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肌肉代谢反射与人体心率的自主调节。

Muscle metaboreflex and autonomic regulation of heart rate in humans.

机构信息

School of Sport and Exercise Sciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

出版信息

J Physiol. 2013 Aug 1;591(15):3777-88. doi: 10.1113/jphysiol.2013.254722. Epub 2013 May 27.

DOI:10.1113/jphysiol.2013.254722
PMID:23713032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3752457/
Abstract

We elucidated the autonomic mechanisms whereby heart rate (HR) is regulated by the muscle metaboreflex. Eight male participants (22 ± 3 years) performed three exercise protocols: (1) enhanced metaboreflex activation with partial flow restriction (bi-lateral thigh cuff inflation) during leg cycling exercise, (2) isolated muscle metaboreflex activation (post-exercise ischaemia; PEI) following leg cycling exercise, (3) isometric handgrip followed by PEI. Trials were undertaken under control (no drug), β1-adrenergic blockade (metoprolol) and parasympathetic blockade (glycopyrrolate) conditions. HR increased with partial flow restriction during leg cycling in the control condition (11 ± 2 beats min(-1); P < 0.05). The magnitude of this increase in HR was similar with parasympathetic blockade (11 ± 2 beats min(-1)), but attenuated with β-adrenergic blockade (4 ± 1 beats min(-1); P < 0.05 vs. control and parasympathetic blockade). During PEI following leg cycling exercise, HR remained similarly elevated above rest under all conditions (11 ± 2, 13 ± 3 and 9 ± 4 beats min(-1), for control, β-adrenergic and parasympathetic blockade; P > 0.05 between conditions). During PEI following handgrip, HR was similarly elevated from rest under control and parasympathetic blockade (4 ± 1 vs. 4 ± 2 beats min(-1); P > 0.05 between conditions) conditions, but attenuated with β-adrenergic blockade (0.2 ± 1 beats min(-1); P > 0.05 vs. rest). Thus muscle metaboreflex activation-mediated increases in HR are principally attributable to increased cardiac sympathetic activity, and only following exercise with a large muscle mass (PEI following leg cycling) is there a contribution from the partial withdrawal of cardiac parasympathetic tone.

摘要

我们阐明了心率(HR)受肌肉代谢反射调节的自主机制。八名男性参与者(22 ± 3 岁)进行了三项运动方案:(1)在腿部循环运动期间通过双侧大腿袖带充气增强代谢反射激活,(2)腿部循环运动后的孤立肌肉代谢反射激活(PEI),(3)等长握力后进行 PEI。在控制(无药物)、β1 肾上腺素能阻断(美托洛尔)和副交感神经阻断(格隆溴铵)条件下进行试验。在控制条件下,腿部循环期间部分血流量限制会导致 HR 增加(11 ± 2 次/分钟;P < 0.05)。在副交感神经阻断的情况下,HR 增加的幅度相似(11 ± 2 次/分钟),但在β肾上腺素能阻断的情况下减弱(4 ± 1 次/分钟;P < 0.05 与控制和副交感神经阻断)。在腿部循环运动后的 PEI 期间,在所有条件下 HR 均保持高于静息水平(控制、β 肾上腺素能和副交感神经阻断分别为 11 ± 2、13 ± 3 和 9 ± 4 次/分钟;P > 0.05 之间的条件)。在手握后进行 PEI 时,在控制和副交感神经阻断条件下 HR 均从静息状态升高(4 ± 1 与 4 ± 2 次/分钟;P > 0.05 之间的条件),但在β肾上腺素能阻断的情况下减弱(0.2 ± 1 次/分钟;P > 0.05 与休息)。因此,肌肉代谢反射激活介导的 HR 增加主要归因于心脏交感神经活动的增加,只有在进行大量肌肉运动(腿部循环后的 PEI)时,才会从心脏副交感神经张力的部分撤回中得到贡献。

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