Abstract：
OBJECTIVE: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.
摘要：
目的：睡眠前应激或过度觉醒是失眠障碍的一个重要病因。尽管如此,睡眠发作期间的生理变化还没有得到很好的理解。特别是,失眠和阻塞性睡眠呼吸暂停(OSA)是非常普遍的合并症，自主调节可能会改变。我们旨在表征睡眠发作期间的心率变异性（HRV），作为睡眠前过度觉醒的潜在量度。
方法：我们描述了睡眠前HRV测量的概况，并探索了自我报告失眠障碍参与者的自主神经差异（没有OSA，n=69；轻度OSA，n=70；中度或重度OSA，n=66),与正常睡眠对照组相比（n=123）。提取睡眠开始过程期间的心率数据用于HRV分析。
结果：在睡眠开始过程中，与正常睡眠对照相比，失眠参与者的HRV改变，心率较高（p=0.004），较低的SDNN(p=0.003)，降低pNN20（p<0.001）和pNN50（p=0.010），降低功率（p<0.001）。与无/轻度OSA失眠患者相比，失眠和中度/重度OSA患者的HRV结果可能进一步恶化，但差异不显着。失眠本身与明显较高的心率有关，较低的pNN20，即使在调整年龄后也较低的高频功率，性别,BMI和OSA严重程度。
结论：失眠的参与者在睡眠发作期迷走神经活动较低，这可能是由OSA复合的，反映在更高的心率和更低的HRV。这些改变的心率动力学可以作为睡前失眠的生理生物标志物，或作为评估针对睡前压力的行为干预措施功效的潜在工具。
方法：我们描述了睡眠前HRV测量的概况，并探索了自我报告失眠障碍参与者的自主神经差异（没有OSA，n=69；轻度OSA，n=70；中度或重度OSA，n=66),与正常睡眠对照组相比（n=123）。提取睡眠开始过程期间的心率数据用于HRV分析。
结果：在睡眠开始过程中，与正常睡眠对照相比，失眠参与者的HRV改变，心率较高（p=0.004），较低的SDNN(p=0.003)，降低pNN20（p<0.001）和pNN50（p=0.010），降低功率（p<0.001）。与无/轻度OSA失眠患者相比，失眠和中度/重度OSA患者的HRV结果可能进一步恶化，但差异不显着。失眠本身与明显较高的心率有关，较低的pNN20，即使在调整年龄后也较低的高频功率，性别,BMI和OSA严重程度。
结论：失眠的参与者在睡眠发作期迷走神经活动较低，这可能是由OSA复合的，反映在更高的心率和更低的HRV。这些改变的心率动力学可以作为睡前失眠的生理生物标志物，或作为评估针对睡前压力的行为干预措施功效的潜在工具。
