Sleep is a fundamental biological process with measurable effects on cardiovascular regulation. Variations in sleep duration—particularly chronic short sleep—have been linked to changes in autonomic nervous system activity that may precede overt cardiometabolic disease. Cardiac autonomic modulation can be quantified noninvasively using heart rate variability (HRV), which reflects beat-to-beat fluctuations in sinus rhythm and is commonly summarized using time-domain indices (e.g., SDNN, RMSSD) and frequency-domain components (e.g., LF, HF, and LF/HF) as standardized by international consensus recommendations. [1]

Experimental evidence supports a mechanistic link between sleep loss and autonomic imbalance. A recent systematic review and meta-analysis of randomized trials reported that sleep deprivation is associated with suppression of cardiac vagal activity, with consistent reductions in parasympathetic-linked HRV metrics such as RMSSD. [2] Controlled laboratory studies similarly indicate that restricting sleep can alter nocturnal autonomic tone, with findings consistent with increased autonomic stress and reduced vagal modulation compared with habitual or unrestricted sleep conditions. [3] Complementing these observations, studies examining partial sleep loss in occupational settings have documented HRV changes suggestive of increased sympathetic dominance and reduced parasympathetic activity during periods of restricted sleep. [4]

However, evidence from observational studies assessing habitual sleep duration and HRV has been heterogeneous, potentially due to differences in populations, sleep measurement approaches, and confounding by lifestyle factors. For example, in a cross-sectional study of adults, sleep quality showed clearer adverse associations with HRV and cardiovascular parameters than sleep duration alone, indicating that the sleep–autonomic relationship may be context-dependent. [5] Data specific to young adults remain comparatively limited despite the relevance of this age group, in whom autonomic alterations may represent early, modifiable physiological changes. Prior work in young adults has suggested that short sleep is associated with less favorable HRV patterns, supporting the premise that inadequate sleep duration may influence autonomic balance even before clinical disease becomes apparent. [6]

Against this background, the present study was designed to examine the association between habitual sleep duration and resting HRV indices in apparently healthy young adults, with the objective of characterizing autonomic differences across sleep-duration categories under standardized recording conditions.

Study design and setting: A cross-sectional, observational study was conducted among apparently healthy young adults to evaluate the association between habitual sleep duration HRV. The study was carried out in a controlled academic research setting over a six-month period.

Study population: Participants were recruited from undergraduate and postgraduate programs through notice-board announcements and direct invitations. Individuals aged 18–25 years of either sex were considered eligible.

Inclusion criteria

• Age between 18 and 25 years
• Self-reported regular sleep–wake schedule for at least the preceding three months
• No history of diagnosed cardiovascular, respiratory, neurological, endocrine, or sleep disorders
• Not on medications known to affect autonomic function (e.g., beta-blockers, antidepressants)

Exclusion criteria

• Current smokers or tobacco users
• Regular alcohol intake (>7 standard drinks/week)
• Shift workers or individuals with frequent trans-meridian travel in the past three months
• Acute illness within two weeks prior to assessment

Sample size estimation:Sample size was calculated assuming a moderate effect size (f = 0.25) for differences in HRV parameters across sleep duration categories, with a power of 80% and a two-sided alpha of 0.05. Based on these assumptions, a minimum of 108 participants was required. To account for potential dropouts and incomplete recordings, 120 participants were enrolled.

Assessment of sleep duration: Habitual sleep duration was assessed using a structured, interviewer-administered sleep questionnaire adapted from validated sleep assessment tools. Participants reported average nightly sleep duration over the previous four weeks. Based on reported sleep duration, participants were categorized into three groups:

• Short sleep: <6 hours per night
• Normal sleep: 6–8 hours per night
• Long sleep: >8 hours per night

Participants were instructed to maintain their usual sleep habits prior to physiological assessment.

Heart rate variability recording: HRV was recorded using a validated digital electrocardiography (ECG) system. All recordings were performed in the morning between 08:00 and 10:00 hours to minimize circadian variation. Participants were advised to avoid caffeine, strenuous physical activity, and heavy meals for at least 12 hours prior to recording.

After a 10-minute acclimatization period in the supine position in a quiet, temperature-controlled room (22–24 °C), a continuous 5-minute ECG recording was obtained at a sampling rate of 1000 Hz. Artefacts and ectopic beats were identified and corrected using automated filtering followed by manual verification.

HRV analysis: Time-domain and frequency-domain HRV parameters were analyzed in accordance with established guidelines. Time-domain measures included:

• Mean RR interval
• Standard deviation of normal-to-normal intervals (SDNN)
• Root mean square of successive differences (RMSSD)

Frequency-domain analysis was performed using fast Fourier transformation, yielding:

• Low-frequency power (LF; 0.04–0.15 Hz)
• High-frequency power (HF; 0.15–0.40 Hz)
• LF/HF ratio

All HRV parameters were expressed in milliseconds or normalized units, as appropriate.

Anthropometric and physiological measurements: Height and weight were measured using standardized techniques, and body mass index (BMI) was calculated as weight (kg)/height (m²). Resting heart rate and blood pressure were recorded prior to HRV acquisition using an automated sphygmomanometer.

Statistical analysis: Data were entered into a predesigned database and analyzed using standard statistical software. Continuous variables were initially assessed for normality using the Shapiro–Wilk test. Variables demonstrating a normal distribution were summarized as mean ± standard deviation, while categorical variables were expressed as frequencies and percentages. Comparisons of baseline demographic and physiological characteristics across the three sleep duration categories were performed using one-way analysis of variance (ANOVA) for continuous variables. Sex distribution among groups was evaluated using the chi-square test. For heart rate variability parameters, intergroup differences in both time-domain and frequency-domain indices were analyzed using one-way ANOVA. When a significant overall effect was observed, post-hoc pairwise comparisons were conducted with Bonferroni adjustment to control for multiple testing. The relationship between habitual sleep duration and HRV indices was examined using Pearson’s correlation coefficient. In instances where variables did not satisfy normality assumptions, the Spearman rank correlation test was applied as an alternative. All statistical tests were two-tailed, and a p-value <0.05 was considered indicative of statistical significance.

A total of 120 young adults were included in the final analysis and categorized according to habitual sleep duration. Baseline demographic characteristics were largely comparable across the three sleep-duration groups, with no statistically significant differences observed in age, sex distribution, body mass index, or blood pressure parameters. However, resting heart rate demonstrated a significant intergroup difference, with individuals reporting shorter sleep duration exhibiting higher resting values compared with those obtaining normal or longer sleep durations (Table 1).

Analysis of time-domain HRV indices revealed a graded improvement in autonomic variability with increasing sleep duration. Participants in the short sleep group demonstrated reduced overall variability and diminished parasympathetic modulation relative to individuals with normal or long sleep duration. In contrast, those reporting longer habitual sleep exhibited more favorable time-domain HRV profiles, indicating enhanced cardiac autonomic regulation (Table 2).

Frequency-domain analysis further supported these findings. Short sleep duration was associated with a relative predominance of sympathetic activity, whereas normal and long sleep durations were characterized by greater parasympathetic influence. The sympathovagal balance shifted progressively toward vagal dominance with increasing sleep duration, reflecting a more favorable autonomic profile among individuals with adequate sleep (Table 3).

Correlation analysis demonstrated a significant association between habitual sleep duration and multiple HRV indices. Longer sleep duration was positively related to measures reflecting overall variability and parasympathetic activity, while an inverse relationship was observed with indices indicative of sympathetic predominance. These findings suggest a continuous relationship between sleep duration and cardiac autonomic modulation rather than a purely categorical effect (Table 4).

. Table 1. Baseline characteristics of study participants according to sleep duration

Table 2. Comparison of time-domain HRV parameters across sleep duration groups

Table 3. Comparison of frequency-domain HRV parameters across sleep duration groups

Table 4. Correlation between sleep duration and HRV parameters

In this study, shorter habitual sleep duration was associated with a less favorable resting autonomic profile, characterized by lower vagally mediated HRV indices and a shift toward sympathetic predominance. This pattern aligns with contemporary evidence linking insufficient sleep to autonomic dysregulation and cardiometabolic risk pathways. Experimental work in healthy young adults shows that sustained sleep restriction can activate cardiovascular stress systems (e.g., higher ambulatory blood pressure and neurohumoral activation), supporting a plausible mechanistic bridge between curtailed sleep and altered autonomic regulation observed in free-living settings [7]. Broader clinical syntheses similarly describe sleep loss as a contributor to increased heart rate and reduced HRV, consistent with reduced parasympathetic modulation and/or enhanced sympathetic tone [8].

The direction and nature of HRV changes in our findings are also consistent with meta-analytic evidence from randomized studies of sleep deprivation, where RMSSD tends to decrease while LF and LF/HF increase—changes interpreted as vagal withdrawal and relative sympathetic dominance [9]. This convergence is important because HRV is sensitive to both acute sleep perturbations and longer-term sleep behavior, and different HRV domains can capture distinct features of autonomic control. In observational contexts, objective multi-day monitoring has demonstrated temporal coupling between sleep metrics and autonomic function, suggesting that sleep and HRV can influence each other over subsequent days, rather than reflecting a purely unidirectional relationship [10]. Such bidirectionality may help explain why inter-individual variability is substantial and why sleep–HRV associations differ across cohorts and measurement approaches.

Beyond sleep duration alone, sleep regularity and sleep quality likely modify autonomic outcomes. Interventions aimed at reducing sleep timing irregularity (without necessarily changing mean sleep duration) have been shown to lower resting heart rate and improve RMSSD, indicating that stabilizing sleep schedules may enhance parasympathetic cardiac control [11]. In parallel, studies in young adult populations—including medical students—report that poorer sleep quality correlates with lower parasympathetic-related HRV indices and higher sympathetic-related indices, reinforcing the concept that qualitative sleep disturbance can mirror (or amplify) the autonomic signature of short sleep [12]. Consistent findings in insomnia phenotypes also demonstrate higher heart rate and lower HRV during critical transition periods such as sleep onset, supporting hyperarousal and reduced vagal activity as plausible physiological substrates [13].

Mechanistically, several interconnected pathways could account for the observed associations, including heightened sympathetic drive, hypothalamic–pituitary–adrenal axis activation, endothelial dysfunction, and inflammatory signaling. Experimental and integrative cardiovascular literature describes sleep loss as a systemic stressor that can affect vascular and autonomic homeostasis, potentially creating a feed-forward loop where autonomic imbalance worsens sleep continuity and vice versa [8,10]. The net effect—particularly if persistent—may have implications for early cardiovascular risk stratification even in ostensibly healthy young adults.

Key strengths include the focused young adult cohort and standardized HRV assessment at rest, enabling detection of sleep-related differences in autonomic markers relevant to early cardiovascular physiology. Several limitations should be considered. First, sleep duration was assessed behaviorally (typical for many epidemiologic designs) and may be affected by recall bias; objective measures such as actigraphy can refine exposure classification and capture sleep regularity [10,11]. Second, cross-sectional inference limits causal interpretation and cannot rule out reverse causality (e.g., lower HRV reflecting stress-related physiology that also disrupts sleep) [10]. Third, residual confounding is possible—particularly from physical activity, caffeine/alcohol timing, psychosocial stress, and chronotype—which can independently influence HRV. Future studies would benefit from longitudinal designs combining actigraphy-derived sleep duration/regularity, standardized HRV protocols, and comprehensive confounder assessment to clarify causal directions and identify modifiable targets.

The findings of this study demonstrate a clear association between habitual sleep duration and cardiac autonomic function in young adults. Shorter sleep duration was linked to an unfavorable autonomic profile characterized by reduced heart rate variability and relative sympathetic predominance, whereas adequate and longer sleep durations were associated with enhanced autonomic flexibility and greater parasympathetic modulation. These observations underscore the importance of sufficient sleep in maintaining optimal cardiovascular autonomic regulation even in a young, ostensibly healthy population. Promoting healthy sleep habits may therefore represent a simple yet effective strategy for supporting early cardiovascular health and autonomic balance.

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