首页> 外文期刊>Proceedings of the Royal Society. Biological sciences >Extensive eccentric contractions in intact cardiac trabeculae: revealing compelling differences in contractile behaviour compared to skeletal muscles
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Extensive eccentric contractions in intact cardiac trabeculae: revealing compelling differences in contractile behaviour compared to skeletal muscles

机译:完整的心脏小梁中的广泛偏心收缩:与骨骼肌相比,揭示了收缩行为的引人注目的差异

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摘要

Force enhancement (FE) is a phenomenon that is present in skeletal muscle. It is characterized by progressive forces upon active stretching-distinguished by a linear rise in force-and enhanced isometric force following stretching (residual FE (RFE)). In skeletal muscle, non-cross-bridge (XB) structures may account for this behaviour. So far, it is unknown whether differences between non-XB structures within the heart and skeletal muscle result in deviating contractile behaviour during and after eccentric contractions. Thus, we investigated the force response of intact cardiac trabeculae during and after isokinetic eccentric muscle contractions (10% of maximum shortening velocity) with extensive magnitudes of stretch (25% of optimum muscle length). The different contributions of XB and non-XB structures to the total muscle force were revealed by using an actomyosin inhibitor. For cardiac trabeculae, we found that the force-length dynamics during long stretch were similar to the total isometric force-length relation. This indicates that no (R)FE is present in cardiac muscle while stretching the muscle from 0.75 to 1.0 optimum muscle length. This finding is in contrast with the results obtained for skeletal muscle, in which (R)FE is present. Our data support the hypothesis that titin stiffness does not increase with activation in cardiac muscle.
机译:力增强(Fe)是骨骼肌中存在的现象。在拉伸(残留Fe(RFE))之后,通过在力 - 和增强的等轴力的线性上升时,其特征在于激活延伸延伸的渐进力。在骨骼肌中,非交叉桥(XB)结构可以解释这种行为。到目前为止,它未知心脏和骨骼肌内非XB结构之间的差异是否导致偏心收缩期间和之后偏离收缩行为。因此,我们调查了在等因内偏心肌收缩期间和后的完整心脏小梁的力响应(最大缩短速度的10%),具有广泛的拉伸大小(占最佳肌肉长度的25%)。通过使用Actomyosin抑制剂揭示了Xb和非Xb结构对总肌肉的不同贡献。对于心脏小梁,我们发现长伸展期间的力长度动态类似于总等轴力长度关系。这表明无(R)Fe存在于心肌中,同时将肌肉从0.75延伸到1.0至1.0最佳肌肉长度。这种发现与骨骼肌的结果相反,存在(R)Fe存在。我们的数据支持假设,即肌肉肌肉激活不增加三肽僵硬。

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