Metaboreceptor activation in heart failure with reduced ejection fraction: Linking cardiac and peripheral vascular haemodynamics

被引:12
作者
Barrett-O'Keefe, Zachary [1 ,2 ]
Lee, Joshua F. [2 ,3 ]
Berbert, Amanda [2 ]
Witman, Melissa A. H. [2 ]
Nativi-Nicolau, Jose [4 ]
Stehlik, Josef [4 ]
Richardson, Russell S. [2 ,3 ,5 ]
Wray, D. Walter [2 ,3 ,5 ]
机构
[1] Univ Utah, Dept Exercise & Sport Sci, Salt Lake City, UT 84148 USA
[2] Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Salt Lake City, UT 84148 USA
[3] Univ Utah, Dept Internal Med, Div Geriatr, Salt Lake City, UT 84148 USA
[4] Univ Utah, Dept Internal Med, Div Cardiol, Salt Lake City, UT 84148 USA
[5] Univ Utah, Dept Nutr & Integrat Physiol, Salt Lake City, UT 84148 USA
基金
美国国家卫生研究院;
关键词
arterial blood pressure; exercise; heart failure; metaboreflex; EXERCISE PRESSOR REFLEX; MUSCLE METABOREFLEX; ARTERIAL-PRESSURE; BLOOD-PRESSURE; STROKE VOLUME; LEFT-VENTRICLE; HUMANS; MECHANISMS; INTOLERANCE; HYPOTHESIS;
D O I
10.1113/EP086948
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
We sought to evaluate the muscle metaboreflex in heart failure with reduced ejection fraction (HFrEF) patients, with an emphasis on the interaction between cardiac and peripheral vascular haemodynamics across multiple levels of metaboreceptor activation. In 23HFrEF patients (63 +/- 2years of age) and 15 healthy control subjects (64 +/- 3years of age), we examined changes in mean arterial pressure, cardiac output, systemic vascular conductance, effective arterial elastance, stroke work and forearm deoxyhaemoglobin concentration during metaboreceptor activation elicited by postexercise circulatory occlusion (PECO) after three levels of static-intermittent handgrip exercise (15, 30 and 45% maximal voluntary contraction). Across workloads, the metaboreflex-induced increase in deoxyhaemoglobin and mean arterial pressure were similar between groups. However, in control subjects, the pressor response was driven by changes () in cardiac output(495 +/- 155, 564 +/- 156 and 666 +/- 217mlmin(-1)), whereas this change was accomplished by intensity-dependent reductions in systemic vascular conductance in patients with HFrEF (-4.9 +/- 1.5, -9.1 +/- 1.9 and -12.7 +/- 1.8mlminmmHg(-1)). This differential response contributed to the exaggerated increases in effective arterial elastance in HFrEF patients compared with control subjects, coupled with a blunted response in stroke work in the HFrEF patients. Together, these findings indicate a preserved role of the metaboreflex-induced pressor response in HFrEF but suggest that this response is governed by changes in the peripheral circulation. The net effect of this response appears to be maladaptive, as it places a substantial haemodynamic load on the left ventricle that may exacerbate left ventricular systolic dysfunction and contribute to exercise intolerance in this patient population.
引用
收藏
页码:807 / 818
页数:12
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