Spectral Power of Slow Wave Sleep is Associated with Reductions of Nocturnal Blood Pressure in Humans

Abstract

Slow wave sleep (SWS) is characterized by high amplitude, low frequency waveforms oscillating at 0.5 to 4 Hz. These slow wave oscillations, also referred to as delta waves, have been implicated as an important component of cardiovascular health. Specifically, SWS is associated with sympathoinhibition and decreased blood pressure, and studies suggest the greatest reductions of nocturnal blood pressure during SWS. Recent studies report that the strength of SWS, quantified using spectral analysis of the delta waves and referred to as delta power density, is related to clinical conditions such as fibromyalgia and depression. To date, the impact of delta power density on nocturnal blood pressure remains unknown. We hypothesized that delta power density would be greater during the first cycle of SWS compared to the second cycle of SWS, and that this would be associated with greater reductions of nocturnal blood pressure. Eight participants (5 female, 23 ± 1 years, 29 ± 2 kg/m2) were equipped with overnight finger plethysmography (NOVA, Finapres) and a standard 10–20 electroencephalography (EEG) for quantification of sleep stages. Overnight EEG was scored by a board certified sleep technician. EEG signals were filtered with a low pass (35 Hz), high pass (0.5 Hz), and notch filter (60 Hz). Central leads (C3 and C4) were analyzed using an original Matlab® code, applying a short‐term Fourier transform function (i.e., spectral analysis) with sliding window parameters of 10 seconds by 5 seconds to detect delta frequencies (i.e., 0.5 to 4 Hz). Delta frequencies were normalized to the entire overnight EEG to quantify delta power density. Beat‐to‐beat systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and heart rate (HR) were compared across a wake baseline (minimum 5 min), the first SWS cycle (18 ± 3 min), and the second SWS cycle (40 ± 13 min) using repeated measures ANOVA (p<0.05). Pearson correlations were used to compare changes of delta power density with changes in blood pressure between SWS cycles 1 and 2. SAP was significantly reduced during the first (111 ± 3 to 96 ± 4 mmHg; p = 0.01), but not second (108 ± 5 mmHg), cycle of SWS when compared to the wake baseline. In contrast, DAP was significantly reduced during both the first (68 ± 3 to 56 ± 3 mmHg; p < 0.02) and second (61 ± 5 mmHg; p = 0.03) cycles of SWS. HR was not statistically different between wake and either cycle of SWS. Delta power density was not different between SWS cycles, but changes in delta power density across SWS cycles was significantly correlated with changes in SAP (r = −0.69, p = 0.03) and DAP (r = −0.71, p = 0.02). Our findings indicate that the strength of SWS, as quantified by delta power density, is significantly associated with greater reductions in nocturnal blood pressure. These results support emerging evidence that sleep is important to cardiovascular health and that the strength of SWS is of particular relevance. This has potential clinical implications, as there are a number of conditions and drugs that can diminish slow wave sleep.Support or Funding InformationSupport provided by the National Institutes of Health (AA‐024892) and the Portage Health Foundation.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.