Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, TX, United States of America.
Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia.
Auton Neurosci. 2020 Nov;228:102698. doi: 10.1016/j.autneu.2020.102698. Epub 2020 Jul 28.
Autonomic alterations at the onset of exercise are critical to redistribute cardiac output towards the contracting muscles while preventing a fall in arterial pressure due to excessive vasodilation within the contracting muscles. Neural mechanisms responsible for these adjustments include central command, the exercise pressor reflex, and arterial and cardiopulmonary baroreflexes. The exercise pressor reflex evokes reflex increases in sympathetic activity to the heart and systemic vessels and decreases in parasympathetic activity to the heart, which increases blood pressure (BP), heart rate, and total peripheral resistance through vasoconstriction of systemic vessels. In this review, we discuss recent advancements in our understanding of exercise pressor reflex function in health and disease. Specifically, we discuss emerging evidence suggesting that sympathetic vasoconstrictor drive to the contracting and non-contracting skeletal muscle is differentially controlled by central command and the metaboreflex in healthy conditions. Further, we discuss evidence from animal and human studies showing that cardiovascular diseases, including hypertension, diabetes, and heart failure, lead to an altered exercise pressor reflex function. We also provide an update on the mechanisms thought to underlie this altered exercise pressor reflex function in each of these diseases. Although these mechanisms are complex, multifactorial, and dependent on the etiology of the disease, there is a clear consensus that several mechanisms are involved. Ultimately, approaches targeting these mechanisms are clinically significant as they provide alternative therapeutic strategies to prevent adverse cardiovascular events while also reducing symptoms of exercise intolerance.
自主神经在运动开始时的改变对于将心输出量重新分配到收缩的肌肉非常重要，同时防止由于收缩肌肉内过度血管扩张导致动脉血压下降。负责这些调整的神经机制包括中枢命令、运动加压反射以及动脉和心肺压力反射。运动加压反射引起交感神经活性对心脏和全身血管的反射性增加，以及对心脏的副交感神经活性的降低，通过全身血管的血管收缩增加血压 (BP)、心率和总外周阻力。在这篇综述中，我们讨论了我们对健康和疾病中运动加压反射功能的理解的最新进展。具体来说，我们讨论了新出现的证据表明，在健康条件下，中枢命令和代谢反射对收缩和非收缩骨骼肌的交感血管收缩驱动力的控制是不同的。此外，我们还讨论了来自动物和人类研究的证据，表明心血管疾病，包括高血压、糖尿病和心力衰竭，导致运动加压反射功能改变。我们还提供了关于这些疾病中运动加压反射功能改变的潜在机制的最新信息。尽管这些机制复杂、多因素且取决于疾病的病因，但有一个明确的共识，即涉及多种机制。最终，针对这些机制的方法在临床上具有重要意义，因为它们提供了替代治疗策略，以预防不良心血管事件，同时减轻运动不耐受的症状。
