Study Objectives Sleep restriction therapy (SRT) effectively treats insomnia but mechanisms are poorly understood. Theoretical models suggest that potentiation of sleep pressure and reduction of arousal are key mechanisms of action. To our knowledge, this has never been directly tested. We designed a randomized controlled trial with embedded mechanistic measurement to investigate if SRT causally modifies multidimensional assessments of sleep pressure and arousal. Methods Participants aged 25–55 who met DSM-5 diagnostic criteria for insomnia disorder were randomized to four weeks of SRT or time in bed regularization (TBR), a control intervention that involves prescription of a regular but not reduced time in bed. Sleep pressure was assessed through daily diary appraisal of morning and evening sleepiness, weekly Epworth sleepiness scale (ESS) scores, psychomotor vigilance, and non-rapid eye movement (NREM) delta power (0.75–4.5 Hz) from ambulatory polysomnographic recordings. Arousal was assessed through daily diary appraisal of cognitive arousal, the pre-sleep arousal scale (PSAS), and NREM beta power (15–32 Hz). Outcomes were assessed at baseline (2-week period prior to randomization), during the intervention phase (1–4 weeks post-randomization), and at 12-week follow-up. We performed intention-to-treat analyses using linear mixed models. For continuous daily measures, the treatment period was split into early (weeks 1–2) and late (weeks 3–4) treatment. Results Fifty-six participants (39 females, mean age = 40.78 ± 9.08) were assigned to SRT (n = 27) or TBR (n = 29). The SRT group showed enhanced sleep pressure relative to TBR, reflected in (1) enhanced sleepiness in the evening during early (d = 1.17) and late treatment (d = 0.92), and in the morning during early treatment (d = 0.47); (2) higher daytime sleepiness on the ESS at weeks-1 and -2 (d = 0.54, d = 0.45); and (3) reduced psychomotor vigilance at week-1 (d = 0.34). The SRT group also showed reduced arousal relative to TBR, reflected in lower levels of daily-monitored cognitive arousal during early treatment (d = 0.53) and decreased PSAS total score at week-4 and week-12 (ds ≥ 0.39). Power spectral analysis of all night NREM sleep revealed an increase in relative, but not absolute, EEG delta power at week-1 and week-4 (ds ≥ 0.52) and a decrease of relative EEG beta power at week-4 (d = 0.11). Conclusion For the first time, we show that SRT increases sleep pressure and decreases arousal during acute implementation, providing support for mechanism-of-action.

中文翻译：

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睡眠限制疗法对失眠症的睡眠压力和觉醒的影响：一项随机对照机制试验

研究目标 睡眠限制疗法 (SRT) 可有效治疗失眠，但对其机制知之甚少。理论模型表明，睡眠压力的增强和觉醒的减少是关键的作用机制。据我们所知，这从未被直接测试过。我们设计了一项带有嵌入式机械测量的随机对照试验，以研究 SRT 是否会改变对睡眠压力和觉醒的多维评估。方法 年龄在 25-55 岁且符合 DSM-5 失眠症诊断标准的参与者被随机分配至 4 周的 SRT 或卧床时间规则化 (TBR)，这是一种控制干预措施，包括规定卧床时间有规律但不缩短。睡眠压力通过每天早晨和晚上嗜睡的日记评估、每周 Epworth 嗜睡量表 (ESS) 评分、来自动态多导睡眠图记录的精神运动警觉性和非快速眼动 (NREM) 增量功率 (0.75–4.5 Hz)。通过认知唤醒的日常日记评估、睡前唤醒量表 (PSAS) 和 NREM β 功率 (15-32 Hz) 来评估唤醒。在基线（随机化前 2 周）、干预阶段（随机化后 1-4 周）和 12 周随访时评估结果。我们使用线性混合模型进行了意向治疗分析。对于连续的每日测量，治疗期分为早期（第 1-2 周）和晚期（第 3-4 周）治疗。结果 56 名参与者（39 名女性，平均年龄 = 40.78 ± 9.08）被分配到 SRT（n = 27）或 TBR（n = 29）。相对于 TBR，SRT 组的睡眠压力增加，体现在（1）治疗早期（d = 1.17）和治疗晚期（d = 0.92）和早期治疗期间（d = 0.47）的早晨嗜睡增加；(2) ESS 在第 1 周和第 -2 周的白天嗜睡程度更高（d = 0.54，d = 0.45）；(3) 在第 1 周时降低精神运动警觉性 (d = 0.34)。与 TBR 相比，SRT 组的唤醒也有所降低，这反映在早期治疗期间每日监测的认知唤醒水平较低（d = 0.53），并且在第 4 周和第 12 周时 PSAS 总分降低（ds ≥ 0.39）。整夜 NREM 睡眠的功率谱分析显示，在第 1 周和第 4 周（ds ≥ 0.52）相对脑电图 delta 功率增加，但不是绝对增加，在第 4 周相对脑电图 β 功率降低（d = 0.11 ）。结论 第一次，