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Sympathetic Neural Control in Chronic Insomnia
Author(s) -
Carter Jason R.,
Grimaldi Daniela,
Fonkoue Ida T.,
Medalie Lisa,
Mokhlesi Babak,
Van Cauter Eve
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1086.6
Subject(s) - baroreflex , medicine , microneurography , blood pressure , heart rate , cardiology , heart rate variability , sympathetic nervous system , anesthesia , autonomic nervous system , supine position , polysomnography , obstructive sleep apnea , diastole , apnea
Heightened sympathetic neural activity and impaired baroreflex function are known contributors to hypertension and cardiovascular risk. Recent epidemiological studies report an association between chronic insomnia and hypertension. In the present study, we 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 and blunted baroreflex control when compared to matched controls. Thirteen insomniacs (40 ± 4 years, 24 ± 1 kg/m 2 ) and 15 matched controls (35 ± 3 years, 26 ± 1 kg/m 2 ; 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. Baseline systolic arterial pressure (110 ± 5 vs. 113 ± 4 mmHg; p=0.673), diastolic arterial pressure (69 ± 3 vs. 66 ± 2 mmHg; p=0.424), heart rate (64 ± 3 vs. 59 ± 2 mmHg; p=0.169), and MSNA (23 ± 3 vs. 25 ± 3 bursts/min; p=0.635) were not different between insomniacs and controls. In contrast, spontaneous sympathetic baroreflex sensitivity (BRS) 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). Cardiovagal BRS was not different between groups when assessed as either up‐up (23 ± 4 vs. 25 ± 6 ms/mmHg; p=0.843) or down‐down (25 ±5 vs. 25 ± 5 ms/mmHg; p=0.955) sequencing methods. In conclusion, insomniacs demonstrated similar levels of MSNA, but substantially blunted sympathetic BRS, at rest when compared to matched controls. These findings support growing evidence of increased risk of hypertension with chronic insomnia. Support or Funding Information Supported by Merck Investigators Studies Program.