Departments of Medicine and Neurology, Division of Sleep and Circadian Disorders, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Division of Sleep Medicine, Harvard Medical School, Massachusetts, Boston, USA.
J Pineal Res. 2022 Aug;73(1):e12805. doi: 10.1111/jpi.12805. Epub 2022 May 25.
Circadian adaptation to shifted sleep/wake schedules may be facilitated by optimizing the timing, intensity and spectral characteristics of light exposure, which is the principal time cue for mammalian circadian pacemaker, and possibly by strategically timing nonphotic time cues such as exercise. Therefore, circadian phase resetting by light and exercise was assessed in 44 healthy participants (22 females, mean age [±SD] 36.2 ± 9.2 years), who completed 8-day inpatient experiments simulating night shiftwork, which included either an 8 h advance or 8 h delay in sleep/wake schedules. In the advance protocol (n = 18), schedules were shifted either gradually (1.6 h/day across 5 days) or abruptly (slam shift, 8 h in 1 day and maintained across 5 days). Both advance protocols included a dynamic lighting schedule (DLS) with 6.5 h exposure of blue-enriched white light (704 melanopic equivalent daylight illuminance [melEDI] lux) during the day and dimmer blue-depleted light (26 melEDI lux) for 2 h immediately before sleep on the shifted schedule. In the delay protocol (n = 26), schedules were only abruptly delayed but included four different lighting conditions: (1) 8 h continuous room-light control; (2) 8 h continuous blue-enriched light; (3) intermittent (7 × 15 min pulses/8 h) blue-enriched light; (4) 8 h continuous blue-enriched light plus moderate intensity exercise. In the room-light control, participants received dimmer white light for 30 min before bedtime, whereas in the other three delay protocols participants received dimmer blue-depleted light for 30 min before bedtime. Both the slam and gradual advance protocols induced similar shifts in circadian phase (3.28 h ± 0.37 vs. 2.88 h ± 0.31, respectively, p = .43) estimated by the change in the timing of timing of dim light melatonin onset. In the delay protocol, the continuous 8 h blue-enriched exposure induced significantly larger shifts than the room light control (-6.59 h ± 0.43 vs. -4.74 h ± 0.62, respectively, p = .02). The intermittent exposure induced ~60% of the shift (-3.90 h ± 0.62) compared with 8 h blue-enriched continuous light with only 25% of the exposure duration. The addition of exercise to the 8 h continuous blue-enriched light did not result in significantly larger phase shifts (-6.59 h ± 0.43 vs. -6.41 h ± 0.69, p = .80). Collectively, our results demonstrate that, when attempting to adapt to an 8 h overnight work shift, delay shifts are more successful, particularly when accompanied by a DLS with high-melanopic irradiance light stimulus during wake.
生物钟适应移位的睡眠/觉醒时间表可能通过优化光暴露的时间、强度和光谱特性来实现,光暴露是哺乳动物生物钟节律器的主要时间线索,并且可能通过有策略地定时非光时间线索(如运动)来实现。因此,在 44 名健康参与者(22 名女性,平均年龄[±SD]36.2±9.2 岁)中评估了光和运动对生物钟相位的重置,他们完成了模拟夜班工作的 8 天住院实验,其中包括睡眠/觉醒时间表提前 8 小时或延迟 8 小时。在提前方案(n=18)中,日程安排逐渐(5 天内每天 1.6 小时)或突然(突然改变,1 天内 8 小时,并在 5 天内保持)改变。这两个提前方案都包括一个动态照明方案(DLS),白天有 6.5 小时暴露于富含蓝色的白光(704 个光生物学等效日光照度[melEDI]勒克斯),在移到时间表上睡觉前的 2 小时内,使用较暗的蓝色耗尽光(26 melEDI 勒克斯)。在延迟方案(n=26)中,日程安排仅突然延迟,但包括四种不同的照明条件:(1)8 小时连续室内光控制;(2)8 小时连续富含蓝色的光;(3)间歇性(7×15 分钟脉冲/8 小时)富含蓝色的光;(4)8 小时连续富含蓝色的光加上中等强度的运动。在室内灯光控制下,参与者在睡前 30 分钟接受较暗的白光,而在其他三种延迟方案中,参与者在睡前 30 分钟接受较暗的蓝色耗尽光。在突然改变和逐渐改变方案中,通过测定褪黑素开始时间的变化,估计生物钟相位的变化相似(分别为 3.28±0.37 小时和 2.88±0.31 小时,p=0.43)。在延迟方案中,连续 8 小时富含蓝色的暴露引起的变化明显大于室内光控制(-6.59±0.43 小时与-4.74±0.62 小时,p=0.02)。间歇性暴露引起的变化约为 60%(-3.90±0.62 小时),而 8 小时连续富含蓝色的光暴露仅持续 25%。将运动添加到 8 小时连续富含蓝色的光中并不会导致相位变化明显增大(-6.59±0.43 小时与-6.41±0.69 小时,p=0.80)。总之,我们的结果表明,当试图适应 8 小时的夜间工作班次时,延迟变化更成功,尤其是当在觉醒期间伴有高光生物学辐照度的 DLS 时。