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去表皮心脏纤维束中的残余力和被动力增强

Residual and passive force enhancement in skinned cardiac fibre bundles.

作者信息

Boldt Kevin, Han Seong-Won, Joumaa Venus, Herzog Walter

机构信息

Faculty of Kinesiology, Human Performance Laboratory, University of Calgary, Canada.

Faculty of Kinesiology, Human Performance Laboratory, University of Calgary, Canada.

出版信息

J Biomech. 2020 Aug 26;109:109953. doi: 10.1016/j.jbiomech.2020.109953. Epub 2020 Jul 15.

DOI:10.1016/j.jbiomech.2020.109953
PMID:32807325
Abstract

In skeletal muscle, steady-state force is consistently greater following active stretch than during a purely isometric contraction at the same length (residual force enhancement; RFE). Similarly, when deactivated, the force remains higher following active stretch than following an isometric condition (passive force enhancement; PFE). RFE and PFE have been associated with the sarcomere protein titin, but skeletal and cardiac titin have different structures, and results regarding RFE in cardiac muscle have been inconsistent and contradictory. Therefore, the purpose of this study was to determine if cardiac muscle exhibits RFE and PFE. Skinned fibre bundles (n = 10) were activated isometrically at a sarcomere length of 2.2 μm and actively stretched by 15% of their length. The resultant active and passive forces were compared to the corresponding forces obtained for purely isometric contractions at the long length. RFE was observed in all fibre bundles, averaging 5.5 ± 2.5% (ranging from 2.3 to 9.4%). PFE was observed in nine of the ten bundles, averaging 11.1 ± 6.5% (ranging from -2.1 to 18.7%). Stiffness was not different between the active isometric and the force enhanced conditions, but was higher following deactivation from the force-enhanced compared to the isometric reference state. We conclude that there is RFE and PFE in cardiac muscle. We speculate that cardiac muscle has the same RFE capability as skeletal muscle, and that the most likely mechanism for the RFE and PFE is the engagement of a passive structural element during active stretching.

摘要

在骨骼肌中,主动拉伸后的稳态力始终比在相同长度下的纯等长收缩时更大(残余力增强;RFE)。同样,当肌肉失活时,主动拉伸后的力仍高于等长收缩后的力(被动力增强;PFE)。RFE和PFE与肌节蛋白肌联蛋白有关,但骨骼肌和心肌的肌联蛋白结构不同,关于心肌中RFE的研究结果一直不一致且相互矛盾。因此,本研究的目的是确定心肌是否表现出RFE和PFE。对皮肤纤维束(n = 10)在肌节长度为2.2μm时进行等长激活,并使其长度主动拉伸15%。将由此产生的主动力和被动力与在该长长度下纯等长收缩所获得的相应力进行比较。在所有纤维束中均观察到RFE,平均为5.5±2.5%(范围为2.3%至9.4%)。在十个纤维束中有九个观察到PFE,平均为11.1±6.5%(范围为-2.1%至18.7%)。主动等长收缩和力增强条件下的刚度没有差异,但与等长参考状态相比,从力增强状态失活后刚度更高。我们得出结论,心肌中存在RFE和PFE。我们推测心肌具有与骨骼肌相同的RFE能力,并且RFE和PFE最可能的机制是在主动拉伸过程中被动结构元件的参与。

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