Contraction-relaxation coupling is unaltered by exercise training and infarction in isolated canine myocardium.

Contraction-relaxation coupling is unaltered by exercise training and infarction in isolated canine myocardium.
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运动训练和心肌梗死均未改变离体犬心肌的收缩-舒张偶联。

DOI:
10.1085/jgp.202012829
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发表时间:
2021-07-05
期刊:
The Journal of general physiology
影响因子:
--
通讯作者:
Janssen PML
Janssen PML
中科院分区:
其他
文献类型:
--
作者:
Fazlollahi F;Santini Gonzalez JJ;Repas SJ;Canan BD;Billman GE;Janssen PML

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Fazlollahi等人的研究表明,在运动训练和/或心肌梗死后,完整犬心肌的收缩和舒张仍然紧密耦合。他们推测心肌肌凝蛋白结合蛋白C对肌动蛋白和肌凝蛋白的作用可能在这一过程中起关键作用。哺乳动物心脏周期的两个主要阶段是收缩和放松;然而,在人类中它们之间是否存在联系尚不清楚。常规运动已被证明可以改善心脏功能、形态学和分子特征。同样,心脏因损伤、疾病和压力而发生的急性和慢性变化也有很好的特征,尽管尚未完全了解。在这项研究中,我们研究了运动和心肌损伤如何影响收缩-松弛耦合。我们回顾性分析了手术诱发心肌梗死后犬心肌最大收缩速度和最大舒张速度之间的相关性,随后进行了10-12周的久坐恢复或运动训练。我们使用分离的右心室小梁,以不同的长度、频率和增加的β-肾上腺素能受体刺激进行电节拍。在所有情况下,收缩和放松都是线性相关的,与受伤或训练史无关。基于这些结果和现有文献,我们假设收缩-松弛耦合是一种基本的心肌特性,它存在于肌节水平的蛋白质结构安排中,这可能受到心肌肌凝蛋白结合蛋白C (cMyBP-C)对肌动蛋白和肌凝蛋白的作用的调节。
Fazlollahi et al. show that contraction and relaxation remain tightly coupled in intact canine myocardium after exercise training and/or myocardial infarction. They postulate that the action of cardiac myosin binding protein C on actin and myosin may play a key role in this process. The two main phases of the mammalian cardiac cycle are contraction and relaxation; however, whether there is a connection between them in humans is not well understood. Routine exercise has been shown to improve cardiac function, morphology, and molecular signatures. Likewise, the acute and chronic changes that occur in the heart in response to injury, disease, and stress are well characterized, albeit not fully understood. In this study, we investigated how exercise and myocardial injury affect contraction–relaxation coupling. We retrospectively analyzed the correlation between the maximal speed of contraction and the maximal speed of relaxation of canine myocardium after receiving surgically induced myocardial infarction, followed by either sedentary recovery or exercise training for 10–12 wk. We used isolated right ventricular trabeculae, which were electrically paced at different lengths, frequencies, and with increasing β-adrenoceptor stimulation. In all conditions, contraction and relaxation were linearly correlated, irrespective of injury or training history. Based on these results and the available literature, we posit that contraction–relaxation coupling is a fundamental myocardial property that resides in the structural arrangement of proteins at the level of the sarcomere and that this may be regulated by the actions of cardiac myosin binding protein C (cMyBP-C) on actin and myosin.
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