Assessing the Impact of Sleep Deprivation on Autonomic Nervous System Regulation and Heart Rate Variability in Healthy Adults

Project Abstract

This study investigates how acute sleep deprivation alters autonomic nervous system (ANS) regulation and heart rate variability (HRV) in healthy adults, aiming to elucidate mechanistic links between sleep loss and cardiovascular risk markers. A randomized cross-over design was conducted with 40 healthy volunteers (20 male, 20 female; aged 20–35 years) who underwent two experimental conditions normal sleep (8 hours) and total sleep deprivation for 24 hours, separated by a two-week washout period. Primary outcomes included time-domain and frequency-domain HRV metrics (SDNN, RMSSD, LF, HF, LF/HF ratio) captured via short-term ECG recordings during seated rest, paced breathing, and a cognitive task to assess autonomic responsiveness under sympathetic and parasympathetic challenges. Secondary outcomes encompassed baroreflex sensitivity (BRS), skin conductance response (SCR), pupil dilation as indices of sympathetic arousal, and salivary cortisol as a HPA-axis marker. Sleep architecture was monitored with actigraphy and polysomnography on the baseline night, while subjective sleepiness and fatigue were quantified using the Stanford Sleepiness Scale and the Karolinska Sleepiness Scale. Statistical analyses employed linear mixed-effects models to compare sleep-deprived and rested states, accounting for period effects, sex, baseline fitness (VO2 max), and circadian timing. We hypothesized that 24-hour sleep deprivation would reduce HRV, particularly decreasing parasympathetic (RMSSD, HF) activity and increasing sympathetic dominance (LF/HF ratio), and would attenuate BRS, reflecting impaired autonomic flexibility. Preliminary findings indicate a significant reduction in time-domain HRV (SDNN and RMSSD) and HF power under sleep deprivation, with a concomitant rise in LF power and LF/HF ratio, suggesting diminished vagal tone and heightened sympathetic dominance. BRS measures showed a notable decline, indicating impaired baroreflex function, while SCR and pupil dilation demonstrated augmented sympathetic arousal in the deprived state. Salivary cortisol levels were elevated post-deprivation, aligning with increased HPA-axis activation. Cognitive task performance deteriorated in the sleep-deprived condition, with slower reaction times and reduced accuracy, correlating with autonomic arousal indices. Sex-specific analyses revealed that female participants exhibited more pronounced reductions in HRV and BRS, potentially reflecting interactions between sex hormones and autonomic regulation. Control analyses confirmed that recent caffeine intake did not confound primary outcomes. The findings advance understanding of how acute sleep loss perturbs cardiovascular autonomic control, emphasizing the vulnerability of HRV metrics and baroreflex function to sleep debt. Implications include potential early identification of individuals at elevated cardiovascular risk due to sleep deprivation and informing interventions to mitigate autonomic dysregulation, such as targeted sleep strategies, chronotherapy, and stress-reduction techniques. Limitations include the controlled laboratory setting, homogenous young adult sample, and the short-term nature of deprivation; future work should extend to diverse age groups, chronic sleep restriction, and real-world occupational contexts to map long-term autonomic consequences of insufficient sleep. Overall, the study provides a comprehensive characterization of how sleep deprivation disrupts autonomic balance and cardiovascular regulation, with robust multimodal corroboration across electrophysiological, hormonal, and behavioral domains.

Project Overview

What This Project Is About

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This project looks at how not getting enough sleep affects the body's automatic functions and how the heart changes its beat-to-beat pattern. Specifically, it examines the autonomic nervous system, which controls involuntary processes like heart rate and digestion, and heart rate variability, which is a measure of how much the time between heartbeats varies. The goal is to see how sleep loss alters these systems in healthy adults.

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The Problem It Addresses

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Many people experience sleep deprivation from work, study, or lifestyle, yet we don’t fully understand how this affects basic bodily regulation. Poor sleep could contribute to higher stress on the heart and other health risks. This project investigates the link between short sleep, autonomic control, and heart rate patterns to inform health recommendations and preventive strategies.

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Objectives of the Project

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1. Describe how sleep deprivation changes heart rate variability.
2. Assess changes in markers of autonomic nervous system activity (e.g., sympathetic and parasympathetic balance).
3. Compare responses between different lengths of sleep deprivation (e.g., one night vs. two nights).

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What You Will Do Step by Step

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1. Review relevant literature on sleep, autonomic function, and heart rate variability.
2. Recruit healthy adult volunteers and obtain informed consent.
3. Subject participants to controlled wakefulness periods and collect ECG data.
4. Analyze heart rate variability and autonomic markers using simple statistical methods.
5. Interpret results in light of existing research and discuss practical implications.

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Expected Outcome

Anticipated findings include measurable reductions in heart rate variability and shifts toward sympathetic dominance after sleep deprivation, with clearer effects after longer deprivation. The study should provide practical insights into how sleep loss can affect everyday bodily regulation and health risk awareness.