bioRxiv Science⌕ Search

bioRxiv · 10.1101/2025.11.01.685631

A broken power-law model of heart rate variability spectra in sleep

Abstract

AimsThe aim of the study was to introduce a parametric description of RR-interval spectra using a broken power-law model, in addition to the parametrization of oscillatory peaks. Furthermore, to use this model to evaluate effects of age, sex and sleep architecture on overnight heart rate variability (HRV) in healthy subjects. Methods & ResultsFrom a polysomnography database, 215 whole-night, high quality electrocardiograms (ECGs) were extracted. The fractal and oscillatory power-spectral densities (PSDs) were calculated from evenly resampled RR-interval time-series, then a broken power-law model was fitted using piecewise linear regression to the double-logarithmic PSD, determining a custom breaking point in the fractal component, and allowing for two independent spectral slopes in the lower and higher frequency domains. The two-slope model provided a more optimal description compared to linear regression in all cases, even when penalizing increased model complexity. Peak detection was applied to the oscillatory component in the LF (0.04-0.15 Hz) and HF (0.15-0.4 Hz) bands, extracting the frequency and prominence of the dominant peak from each. The high frequency domain intercept, the breaking point frequency and the LF peak frequency decreased significantly with age. Both slopes were flatter in females, while the high domain intercept and the HF peak prominence was significantly increased. Waking after sleep onset and lightest sleep (N1) were associated with lower intercept values, while REM sleep had an opposite effect. ConclusionsThe broken power-law model proved to be more appropriate for the description of RR-interval spectra than the single-slope model, and also captured effects of age, sex and sleep structure that were corroborated by the literature. We would like to highlight that while HRV changes are often assumed to be of oscillatory origin, the fractal component has a major contribution to the total PSD, and thus to all measures derived from it.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Schneider, B., Dresler, M., Gombos, F., Kovacs, I., Bodizs, R.. 2025-11-03. A broken power-law model of heart rate variability spectra in sleep. https://doi.org/10.1101/2025.11.01.685631

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Thoracoabdominal pressure transmission during prone and supine cardiopulmonary resuscitation in fresh-frozen human cadavers

Background: Prone cardiopulmonary resuscitation (CPR) may be necessary when turning a prone patient supine would delay chest compressions. Although prone compressions can generate arterial pressures comparable with or greater than supine CPR, the pathway of pressure transmission is uncertain. We examined synchronized intrathoracic, intra-abdominal, and central arterial pressures in both supine and prone positions. Methods: Two thawed fresh-frozen adult cadavers underwent three, 2-minute mechanical CPR trials per position in a counterbalanced crossover sequence. Solid-state catheters recorded pleural, peritoneal, and central arterial pressures simultaneously. Trial-level outcomes included peak pressure, mean pressure, pressure-time area, and the mean peritoneal-to-pleural pressure gradient. Exploratory fixed-effects models included position, cadaver, and their interaction. Results: Prone CPR increased peak intrathoracic pressure by 7.04 mmHg, peak intra-abdominal pressure by 21.69 mmHg, and peak arterial pressure by 15.40 mmHg. Mean intra-abdominal and arterial pressures increased by 16.22 and 9.90 mmHg, respectively. The mean peritoneal-to-pleural gradient reversed direction from -8.46 mmHg supine to 4.85 mmHg prone. Intrathoracic pressure-time area increased 3.4-fold, from 1.62 to 5.46 mmHg{middle dot}s, and arterial pressure-time area increased 2.2-fold, from 2.96 to 6.42 mmHg{middle dot}s. Conclusions: Compared to supine, prone mechanical CPR generated higher arterial pressures and reversed the pressure relationship across the thoracoabdominal boundary in both cadavers. Higher abdominal pressure coincided with a larger intrathoracic pressure-time area, a pattern compatible with reduced caudal pressure dissipation.

physiology↗

Hypothalamic Farnesoid X Receptor deficiency alters energy balance by modulating hepatic glucose production and adipose tissue metabolism through central insulin signaling.

Objectives: The bile acid nuclear receptor Farnesoid X Receptor (FXR, NR1H4) is a major regulator of metabolism and energy homeostasis in peripheral organs. It modulates bile acid, glucose, and lipid metabolism, as well as fat mass and body weight. However, FXR is also expressed in the brain, particularly in the hypothalamus, a key center for the regulation of energy homeostasis. Although one study has demonstrated a role for brain FXR activation in energy balance, its specific hypothalamic role is still unknown. Here, we examined the role of FXR in the mediobasal hypothalamus in the regulation of energy balance. Methods: We used a genetic approach combined with metabolic phenotyping to determine the effect of FXR invalidation in the mediobasal hypothalamus on metabolic parameters involved in the central regulation of energy homeostasis. Results: Our results demonstrate that hypothalamic FXR deficiency induces a positive energy balance, resulting in a reduction in energy expenditure due to alterations in glucose metabolism accompanied by structural changes in white adipose tissues. Conclusion: This study uncovers a previously unrecognized role for hypothalamic FXR in the central homeostatic control of energy balance, providing new insights into its contribution to peripheral glucose metabolism and adipose tissue structural remodeling.

physiology↗

Rad and Phospholamban are Key Drivers of the Ventricular Adrenergic Response and Stress-Induced Arrhythmia

The adrenergic response is a fundamental mechanism that regulates heart rate (chronotropy), cardiac contractility (inotropy) and relaxation (lusitropy). Adrenergic stress is also a recognized trigger of arrhythmia in disease. Yet, our understanding of the underlying molecular basis remains incomplete. Protein kinase A (PKA) and the calcium/calmodulin-dependent kinase II (CaMKII) phosphorylate multiple targets proposed to participate in the adrenergic response, including the GTP-binding protein Rad, phospholamban (PLB) and ryanodine receptor 2 (RyR2). Here we demonstrate that phosphorylation of both Rad and PLB is necessary for inotropy and lusitropy. We show that changes in cardiac contractility and relaxation are primarily dependent on intracellular calcium handling. Finally, we report that Rad and PLB control stress-induced arrhythmogenesis, despite the phosphorylation of other pro-arrhythmic targets. We have identified the essential molecular components of the adrenergic response, resolving a long-standing debate in cardiac excitation-contraction coupling and refining current models of sympathetic regulation in health and disease.

physiology↗