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Updated: Jan 5, 2026

Through-the-Wall Blood Sampling Method to Minimize Sleep Disruption in Clinical Settings
Published on: June 13, 2025
Night-time cardiac autonomic modulation as a function of sleep-wake stages is modified in otherwise healthy
Rodrigo Chamorro1, Cecilia Algarín2, Oliver Rojas2
1Sleep and Functional Neurobiology Laboratory, Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile; Department of Nutrition, Faculty of Medicine, University of Chile, Santiago, Chile.
Objective:
Even though sympathetic dominance during the daytime period is well known, currently, scarce data exist on autonomic nervous system (ANS) regulation during sleep in pediatric obesity. We aimed to evaluate sleep cardiac ANS regulation in normal-weight (NW) and overweight and obese (OW) adolescents.
Patients/Methods:
In this study, 60 healthy adolescents (15.7 ± 0.7 years) belonging to a birth cohort since infancy were classified based on body mass index percentiles criteria as: OW (N = 27) or NW (N = 33). Sleep was evaluated by polysomnography (PSG) during two consecutive in-lab overnight sessions. Non-rapid eye movement (non-REM) sleep stages (stages 1, 2, and slow-wave sleep [SWS]), rapid eye movement (REM) sleep, and wakefulness (Wake) were scored. R-waves were detected automatically in the electrocardiographic (ECG) signal. An all-night heart rate variability analysis was conducted in the ECG signal, with several time- and frequency-domain measures calculated for each sleep-wake stage. Sleep time was divided into thirds (T1, T2, T3). The analysis was performed using a mixed-effects linear regression model.
Results:
Sleep organization was comparable except for reduced REM sleep percentage in the OW group (p < 0.04). Shorter R-R intervals were found for all sleep stages in the OW group; time-domain measured standard deviation of all R-R intervals (RRSD) was lower during stage 2, SWS and REM sleep (all p < 0.05). The square root of the mean of the sum of the squares of differences between adjacent R-R intervals (RMSSD) was also lower only during wake after sleep onset (WASO) in T1 and T3 (p < 0.05). The OW group had increased very low- and low-frequency (LF) power during WASO (in T1 and T2), and LF power during stage 2 and REM sleep (in T2). During WASO in the OW group, high-frequency (HF) power was lower (in T1 and T2), and LF/HF ratio was higher (in T2, p < 0.007).
Conclusions:
Several sleep-stage-dependent changes in cardiac autonomic regulation characterized the OW group. As sleep-related ANS balance was disturbed in the absence of concomitant metabolic alterations in this sample of otherwise healthy OW adolescents, their relevance for pediatric obesity should be further explored throughout development.
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