0397 REPETITIVE SLEEP DISRUPTION, AN EXPERIMENTAL MODEL OF INSOMNIA, LEADS TO INCREASED SYMPATHETIC ACTIVITY

• Published in: Sleep (New York, N.Y.) N.Y.), 2017-04, Vol.40 (suppl_1), p.A148-A148
• Main Authors: Yang, H, Haack, M, Mullington, J
• Format: Article
• Language: English
• Subjects: Hypertension; Insomnia; Sleep deprivation; Spectrum analysis
• ISSN: 0161-8105; 1550-9109
• DOI: 10.1093/sleepj/zsx050.396

Abstract Introduction: Sympathetic over-activity is an important feature of hypertension and might be the underlying mechanism of the link between insomnia with reduced total sleep time and hypertension. The normalized low frequency component of heart rate variability (HRV) spectra is considered a quantitative index of sympathetic activation. Thus, we investigated autonomic modulation via HRV in response to a novel repetitive sleep disruption protocol, an experimental model of insomnia. Methods: Eight healthy participants (age 28 ± 2 yrs; BMI 23 ± 1 kg/m2) completed a 19-day in-hospital protocol. Following 3 nights of consolidated sleep (8h/night from 2300-0700), participants were exposed to three nights of sleep disruption (40 min sleep opportunity and 20 min experimental awakening monitored by staff, repeated between midnight and 6am) followed by one night 8h recovery sleep. This sleep disruption protocol repeated three times, followed by three additional nights of recovery sleep at the end of the study. Two-lead electrocardiography was recorded during 5min controlled breathing (15 breaths/min) in the morning at baseline, each sleep disruption block and recovery. Lomb-scargle periodogram algorithm was performed to generate the power spectrum analysis of R-R interval. Spectral power of LF (0.04–0.15 Hz) was analyzed in normalized units (nu; LF/[total power- very LF component]) as indicator of sympathetic modulation. Results: There was a significant intervention effect (p=0.045) on normalized LF measured during controlled breathing. Specifically, normalized LF showed a trend towards an increase over baseline (14 ± 8 nu, p=0.094) following the first block of sleep disruption, and significantly increased during the second (22 ± 8 nu, p=0.009) and third (21 ± 8 nu, p=0.015) blocks of sleep disruption. Furthermore, normalized LF was still elevated after two nights of recovery sleep (23 ± 8 nu, p=0.009) compared to baseline. Conclusion: Sympathetic activity was exacerbated by repetitive experimental sleep disruption and was still elevated following two nights of recovery sleep. Our preliminary results indicate a disrupted autonomic function due to repetitive exposure to sleep disruption, an experimental model of insomnia. Support (If Any): NIH/NINDS (NS-091177); NIH/UL1 RR02758 and M01-RR-01032 from the National Center for Research Resources to the Harvard Clinical and Translational Science Center.