Spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading

Abstract Force enhancement is one kind of myogenic spontaneous fasciculation in lengthening preload striated muscles. In cardiac muscle, the role of this biomechanical event is not well established. The physiological passive property is an essential part for maintaining normal diastole in the heart....

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Autores principales: Shouyan Fan, Lingfeng Gao, Annie Christel Bell, Joseph Akparibila Azure, Yang Wang
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/1258098edb734f7e9a88c445d11fdf91
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spelling oai:doaj.org-article:1258098edb734f7e9a88c445d11fdf912021-12-02T16:50:24ZSpontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading10.1038/s41598-021-94335-w2045-2322https://doaj.org/article/1258098edb734f7e9a88c445d11fdf912021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94335-whttps://doaj.org/toc/2045-2322Abstract Force enhancement is one kind of myogenic spontaneous fasciculation in lengthening preload striated muscles. In cardiac muscle, the role of this biomechanical event is not well established. The physiological passive property is an essential part for maintaining normal diastole in the heart. In excessive preload heart, force enhancement relative erratic passive properties may cause muscle decompensating, implicate in the development of diastolic dysfunction. In this study, the force enhancement occurrence in mouse cardiac papillary muscle was evaluated by a microstepping stretch method. The intracellular Ca2+ redistribution during occurrence of force enhancement was monitored in real-time by a Flou-3 (2 mM) indicator. The force enhancement amplitude, the enhancement of the prolongation time, and the tension–time integral were analyzed by myography. The results indicated that the force enhancement occurred immediately after active stretching and was rapidly enhanced during sustained static stretch. The presence of the force and the increase in the amplitude synchronized with the acquisition and immediate transfer of Ca2+ to adjacent fibres. In highly preloaded fibres, the enhancement exceeded the maximum passive tension (from 4.49 ± 0.43 N/mm2 to 6.20 ± 0.51 N/mm2). The occurrence of force enhancement were unstable in each static stretch. The increased enhancement amplitude combined with the reduced prolongation time to induce a reduction in the tension–time integral. We concluded that intracellular Ca2+-synchronized force enhancement is one kind of interruption event in excessive preload cardiac muscle. During the cardiac muscle in its passive relaxation period, the occurrence of this interruption affected the rhythmic stability of the cardiac relaxation cycle.Shouyan FanLingfeng GaoAnnie Christel BellJoseph Akparibila AzureYang WangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-10 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Shouyan Fan
Lingfeng Gao
Annie Christel Bell
Joseph Akparibila Azure
Yang Wang
Spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading
description Abstract Force enhancement is one kind of myogenic spontaneous fasciculation in lengthening preload striated muscles. In cardiac muscle, the role of this biomechanical event is not well established. The physiological passive property is an essential part for maintaining normal diastole in the heart. In excessive preload heart, force enhancement relative erratic passive properties may cause muscle decompensating, implicate in the development of diastolic dysfunction. In this study, the force enhancement occurrence in mouse cardiac papillary muscle was evaluated by a microstepping stretch method. The intracellular Ca2+ redistribution during occurrence of force enhancement was monitored in real-time by a Flou-3 (2 mM) indicator. The force enhancement amplitude, the enhancement of the prolongation time, and the tension–time integral were analyzed by myography. The results indicated that the force enhancement occurred immediately after active stretching and was rapidly enhanced during sustained static stretch. The presence of the force and the increase in the amplitude synchronized with the acquisition and immediate transfer of Ca2+ to adjacent fibres. In highly preloaded fibres, the enhancement exceeded the maximum passive tension (from 4.49 ± 0.43 N/mm2 to 6.20 ± 0.51 N/mm2). The occurrence of force enhancement were unstable in each static stretch. The increased enhancement amplitude combined with the reduced prolongation time to induce a reduction in the tension–time integral. We concluded that intracellular Ca2+-synchronized force enhancement is one kind of interruption event in excessive preload cardiac muscle. During the cardiac muscle in its passive relaxation period, the occurrence of this interruption affected the rhythmic stability of the cardiac relaxation cycle.
format article
author Shouyan Fan
Lingfeng Gao
Annie Christel Bell
Joseph Akparibila Azure
Yang Wang
author_facet Shouyan Fan
Lingfeng Gao
Annie Christel Bell
Joseph Akparibila Azure
Yang Wang
author_sort Shouyan Fan
title Spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading
title_short Spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading
title_full Spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading
title_fullStr Spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading
title_full_unstemmed Spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading
title_sort spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/1258098edb734f7e9a88c445d11fdf91
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