Osher Center for Integrative Health, Division of Preventive Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States.
Sleep and Inflammatory Systems Laboratory, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, United States.
Sleep Med. 2024 Oct;122:92-98. doi: 10.1016/j.sleep.2024.07.034. Epub 2024 Aug 7.
Pre-sleep stress or hyperarousal is a known key etiological component in insomnia disorder. Despite this, physiological alterations during the sleep onset are not well-understood. In particular, insomnia and obstructive sleep apnea (OSA) are highly prevalent co-morbid conditions, where autonomic regulation may be altered. We aimed to characterize heart rate variability (HRV) during sleep onset as a potential measure of pre-sleep hyperarousal.
We described the profile of pre-sleep HRV measures and explore autonomic differences in participants with self-reported insomnia disorder (with no OSA, n = 69; with mild OSA, n = 70; with moderate or severe OSA, n = 66), compared to normal sleep controls (n = 123). Heart rate data during the sleep onset process were extracted for HRV analyses.
During the sleep onset process, compared to normal sleep controls, participants with insomnia had altered HRV, indicated by higher heart rate (p = 0.004), lower SDNN (p = 0.003), reduced pNN20 (p < 0.001) and pNN50 (p = 0.010) and lower powers (p < 0.001). Participants with insomnia and moderate/severe OSA may have further deteriorated HRV outcomes compared to no/mild OSA patients with insomnia but differences were not significant. Insomnia itself was associated with significantly higher heart rate, lower pNN20, and lower high frequency power even after adjustment for age, gender, BMI and OSA severity.
Participants with insomnia had lower vagal activity during the sleep onset period, which may be compounded by OSA, reflected in higher heart rates and lower HRV. These altered heart rate dynamics may serve as a physiological biomarker for insomnia during bedtime wakefulness, or as a potential tool to evaluate the efficacy of behavioral interventions which target bedtime stress.
睡前应激或过度觉醒是失眠障碍的一个已知关键病因学组成部分。尽管如此，睡眠起始期间的生理变化仍未得到很好的理解。特别是，失眠和阻塞性睡眠呼吸暂停（OSA）是高度普遍的共病情况，自主调节可能会发生改变。我们旨在描述睡眠起始期间的心率变异性（HRV）作为潜在的睡前过度觉醒测量指标。
我们描述了睡前 HRV 指标的特征，并探索了有或无 OSA（n=69）、有轻度 OSA（n=70）、有中度或重度 OSA（n=66）的自述失眠症患者与正常睡眠对照者（n=123）之间的自主神经差异。从 HRV 分析中提取睡眠起始过程中心率数据。
与正常睡眠对照组相比，失眠症患者在睡眠起始过程中心率变异性发生改变，表现为心率较高（p=0.004）、SDNN 较低（p=0.003）、pNN20 减少（p<0.001）、pNN50 减少（p=0.010）和功率降低（p<0.001）。与无/轻度 OSA 的失眠症患者相比，中度/重度 OSA 的失眠症患者的 HRV 结果可能进一步恶化，但差异无统计学意义。即使在调整年龄、性别、BMI 和 OSA 严重程度后，失眠症本身与心率显著升高、pNN20 显著降低和高频功率显著降低有关。
失眠症患者在睡眠起始期间的迷走神经活动较低，这可能因 OSA 而更加严重，表现为心率升高和 HRV 降低。这些改变的心率动力学可能作为睡前清醒期间失眠的生理生物标志物，或作为评估针对睡前应激的行为干预效果的潜在工具。
