0110 Sleep Fragmentation Elevates Blood Pressure and Alters Parasympathetic Activity During Slow Wave Sleep in Rats

Abstract Introduction Sleep plays a major role in health and chronic sleep disruption can increase cardiometabolic disease risk. Spectral analysis of physiologic data quantifies signal power across defined frequency bands, providing a measure of sleep architecture and heart rate variability (HRV). HRV reflects the body’s capacity to adapt to physiological stressors, including sleep fragmentation (SF), because it indexes autonomic regulation of vascular tone and blood pressure (BP). This study evaluates whether SF increases cardiovascular disease risk by altering BP and autonomic regulation, as measured by HRV. Methods Male Wistar–Kyoto rats were implanted with telemetry transmitters to record BP and cortical electroencephalogram (EEG) signals (Data Sciences International). Animals were maintained on a 12:12 light–dark cycle (Zeitgeber Time [ZT]0–12 light; ZT12–24 dark). Rats were randomized to 8 hours (ZT1-9) of daily SF via a mechanical sweeper bar (n=8) or undisturbed controls (n=7). EEG were recorded over intervention (28-days) and recovery (7-days). HRV and BP during slow wave sleep (SWS) in the bar on period were quantified from systolic peak intervals (aortic BP tracing) to generate high frequency (HF) band power and square root of the mean squared RR-interval difference (rMSSD) metrics. Results The SF intervention increased mean arterial pressure (MAP) during SWS over time (group x time, p<.0001), where at day 28, SF rats had elevated MAP vs. controls (+7.24, p =.016). SF also differentially impacted HRV responsiveness in SF rats vs. controls across intervention and recovery in metrics including HF band power and rMSSD (both group x time p<.01). Notably, rMSSD was elevated in SF vs. control animals at int10 (+2.30, p=.007) and int28 (+2.39, p=.009), which normalized during recovery (p>.05 across all days). Conclusion Increased HF power and rMSSD may reflect enhanced parasympathetic activation as a homeostatic autonomic nervous system response to SF-induced BP elevations during SWS. Ongoing analyses are evaluating whether changes in HRV are sustained during bar off periods and the relationships between sleep quality, HRV, and BP outcomes. Support (if any) This work was funded through R00NR014369 to AMF. SX, SML, JJB, LY and KAM are supported by intramural research funds from the National Institutes of Health, Clinical Center.