European Journal of Cardiovascular Medicine

Cardiovascular diseases (CVDs) remain the leading cause of mortality globally, creating an urgent need to identify and mitigate modifiable risk factors [1]. Beyond traditional factors like diet, physical activity, and smoking, sleep has emerged as a fundamental pillar of cardiovascular health. Modern societal pressures have contributed to a widespread pattern of insufficient sleep, with estimates suggesting over one-third of adults in industrialized nations fail to obtain the recommended amount of sleep on a regular basis [2].

A growing body of epidemiological evidence has established a robust association between chronic short sleep duration (<6 hours per night) and an increased risk of hypertension, coronary artery disease, and overall cardiovascular mortality [3]. The physiological mechanisms thought to underpin this relationship are multifaceted, involving dysregulation of the autonomic nervous system (ANS), endocrine disruption, and the promotion of a low-grade systemic inflammatory state [4]. Specifically, sleep loss is hypothesized to induce a shift in autonomic balance towards sympathetic hyperactivity and parasympathetic (vagal) withdrawal, which can acutely elevate blood pressure and heart rate [5]. Concurrently, sleep restriction has been shown to upregulate the production of pro-inflammatory cytokines such as Interleukin-6 (IL-6) and acute-phase reactants like C-reactive protein (CRP), both of which are implicated in the pathogenesis of atherosclerosis [6].

While the long-term consequences of poor sleep are well-documented, the immediate physiological impact of a single night of sleep restriction is less comprehensively understood. Most studies have either focused on total sleep deprivation (i.e., no sleep) or examined a limited array of physiological markers. Investigating the acute effects of partial sleep restriction, a common real-world scenario, on a broad panel of cardiovascular and inflammatory markers is crucial for understanding the initial pathogenic events that may, with repeated exposure, contribute to chronic disease. Elucidating these acute responses can provide mechanistic insight into the sleep-CVD relationship and emphasize the importance of consistent, nightly sleep for maintaining physiological homeostasis.

Therefore, this study fills a critical research gap by employing a rigorous, controlled crossover design to investigate the acute effects of one night of partial sleep restriction (4 hours) compared to adequate sleep (8 hours) on hemodynamic (blood pressure, heart rate), autonomic (heart rate variability), and inflammatory (hs-CRP, IL-6) parameters in a cohort of healthy young adults. We hypothesized that a single night of partial sleep restriction would result in significantly elevated blood pressure and heart rate, reduced heart rate variability, and increased levels of systemic inflammatory markers.

Study Design

This study utilized a randomized, single-blind, crossover design conducted in a controlled sleep laboratory environment. Each participant completed two experimental conditions: (1) an Adequate Sleep (AS) condition, with 8 hours of time in bed (TIB) from 23:00 to 07:00, and (2) a Sleep Restriction (SR) condition, with 4 hours of TIB from 03:00 to 07:00. The order of the conditions was randomized and counterbalanced. A minimum one-week washout period was implemented between the two experimental nights to prevent carryover effects. Participants were blinded to the specific hypotheses of the study. The study protocol was approved by the Institutional Review Board, and all participants provided written informed consent.

Participants
Thirty-two healthy, non-smoking volunteers (16 female, 16 male) aged 20–35 years were recruited from the local university and community via flyers and online advertisements. Inclusion criteria included having a body mass index (BMI) between 18.5 and 24.9 kg/m², self-reported habitual sleep duration of 7–9 hours per night, and a regular sleep-wake schedule. Exclusion criteria comprised any history of cardiovascular, respiratory, endocrine, or psychiatric disorders; current diagnosis of a sleep disorder (e.g., insomnia, sleep apnea); working night shifts; consuming more than 200 mg of caffeine or 2 alcoholic drinks per day; and use of any medication known to affect sleep or cardiovascular function.

Procedures
Participants were instructed to maintain a consistent sleep-wake schedule (verified with wrist actigraphy) and abstain from caffeine, alcohol, and strenuous exercise for 48 hours prior to each laboratory visit. On the evening of each experimental session, participants arrived at the laboratory at 19:00. They were provided a standardized meal and were not permitted further caloric intake until the following morning. During the SR condition, participants remained awake in the laboratory from 23:00 to 03:00 under constant staff supervision in a dimly lit room, engaging in sedentary activities such as reading or watching movies.

All cardiovascular and biochemical measurements were performed the following morning between 08:00 and 09:00, approximately one hour after awakening.

Measurements

• Hemodynamic Parameters:After the participant had been sitting quietly for 10 minutes, brachial blood pressure (systolic, SBP; diastolic, DBP) and resting heart rate (HR) were measured using a validated automated oscillometric device (OMRON HEM-907XL). Three consecutive readings were taken two minutes apart, and the average of the last two readings was used for analysis.
• Heart Rate Variability (HRV):A 5-minute, 3-lead electrocardiogram (ECG) was recorded with participants in a supine position using a Biopac MP160 system. The ECG data were visually inspected for artifacts, and R-R intervals were processed using Kubios HRV Standard software. The time-domain parameters analyzed were the standard deviation of all normal-to-normal (NN) intervals (SDNN), a measure of overall variability, and the root mean square of successive differences between normal heartbeats (RMSSD), a marker of vagal-mediated cardiac autonomic control.
• Inflammatory Biomarkers:A 5 mL venous blood sample was drawn from the antecubital vein into a serum-separating tube. Samples were centrifuged at 3000 rpm for 15 minutes, and the resulting serum was aliquoted and stored at -80°C until analysis. Serum concentrations of high-sensitivity C-reactive protein (hs-CRP) and Interleukin-6 (IL-6) were quantified using commercially available high-sensitivity enzyme-linked immunosorbent assay (ELISA) kits according to the manufacturer’s protocols.

Statistical Analysis
All statistical analyses were performed using SPSS Statistics for Windows, Version 28.0 (IBM Corp., Armonk, NY). Data were checked for normality using the Shapiro-Wilk test. Descriptive statistics were calculated and are presented as mean ± standard deviation (SD). To compare the effects of the two sleep conditions (AS vs. SR) on the dependent variables (SBP, DBP, HR, SDNN, RMSSD, hs-CRP, IL-6), paired-samples t-tests were used, leveraging the crossover design where each participant served as their own control. A two-tailed p-value of < 0.05 was considered statistically significant.

All 32 enrolled participants successfully completed both experimental conditions of the study protocol without any adverse events. The demographic and baseline characteristics of the study cohort are presented in Table 1. The participants represented a homogenous group of healthy young adults.

Table 1. Participant Demographics and Baseline Characteristics (N=32)

Effects on Hemodynamic Parameters
The partial sleep restriction condition had a significant impact on all measured hemodynamic parameters. As detailed in Table 2, mean SBP was significantly higher following the SR condition compared to the AS condition. A similar significant increase was observed for DBP. Furthermore, resting HR was significantly elevated after the night of restricted sleep.

Table 2. Comparison of Hemodynamic Parameters Between Sleep Conditions (N=32)

Effects on Autonomic and Inflammatory Markers
The analysis of autonomic function and systemic inflammation revealed significant adverse changes following sleep restriction (Table 3). Both HRV parameters, SDNN and RMSSD, were significantly lower after the SR condition compared to the AS condition, indicating a reduction in overall heart rate variability and vagal tone. Concurrently, serum concentrations of both inflammatory markers, hs-CRP and IL-6, were significantly elevated following the night of partial sleep restriction.

Table 3. Comparison of Autonomic and Inflammatory Markers Between Sleep Conditions (N=32)

The primary finding of this study is that a single night of partial sleep restriction acutely and significantly impairs cardiovascular function in healthy young adults. Specifically, we demonstrated that reducing sleep from 8 to 4 hours resulted in elevated blood pressure and heart rate, a shift in autonomic balance towards sympathetic dominance, and an increase in systemic inflammatory markers. These results provide compelling evidence that the negative cardiovascular consequences of inadequate sleep manifest rapidly, even in a low-risk population.

The observed increase in both systolic and diastolic blood pressure is consistent with a large body of literature linking sleep loss to hypertension risk [7]. Our findings align with previous laboratory studies that have shown blood pressure elevations after one or more nights of sleep restriction [8]. The magnitude of the SBP increase (~7 mmHg) is clinically relevant, as sustained elevations of this degree are associated with a substantial increase in long-term CVD risk [9]. This pressor effect is likely driven by the observed dysregulation of the autonomic nervous system.

Our heart rate variability analysis supports this mechanistic link. The significant reductions in both SDNN (overall variability) and RMSSD (a proxy for vagal tone) after sleep restriction indicate a withdrawal of parasympathetic influence on the heart and a relative increase in sympathetic activity. This autonomic imbalance is a well-established pathway to cardiovascular pathology, predisposing individuals to arrhythmias and higher resting blood pressure and heart rate [10]. The findings corroborate those of other acute sleep restriction studies which have also reported diminished HRV [5].

A novel aspect of our study is the concurrent measurement of hemodynamic, autonomic, and inflammatory markers, providing a more holistic view of the acute physiological stress response. The significant elevation in hs-CRP and IL-6 after just one night of insufficient sleep is particularly striking. These results support the theory that sleep loss triggers a pro-inflammatory cascade [6], [11]. IL-6 is a key cytokine that stimulates the liver to produce CRP, and both are implicated in endothelial dysfunction and the development of atherosclerosis. While the increases were within a subclinical range, repeated nightly occurrences of such inflammatory surges could plausibly contribute to the cumulative vascular damage seen in chronic short sleepers.

The strengths of this study include its randomized crossover design, which minimizes inter-individual variability and enhances statistical power. The controlled laboratory setting eliminated confounding variables such as diet, activity, and environmental factors. The inclusion of a comprehensive panel of markers allowed for an integrated assessment of cardiovascular dysregulation [12-15]. However, some limitations must be acknowledged. First, the sample size was relatively small and consisted exclusively of healthy, young adults; therefore, the findings may not be generalizable to older individuals or those with pre-existing medical conditions. Second, we assessed the effect of only one night of sleep restriction, which does not capture the cumulative impact of chronic sleep debt. Future research should explore these effects in more diverse populations and over longer durations.

In conclusion, this study demonstrates that even a single night of partial sleep restriction acts as a significant physiological stressor, triggering immediate and adverse shifts in cardiovascular and inflammatory profiles. These results highlight the critical role of adequate nightly sleep in maintaining short-term cardiovascular homeostasis and provide a mechanistic basis for the observed association between chronic sleep loss and long-term cardiovascular disease.

This study provides clear evidence that one night of partial sleep restriction to four hours is sufficient to cause significant increases in blood pressure, heart rate, and key inflammatory biomarkers (hs-CRP, IL-6), while concurrently reducing heart rate variability in healthy young adults. These findings underscore the immediate and multifaceted negative impact of inadequate sleep on the cardiovascular system. The results emphasize the public health importance of promoting sleep hygiene not only for long-term health but also for maintaining daily physiological well-being. The data suggest that the pathway linking poor sleep to cardiovascular disease may be initiated by acute, nightly episodes of autonomic and inflammatory dysregulation.

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