Abstract
Introduction: Recent epidemiological studies suggest that insomnia is associated with heightened cardiovascular risk, but underlying physiological mechanisms remain unclear. The present study examined sympathetic neural and cardiovascular regulation in clinically diagnosed insomniacs and controls. Consistent with the hyperarousal theory of insomnia, we hypothesized that insomniacs would demonstrate higher sympathetic neural outflow, blunted baroreflex control, and augmented neural cardiovascular reactivity to stress when compared to matched controls. Methods: Thirteen insomniacs (40 ± 4 years, 24 ± 1 kg/m2) and 15 matched controls (35 ± 3 years, 26 ± 1 kg/m2; p>0.05) participated in an overnight laboratory polysomnography to exclude obstructive sleep apnea and other sleep disorders, two weeks of at-home actigraphy, and an overnight laboratory visit with an autonomic function test the subsequent morning. The autonomic function test included simultaneous recordings of heart rate (electrocardiogram), beat-to-beat blood pressure (finger plethysmography), and muscle sympathetic nerve activity (MSNA; microneurography) during 10 min supine baseline and 2 min cold pressor test. Results: Baseline blood pressure, heart rate, and MSNA were not different between insomniacs and controls (p>0.05), but sympathetic baroreflex sensitivity was significantly blunted in insomniacs when compared to controls (-2.1 ± 0.3 vs. -4.3 ± 0.4 bursts/100 heart beats/ mmHg; p<0.001). During cold pressor test, systolic blood pressure (Δ20 ± 3 vs. Δ11 ± 2mmHg; time × group = 0.031) and total MSNA (Δ131 ± 29% vs. Δ65 ± 17%; time × group = 0.038) reactivity were significantly augmented in insomniacs compared to controls. Heart rate reactivity to cold pressor test was not different between insomniacs and controls (Δ10 ± 4 vs. Δ9 ± 3 beats/min; time × group = 0.677). Conclusion: Patients with insomnia demonstrated a blunted sympathetic baroreflex and augmented MSNA and blood pressure responsiveness to cold pressor test compared to matched controls. These findings support growing evidence of increased cardiovascular risk and physiological hyperarousal with chronic insomnia.
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CITATION STYLE
Carter, J., Grimaldi, D., Fonkoue, I., Medalie, L., Mokhlesi, B., & Van Cauter, E. (2017). 0305 SYMPATHONEURAL AND CARDIOVASCULAR HYPERAROUSAL IN CHRONIC INSOMNIA. Sleep, 40(suppl_1), A113–A113. https://doi.org/10.1093/sleepj/zsx050.304
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