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迷走神经介导的低频心率变异性在缓慢瑜伽呼吸期间。

Vagal Mediation of Low-Frequency Heart Rate Variability During Slow Yogic Breathing.

机构信息

From the Department of Psychiatry (Kromenacker, Sanova, Lane), University of Arizona, Tucson, Arizona; Department of Psychology (Kromenacker, Allen, Lane), University of Arizona, Tucson, Arizona; and Department of Medicine (Marcus), University of Arizona, Tucson, Arizona.

出版信息

Psychosom Med. 2018 Jul/Aug;80(6):581-587. doi: 10.1097/PSY.0000000000000603.

Abstract

OBJECTIVE

Changes in heart rate variability (HRV) associated with breathing (respiratory sinus arrhythmia) are known to be parasympathetically (vagally) mediated when the breathing rate is within the typical frequency range (9-24 breaths per minute [bpm]; high-frequency HRV). Slow yogic breathing occurs at rates below this range and increases low-frequency HRV power, which may additionally reflect a significant sympathetic component. Yogic breathing techniques are hypothesized to confer health benefits by increasing cardiac vagal control, but increases in low-frequency HRV power cannot unambiguously distinguish sympathetic from parasympathetic contributions. The aim of this study was to investigate the autonomic origins of changes in low-frequency HRV power due to slow-paced breathing.

METHODS

Six healthy young adults completed slow-paced breathing with a cadence derived from yogic breathing patterns. The paced breathing took place under conditions of sympathetic blockade, parasympathetic (vagal) blockade, and placebo. HRV spectral power was compared under 11 breathing rates during each session, in counterbalanced order with frequencies spanning the low-frequency range (4-9 bpm).

RESULTS

HRV power across the low-frequency range (4-9 bpm) was nearly eliminated (p = .016) by parasympathetic blockade (mean (SD) spectral power at breathing frequency = 4.1 (2.1)) compared with placebo (69.5 (8.1)). In contrast, spectral power during sympathetic blockade 70.2 (9.1) and placebo (69.5 (8.1)) was statistically indistinguishable (p = .671).

CONCLUSIONS

These findings clarify the interpretation of changes in HRV that occur during slow-paced breathing by showing that changes in low-frequency power under these conditions are almost entirely vagally mediated. Slow-paced breathing is an effective tool for cardiac vagal activation.

摘要

目的

当呼吸频率在典型范围内(9-24 次/分钟[bpm];高频 HRV)时,与呼吸相关的心率变异性(HRV)的变化已知是由副交感神经(迷走神经)介导的。慢瑜伽呼吸发生在该范围以下的频率,并增加低频 HRV 功率,这可能额外反映出重要的交感成分。瑜伽呼吸技术被假设通过增加心脏迷走神经控制来带来健康益处,但低频 HRV 功率的增加不能明确区分交感神经和副交感神经的贡献。本研究旨在调查由于慢节奏呼吸而导致低频 HRV 功率变化的自主神经起源。

方法

六名健康的年轻人按照源自瑜伽呼吸模式的节奏进行慢节奏呼吸。在交感神经阻滞、副交感神经(迷走神经)阻滞和安慰剂条件下进行有节奏的呼吸。在每个会话中,以 11 种呼吸频率比较 HRV 频谱功率,以平衡的顺序涵盖低频范围(4-9 bpm)的频率。

结果

与安慰剂(4.1(2.1))相比,副交感神经阻滞时低频范围(4-9 bpm)的 HRV 功率几乎完全消除(p =.016)(呼吸频率的平均(SD)频谱功率)。相比之下,交感神经阻滞时的频谱功率 70.2(9.1)和安慰剂时的频谱功率(69.5(8.1))在统计学上无显着差异(p =.671)。

结论

这些发现通过表明在这些条件下低频功率的变化几乎完全是由迷走神经介导的,澄清了在慢节奏呼吸过程中发生的 HRV 变化的解释。慢节奏呼吸是心脏迷走神经激活的有效工具。

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