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

Shouyan Fan,Lingfeng Gao,Annie Christel Bell,Joseph Akparibila Azure,Yang Wang

doi:10.1038/s41598-021-94335-w

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.

Highlights

Force enhancement is one kind of myogenic spontaneous fasciculation in lengthening preload striated muscles
During fulminant COVID-19, there were increasing numbers of cases of reverse takotsubo cardiomyopathy associated with the infection[21,22,23] and epidemiological reports of 1.5% takotsubo cardiomyopathy in COVID-19 p atients[24] that prove the urgency and demands for understanding the mechanism of cardiac muscle akinesia
The force enhancement corresponded to the magnitude of the stretch was gradually revealed in recent s tudies[29]

Summary

Introduction

Force enhancement is one kind of myogenic spontaneous fasciculation in lengthening preload striated muscles. Force enhancement relative erratic passive properties may cause muscle decompensating, implicate in the development of diastolic dysfunction. We concluded that intracellular Ca2+-synchronized force enhancement is one kind of interruption event in excessive preload cardiac muscle. Over the past few years, a specific heart failure syndrome has been reported: takotsubo cardiomyopathy, which is characterized by the sudden acute, reversible enlargement of the left ventricle chamber so that it resembles an octopus trap when viewed by ventricular chamber imaging[2] In this type of myopathy, the cardiac muscle developed extreme lengthening that initiated intrinsic myogenic autoregulation in the muscle. This non-invasive method analysed muscle diastole and systole functions at the anterior wall or posterior wall of left ventricle.

Methods

Results

Conclusion