Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA.
Exp Physiol. 2021 Feb;106(2):401-411. doi: 10.1113/EP089053. Epub 2020 Dec 9.
What is the central question of this study? Does the muscle metaboreflex affect the ratio of left ventricular contraction/relaxation rates and does heart failure impact this relationship. What is the main finding and its importance? The effect of muscle metaboreflex activation on the ventricular relaxation rate was significantly attenuated in heart failure. Heart failure attenuates the exercise and muscle metaboreflex-induced changes in the contraction/relaxation ratio. In heart failure, the reduced ability to raise cardiac output during muscle metaboreflex activation may not solely be due to attenuation of ventricular contraction but also alterations in ventricular relaxation and diastolic function.
The relationship between contraction and relaxation rates of the left ventricle varies with exercise. In in vitro models, this ratio was shown to be relatively unaltered by changes in sarcomere length, frequency of stimulation, and β-adrenergic stimulation. We investigated whether the ratio of contraction to relaxation rate is maintained in the whole heart during exercise and muscle metaboreflex activation and whether heart failure alters these relationships. We observed that in healthy subjects the ratio of contraction to relaxation increases from rest to exercise as a result of a higher increase in contraction relative to relaxation. During muscle metaboreflex activation the ratio of contraction to relaxation is significantly reduced towards 1.0 due to a large increase in relaxation rate matching contraction rate. In heart failure, contraction and relaxation rates are significantly reduced, and increases during exercise are attenuated. A significant increase in the ratio was observed from rest to exercise although baseline ratio values were significantly reduced close to 1.0 when compared to healthy subjects. There was no significant change observed between exercise and muscle metaboreflex activation nor was the ratio during muscle metaboreflex activation significantly different between heart failure and control. We conclude that heart failure reduces the muscle metaboreflex gain and contraction and relaxation rates. Furthermore, we observed that the ratio of the contraction and relaxation rates during muscle metaboreflex activation is not significantly different between control and heart failure, but significant changes in the ratio in healthy subjects due to increased relaxation rate were abolished in heart failure.
这项研究的核心问题是什么?肌肉代谢反射是否会影响左心室收缩/舒张速率的比值,心力衰竭是否会影响这种关系。主要发现及其重要性是什么?在心力衰竭中,肌肉代谢反射激活对心室舒张率的影响明显减弱。心力衰竭减弱了运动和肌肉代谢反射引起的收缩/舒张比的变化。在心力衰竭中,在肌肉代谢反射激活期间心输出量增加的能力降低可能不仅仅是由于心室收缩的减弱,还可能是由于心室舒张和舒张功能的改变。
左心室收缩和舒张速率之间的关系随运动而变化。在体外模型中,这种比值相对不受肌节长度、刺激频率和β-肾上腺素能刺激变化的影响。我们研究了在整个心脏中,收缩与舒张速率的比值在运动和肌肉代谢反射激活期间是否保持不变,以及心力衰竭是否改变了这些关系。我们观察到,在健康受试者中,由于收缩相对于舒张的增加,收缩与舒张的比值从休息增加到运动。在肌肉代谢反射激活期间,由于舒张速率的大幅增加与收缩速率相匹配,收缩与舒张的比值显著降低至 1.0。在心力衰竭中,收缩和舒张速率显著降低,运动时的增加幅度减弱。与休息时相比,运动时观察到比值显著增加,尽管与健康受试者相比,基线比值值显著降低接近 1.0。在运动和肌肉代谢反射激活之间没有观察到显著变化,在肌肉代谢反射激活期间,心力衰竭和对照组之间的比值也没有显著差异。我们得出结论,心力衰竭降低了肌肉代谢反射增益和收缩与舒张速率。此外,我们观察到在肌肉代谢反射激活期间,收缩与舒张速率的比值在对照组和心力衰竭组之间没有显著差异,但由于舒张速率增加,健康受试者的比值发生了显著变化,而在心力衰竭中则被消除。