Crooks Elena, Hansen Devon A, Satterfield Brieann C, Layton Matthew E, Van Dongen Hans P A
Sleep and Performance Research Center, Washington State University, PO Box 1495, Spokane, WA 99210-1495, USA; Department of Physical Therapy, Eastern Washington University, 310 N. Riverpoint Blvd., Spokane, WA 99202-0002, USA.
Sleep and Performance Research Center, Washington State University, PO Box 1495, Spokane, WA 99210-1495, USA; Elson S. Floyd College of Medicine, Washington State University, PO Box 1495, Spokane, WA 99210-1495, USA.
Physiol Behav. 2019 Oct 15;210:112643. doi: 10.1016/j.physbeh.2019.112643. Epub 2019 Aug 6.
Caffeine is often consumed to mitigate degraded alertness associated with sleep deprivation. Both caffeine and sleep deprivation have been implicated in cardiovascular disease, but evidence is largely anecdotal. We determined the effects of sleep deprivation and caffeine on markers of cardiac autonomic activity. Twelve healthy young adults completed an 18-day laboratory study. They were exposed to three 48 h sessions of acute total sleep deprivation (TSD), each separated by three recovery days. In randomized, counter-balanced order, subjects received 0 mg (placebo), 200 mg, or 300 mg of caffeine at 12 h intervals during each sleep deprivation session. Every 2 h during scheduled wakefulness, a 15-minute neurobehavioral task battery was administered, during which heart rate (HR) and the high frequency (HF) component of the HR variability power spectrum (HF-HRV) were measured. Caffeine administration decreased HR and increased HF-HRV, indicating elevated parasympathetic activity. The 300 mg caffeine dose did not significantly affect autonomic activity to a greater extent than the 200 mg dose. There was no significant effect of 48 h of TSD on HR, whereas there was a small increase across hours awake in HF-HRV. There was no significant interaction of TSD with caffeine. Circadian rhythmicity in HR and HF-HRV surpassed the magnitude of the effects of caffeine and TSD. Caffeine and acute TSD thus produced only modest changes in cardiac autonomic activity, unlikely to have immediate clinical implications in healthy young adults. However, further research is needed to determine the long-term effects of chronic exposure to sleep loss and/or caffeine on cardiac health, and to determine the generalizability of our findings to non-healthy populations.
人们常常摄入咖啡因以缓解与睡眠剥夺相关的警觉性下降。咖啡因和睡眠剥夺都与心血管疾病有关,但证据大多是传闻。我们确定了睡眠剥夺和咖啡因对心脏自主神经活动标志物的影响。12名健康的年轻成年人完成了一项为期18天的实验室研究。他们经历了三个48小时的急性完全睡眠剥夺(TSD)阶段,每个阶段之间间隔三天恢复期。在每个睡眠剥夺阶段,受试者按照随机、平衡的顺序,每隔12小时接受0毫克(安慰剂)、200毫克或300毫克的咖啡因。在预定的清醒期间,每2小时进行一次为期15分钟的神经行为任务组,在此期间测量心率(HR)和心率变异性功率谱的高频(HF)成分(HF-HRV)。服用咖啡因可降低心率并增加HF-HRV,表明副交感神经活动增强。300毫克咖啡因剂量对自主神经活动的影响并不比200毫克剂量显著更大。48小时的TSD对心率没有显著影响,而HF-HRV在清醒时间内有小幅增加。TSD与咖啡因之间没有显著的相互作用。心率和HF-HRV的昼夜节律超过了咖啡因和TSD的影响程度。因此,咖啡因和急性TSD对心脏自主神经活动仅产生适度变化,在健康年轻成年人中不太可能有直接的临床意义。然而,需要进一步研究以确定长期暴露于睡眠不足和/或咖啡因对心脏健康的长期影响,并确定我们的研究结果对非健康人群的普遍性。