3.9 Article

SWS SUPPRESSION ADVERSELY AFFECTS GLUCOSE HOMEOSTASIS. THE ROLE OF AUTONOMOUS NERVOUS SYSTEM AND HYPOTHALAMO-PITUITARY-ADRENAL AXIS

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MEZHDUNARODNAYA KNIGA
DOI: 10.1134/S0044467719040105

Keywords

slow-wave sleep suppression; glucose intolerance; autonomous nervous system; heart rate; cortisol

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It was repeatedly shown that slow-wave sleep (SWS) plays a major role in the regulation of insulin sensitivity and SWS suppression impairs morning glucose tolerance. However, the underlying mechanism of this effect remains unclear. The present study aimed to explore a possible role of the activity of autonomous nervous system (ANS), and hypothalamo-pituitary-adrenal axis (HPA) in glucose tolerance impairment after SWS suppression. Fourteen healthy male volunteers with a regular sleep-wake cycle participated in the study. Due to the study's randomized, balanced crossover design, each volunteer participated in two experimental sessions: a session with selective SWS suppression during night sleep and a session with regular night sleep (control). SWS suppression was achieved by presenting an acoustic tone. For analyzing cardiac autonomic activity parameters of heart rate variability were assessed. Salivary samples were collected five times: at 20.00, at 01.30, at 04.00, at 07.00, and at 07.40. The samples were analyzed by liquid chromatography-tandem mass spectrometry for cortisol. In the morning an oral glucose tolerance test was performed and blood glucose was measured. The SWS suppression resulted in a reduction of its overall length by 54%. Morning glucose tolerance was impaired after selective SWS suppression: blood glucose 1 hour after glucose intake was significantly higher in disturbed SWS condition versus control. Comparing to control night SWS suppression was accompanied by increase in low frequency to high frequency (LF/HF) power ratio of heart rate variability suggesting increased sympathetic activity. Salivary cortisol levels remained unaffected. In conclusion, we showed that selective SWS suppression prevents physiological nighttime decrease of sympathetic activity. Such persistent increase in sympathetic activity during night can be one of the mechanisms of glucose intolerance in the conditions of SWS deficiency.

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