它与处于不同状态的横桥有关。

方法

肌原纤维连接在悬臂和微针之间,并用Ca(2+)或MgADP激活。在激活过程中,肌原纤维以10 SLo·s(-1)的速度被拉伸3% SLo。开发了一个横桥模型以更好地理解MgADP在肌原纤维激活中的作用。

结果

尽管拉伸幅度相似,但MgADP激活产生的Pc(1.37 ± 0.07 P/Po)高于Ca(2+)激活(Pc = 1.23 ± 0.03 P/Po)。这些结果表明,用MgADP激活的肌原纤维比用Ca(2+)激活的肌原纤维更硬。

结论

MgADP诱导一部分横桥形成一种在ADP释放之前的“强直样”状态,并且这种状态可能对等长力没有贡献。用开发的横桥模型获得的结果加强了这种解释,该模型表明MgADP使横桥偏向强直样状态。这种状态对于启动横桥和肌动蛋白的协同激活以及在肌原纤维拉伸时抵抗从肌动蛋白上解离至关重要。

意义

我们的结果提出了一种有助于拉伸过程中力量输出的新机制,这是肌肉收缩基本机制的基础。

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