Abstract

Introduction: Cardiac function is modulated by multiple factors including exogenous (circadian rhythm) and endogenous (ultradian 90–110 min sleep cycle) factors. By evaluating heart rate variability (HRV) during sleep, we will better understand their influence on cardiac activity. The aim of this study was to evaluate HRV in the dark phase of the circadian rhythm during sleep in healthy children and adolescents.Methods: One 3 min segment of pre-sleep electrocardiography (EEG) and 3, 6 min segments of electrocardiography recorded during polysomnography from 75 healthy children and adolescents were sampled during progressive cycles of slow wave sleep (SWS1, SWS2, SWS3). Three, 3 min segments of rapid eye movement sleep (REM) were also assessed, with REM1 marked at the last REM period before awakening. Studies that recorded REM3 prior to SWS3 were used for assessment. HRV variables include the following time domain values: mean NN (average RR intervals over given time), SDNN (Standard Deviation of RR intervals), and RMSSD (root Mean Square of beat-to-beat Differences). Frequency domain values include: low frequency (LF), high frequency (HF), and LF:HF.Results: Mixed linear effects model analysis revealed a significant difference in time and frequency domain values between sleep cycles and stages. Mean NN was lowest (highest heart rate) during pre—sleep then significantly increased across SWS1-3. Mean NN in SWS1 was similar to all REM periods which was significantly lower than both SWS2 and SWS3. SDNN remained at pre-sleep levels until SWS3, and then significantly increased in REM1&2. There was a large drop in LF from pre-sleep to SWS1. As cycles progressed through the night, LF remains lower than awake but increases to awake like levels by REM2. RMSSD and HF were lowest in pre-sleep and increased significantly by SWS1 and remain high and stable across stages and cycles except during the REM3 period where RMSSD decreased.Conclusion: Our results demonstrate that there are considerable changes in the spectral analysis of cardiac function occurring during different sleep stages and between sleep cycles across the night. Hence, time of night and sleep stage need to be considered when reporting any HRV differences.

Highlights

  • IntroductionCardiac function is modulated by multiple factors including exogenous (circadian rhythm) and endogenous (ultradian 90–110 min sleep cycle) factors

  • Cardiac function is modulated by multiple factors including exogenous and endogenous factors

  • rapid eye movement sleep (REM) cycles are labeled relative to sleep offset: REM cycle prior to sleep offset = REM1, REM cycle preceding sleep offset but one = REM2 and REM cycle preceding sleep offset but two = REM3

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Summary

Introduction

Cardiac function is modulated by multiple factors including exogenous (circadian rhythm) and endogenous (ultradian 90–110 min sleep cycle) factors. The factors can be divided into those which are [1] organ specific (the composition–muscle fiber/connective tissue) and basal metabolic state (cell size/connectivity) of the cardiac muscle tissue) and [2] those which operate on the cardiovascular system (e.g., exogenous factors such as light exposure and ambient temperature and endogenous factors such as central pattern generators) and activate afferent pathways or influence central neural networks and reflex circuits needed to maintain metabolic functioning, homeostasis and permit adaptive behaviors such as digestion and sleep [1,2,3] These latter influences on cardiac function can be assessed using heart rate variability, a commonly used mathematical manipulation of the electrocardiogram signal. These variables have been proposed to be indicators of the relative tone of the two arms of the autonomic nervous system, the parasympathetic (HF) and sympathetic nervous systems (LF) and sympathovagal activity (LF:HF) acting directly on the cardiac tissue [3,4,5]

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