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肌肉长度对 C57BL/6 和 skMLCK 小鼠 EDL 肌肉强直后增强的影响。

The effect of muscle length on post-tetanic potentiation of C57BL/6 and skMLCK mouse EDL muscles.

机构信息

Department of Kinesiology, Centre for Bone and Muscle Health, Brock University, 1812 Sir Isaac Brock Way, St. Catharines, ON, L2S 3A1, Canada.

出版信息

J Muscle Res Cell Motil. 2022 Sep;43(3):99-111. doi: 10.1007/s10974-022-09620-6. Epub 2022 Jun 30.

Abstract

Post-tetanic potentiation of fast-twitch skeletal muscle is dependent on muscle length, with greater potentiation observed at shorter compared to longer lengths. The structural effects of the primary potentiation mechanism, phosphorylation of the regulatory light chain (RLC) of myosin, are thought to explain this relationship. The purpose of these experiments was to determine whether the length-dependence of potentiation would be attenuated in the absence of RLC phosphorylation. To this end, we compared isometric twitch potentiation of mouse extensor digitorum longus (EDL) muscles with (wildtype, WT) and without (skeletal myosin light chain kinase knockout, skMLCK) phosphorylation. Force was measured at five muscle lengths (0.90 L, 0.95 L, L, 1.05 L, 1.10 L, where L refers to optimal length) prior to and following a tetanic train. In accordance with prior findings, potentiation was dependent on muscle length, with greater values observed at short (e.g., 44.3 ± 4.6% for WT, 33.5 ± 6.2% for skMLCK, at 0.90 L) compared to long lengths (e.g., 16.9 ± 1.3% for WT, 9.1 ± 1.8% for skMLCK, at 1.10 L) in both genotypes. WT muscles displayed greater potentiation compared to their skMLCK counterparts across lengths (e.g., 16.9 ± 1.6% vs 7.3 ± 1.5% at L). However, the relationship between potentiation and muscle length was not different between genotypes. Thus, the alternative mechanisms of potentiation, present in the skMLCK EDL, display a length-dependence of post-tetanic potentiation similar to RLC phosphorylation-dominant potentiation. Additional mechanisms may be required to explain the length-dependence of potentiation.

摘要

快肌强直后增强依赖于肌肉长度,与较长长度相比,较短长度时观察到的增强更大。初级增强机制,肌球蛋白调节轻链(RLC)的磷酸化的结构效应被认为解释了这种关系。这些实验的目的是确定在没有 RLC 磷酸化的情况下,增强的长度依赖性是否会减弱。为此,我们比较了具有(野生型,WT)和不具有(骨骼肌肌球蛋白轻链激酶敲除,skMLCK)磷酸化的小鼠伸趾长肌(EDL)的等长抽搐增强。在强直训练之前和之后,在五个肌肉长度(0.90 L、0.95 L、L、1.05 L、1.10 L,其中 L 指最佳长度)下测量力。与先前的发现一致,增强依赖于肌肉长度,与较短长度(例如,WT 为 44.3±4.6%,skMLCK 为 33.5±6.2%,在 0.90 L)相比,较长长度(例如,WT 为 16.9±1.3%,skMLCK 为 9.1±1.8%,在 1.10 L)观察到更大的增强。WT 肌肉在各个长度下的增强均大于其 skMLCK 对应物(例如,在 L 处为 16.9±1.6%比 7.3±1.5%)。然而,增强与肌肉长度之间的关系在两种基因型之间没有差异。因此,存在于 skMLCK EDL 中的增强的替代机制显示出与 RLC 磷酸化主导的增强相似的强直后增强的长度依赖性。可能需要其他机制来解释增强的长度依赖性。

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