Physiological and Cognitive Effects of 24-Hour Sleep Deprivation: A Gender-Specific Comparison of Nap and Caffeine Interventions

Objective The objective of this study was to examine the impact of acute total sleep deprivation (24 hours) and subsequent recovery interventions (caffeine intake or a short nap) on subjective sleepiness, perceived cognitive difficulty, cardiovascular responses, and heart rate variability (HRV) parameters. Additionally, the moderating role of sex in these physiological and perceptual responses was evaluated. Methods A randomized controlled design was employed involving thirty healthy young adults (15 females, 15 males; mean age = 19.9 ± 1.5 years), who were allocated to one of three groups: caffeine, nap, or control. Each participant underwent three repeated assessments—baseline, post-sleep deprivation, and post-intervention. Measurements included the modified Karolinska Sleepiness Scale (mKSS), visual analog scales for task difficulty, systolic and diastolic blood pressure (SBP/DBP), and a range of HRV indices. Data were analyzed using linear mixed-effects models to account for repeated measures and individual variability. Results Sleep deprivation significantly increased subjective sleepiness and cognitive task difficulty, with more pronounced effects in females. Caffeine was more effective than napping or no intervention in reducing sleepiness. Across all sessions, females consistently reported higher task difficulty. Males showed elevated blood pressure under both rest and stress conditions. Caffeine attenuated stress-induced systolic blood pressure increases, especially among males. HRV analysis revealed increased sympathetic activity (LF) and decreased parasympathetic modulation (HF) after sleep deprivation. Group × sex and time × sex interactions for HRV indicated sex-specific recovery patterns. Parasympathetic activity recovered more in males who consumed caffeine, while napping reduced sympathovagal imbalance in both sexes. Conclusion The findings indicate that acute sleep deprivation adversely affects both cognitive and autonomic functioning, with sex-specific differences modulating the magnitude of these effects and the efficacy of subsequent interventions. While caffeine and short naps were each found to offer partial recovery benefits, their mechanisms and effectiveness appeared to vary by sex. These results underscore the importance of personalized fatigue countermeasures in high-demand or safety-critical settings. Physiological and Cognitive Effects of 24-Hour Sleep Deprivation: A Gender-Specific Comparison of Nap and Caffeine Interventions Nurcan Erdoğan Kurtaran 1, Gülnur Öztürk 2, Samime Şarlı Gündüz 1, Elif Ezgi Gürel 3, Ümmühan Erge 4, Levent Öztürk 4 1 Electroneurophysiology Program, Vocational School of Health Services, Trakya University, Edirne-Türkiye 2 Department of Physiotherapy and Rehabilitation, Faculty of Health Science, Trakya University, Edirne-Türkiye 3 Department of Emergency Aid and Disaster Management, Keşan Hakkı Yörük School of Health, Trakya University, Edirne-Türkiye 4 Department of Physiology, Faculty of Medicine, Trakya University; Edirne-Türkiye Author Emails: Conflicts of Interest The authors declare no conflicts of interest. Corresponding Author: Nurcan Erdoğan Kurtaran, Trakya University Edirne, Turkey E-mail address: [email protected]

Objective The objective of this study was to examine the impact of acute total sleep deprivation (24 hours) and subsequent recovery interventions (caffeine intake or a short nap) on subjective sleepiness, perceived cognitive difficulty, cardiovascular responses, and heart rate variability (HRV) parameters. Additionally, the moderating role of sex in these physiological and perceptual responses was evaluated.

A randomized controlled design was employed involving thirty healthy young adults (15 females, 15 males; mean age = 19.9 ± 1.5 years), who were allocated to one of three groups: caffeine, nap, or control. Each participant underwent three repeated assessments—baseline, post-sleep deprivation, and post-intervention. Measurements included the modified Karolinska Sleepiness Scale (mKSS), visual analog scales for task difficulty, systolic and diastolic blood pressure (SBP/DBP), and a range of HRV indices. Data were analyzed using linear mixed-effects models to account for repeated measures and individual variability.

Sleep deprivation significantly increased subjective sleepiness and cognitive task difficulty, with more pronounced effects in females. Caffeine was more effective than napping or no intervention in reducing sleepiness. Across all sessions, females consistently reported higher task difficulty. Males showed elevated blood pressure under both rest and stress conditions. Caffeine attenuated stress-induced systolic blood pressure increases, especially among males. HRV analysis revealed increased sympathetic activity (LF) and decreased parasympathetic modulation (HF) after sleep deprivation. Group × sex and time × sex interactions for HRV indicated sex-specific recovery patterns. Parasympathetic activity recovered more in males who consumed caffeine, while napping reduced sympathovagal imbalance in both sexes.

The findings indicate that acute sleep deprivation adversely affects both cognitive and autonomic functioning, with sex-specific differences modulating the magnitude of these effects and the efficacy of subsequent interventions. While caffeine and short naps were each found to offer partial recovery benefits, their mechanisms and effectiveness appeared to vary by sex. These results underscore the importance of personalized fatigue countermeasures in high-demand or safety-critical settings.

Sleep deprivation, heart rate variability, blood pressure, cognitive performance, caffeine, napping

Sleep deprivation (SD) is a consequence of inadequate amount or quality of sleep that may lead to sleepiness, decreased performance, and deterioration in physiology of bodily systems (1). SD may result from lifestyle habits such as shift work, extended work hours, social life events, or spending time on social media and diseases that may interfere with sleep health (2). SD increases the risk of stroke, obesity, diabetes, cancer, cognitive disorders, osteoporosis, and cardiovascular disease (3). Experimental studies have shown that chronic absolute SD leads to death (4). SD has been significantly associated with an increased incidence of cardiovascular disease (5, 6, 7, 8). The American Heart Association’s 2019 Guide emphasized that sleep of less than 6 hours was associated with high blood pressure (6). In a large cross-sectional study, a positive correlation was found between short sleep duration and the frequency of ischemic changes in electrocardiography (8). This relationship has been interpreted as short sleep increases the risk of ischemic heart disease (8). Suggested mechanisms that may increase the risk of cardiovascular disease under the conditions of SD include autonomic nervous system alterations, increased oxidative stress, changes in the inflammatory process, development of atherosclerotic plaques, endothelial dysfunction (2, 9). Changes in the balance between sympathetic and parasympathetic nervous systems is one of the major key factors in all of these (10). Heart rate variability (HRV) provides a non-invasive tool for assessment of cardiac autonomic regulation (11) . In this context, LF power is interpreted as an index of sympathetic modulation, whereas HF power reflects parasympathetic (vagal) activity; the LF/HF ratio represents the sympathovagal balance. Inconsistent results have been reported for HRV studies in SD. In an earlier study, 36-h SD led to decrease in the high frequency (HF) parameter of HRV which indicates less parasympathetic activity and shift in the balance of autonomic nervous system in favor of sympathetic system (10). In healthy men, one night of SD was not found to alter HRV as measured in the supine position (12). In another study, a decrease in the HF component of HRV and an increase in the LF component were detected, which indicates a decrease in parasympathetic activity and an increase in sympathetic activity (13). Several other HRV studies have shown that SD can increase sympathetic activity and arterial blood pressure in healthy individuals (14, 15), while some studies reported no change in resting arterial blood pressure, heart rate, or plasma catecholamine levels (16, 17, 18). SD or sleep loss can affect the autonomic nervous system response to stress conditions. Short-term SD altered blood pressure responses to cardiac autonomic stress tests without affecting resting blood pressure levels (19). This indicates that short-term SD may lead to subtle changes in the autonomic regulatory mechanisms which become apparent under stress conditions. The Stroop test can be used specifically for mental stress response. Accordingly, it has been demonstrated that 36 hours of acute SD during a Stroop test increased sympathetic activity and decreased parasympathetic activity. And the baroreflex sensitivity was also reduced, and these effects were visible as early as at the 12th hour of SD (10). There are common strategies such as caffeine intake and naps used to cope with the effects of SD (20, 21, 22). One study found that naps were more effective than caffeine for reducing sleepiness (22). In another study, in which caffeine was administered after SD, it was observed that the heart rate decreased during the cognitive test, the HF component in HRV increased, and the parasympathetic activity increased (23). There are also studies examining the effect of a nap on HRV (24). Napping after partial SD has been shown to improve cognitive performance (25). Despite the growing body of research examining the physiological consequences of sleep deprivation, the comparative efficacy of caffeine and short-term napping in mitigating autonomic dysregulation -particularly under cognitive stress conditions- remains insufficiently explored. While individual studies have shown that both caffeine and napping can modulate HRV and improve cognitive performance following sleep loss, few have systematically assessed their differential effects on cardiovascular and autonomic responses in a stress-inducing context. Notably, the impact of these interventions on HRV parameters during mental stress has not been directly compared. Therefore, the present study aims to (i) investigate the effects of 24-hour total sleep deprivation on HRV and arterial blood pressure during both resting and cognitive stress conditions, and (ii) evaluate and compare the efficacy of caffeine intake and short-duration napping in reversing sleep deprivation-induced autonomic and hemodynamic alterations. By integrating both resting and stress conditions, and focusing on sex-specific responses, this study provides a novel perspective on recovery strategies following acute sleep deprivation.

Approval for the study was obtained from the Local Ethics Committee (Date: 21/03/2022, Decision Number: 06/03). The study was conducted in accordance with the Declaration of Helsinki, and all participants provided written informed consent. Subjects Thirty healthy young adults (15 females, 15 males; mean age ± SD: 19.9 ± 1.5 years; mean BMI ± SD: 23.8 ± 3.8 kg/m²) participated in this study. Inclusion criteria required participants to be healthy young adults aged between 18 and 28 years. Exclusion criteria included the presence of any sleep disorder, cardiovascular disease, psychiatric disease, cognitive impairment, color blindness, substance abuse, drug use, and a daily caffeine intake exceeding 400 mg (23). Anthropometric data and hand preference were recorded during the initial visit; one participant was left-handed, while the remaining were right-handed. Additionally, the medical records of all participants were reviewed. All participants completed the Pittsburgh Sleep Quality Index (PSQI), and individuals with a PSQI score greater than 5 (mean±SD=3.5±1.3) were excluded from the study. Prior to the study, participants were instructed to maintain their regular sleep schedule, avoid napping, and complete a sleep diary for one week, documenting their sleep and wake times. Participants with any indication of sleep disorders, as determined by their medical history, questionnaire responses, and sleep diary entries, were excluded from the study. Experimental design The study employed a randomized design in which participants were allocated to one of three groups (caffeine, nap, or control; n = 10 per group) from the outset. All participants were instructed to abstain from any products containing caffeine or alcohol for 24 hours prior to the experiment. After a regular 7–8 hour night’s sleep and a light breakfast, participants arrived at the laboratory between 08:00 and 10:00 hours. Upon arrival, they rested for 15 minutes and then completed the modified Karolinska Sleepiness Scale (mKSS) to assess their sleepiness levels. Resting blood pressure was measured, and a 5-electrode electrocardiography (ECG) recording was performed to obtain HRV data. The ECG recording lasted 10 minutes in a seated position, comprising a 5-minute pre-task resting period followed by a 5-minute period during which a computer-based cognitive test was administered. Immediately after the cognitive test, systolic and diastolic blood pressures were rapidly measured, and participants provided a subjective rating of the task’s difficulty. Following the initial session, all participants underwent 24 hours of continuous wakefulness, which was verified using actigraphic monitoring (Actiwatch 2.0, Phillips Respironics, US). After the 24-hour sleep deprivation period, participants returned to the laboratory between 08:00 and 10:00 hours the following morning, and the same set of tests and measurements was repeated. Thereafter, participants received their designated interventions: the caffeine group consumed a cup of coffee containing 200 mg of caffeine, the nap group was allowed a 1-hour nap, and the control group remained awake. Final measurements were conducted approximately six hours after the interventions, corresponding to the 30th hour of continuous wakefulness. This design enables the investigation of how 24-hour sleep deprivation affects HRV and blood pressure under conditions of rest and mental stress, and it evaluates the subsequent impact of caffeine and nap interventions compared to a no-intervention control condition. Caffeine and Nap Administration Following a 29-hour period of sleep deprivation, participants assigned to Group 1 consumed coffee containing 200 mg of caffeine. Participants in the nap group (Group 2) were permitted to take a medium-length nap lasting between 40 and 60 minutes in a controlled sleep laboratory environment, with sleep verified via actigraphic monitoring. Given that all participants had been awake for over 24 hours, those in the nap group were able to fall asleep without difficulty. To mitigate the effects of sleep inertia, a waiting period of approximately 30 minutes was observed after awakening, after which all participants completed the same assessments as in the previous sessions. Measurements 1. Sleepiness Assessment At the beginning of each session, participants completed the modified Karolinska Sleepiness Scale (mKSS) (26), a 10-point instrument designed to evaluate subjective sleepiness. The scale ranges from “very alert” (1) to “extremely sleepy, falls asleep all the time” (10). 2. Blood Pressure Measurement Blood pressure was measured using a manual sphygmomanometer with a sensitivity of 2 mmHg, administered by the same examiner throughout the study. Measurements were taken at the start of each session and immediately after the cognitive test, resulting in a total of six readings across the three sessions. 3. HRV Analysis Electrocardiography (ECG) recordings were obtained using a Holter recorder (BI9800TL+Series, Biomedical Instruments Co., Guangdong, China) with a three-channel, five-lead electrode configuration. The recordings were segmented into 5-minute intervals and analyzed using the ECGLab 1.0.5 software. Although several time-domain metrics are available for HRV assessment—including SDNN, the HRV triangular index, SDANN, and RMSSD (11) for the purposes of this study, only two parameters were selected: SDNN and RMSSD. SDNN, the standard deviation of NN intervals, provides an estimate of total HRV by capturing all cyclic variations over the recording period. It is crucial that the recording durations remain consistent (e.g., short-term 5-minute recordings). RMSSD, the square root of the mean squared differences between successive NN intervals, is preferred over NN50 and pNN50 due to its superior statistical properties. Spectral analysis of short-term recordings (2 to 5 minutes) distinguishes three primary frequency bands: Very Low Frequency (VLF; <0.04 Hz), Low Frequency (LF; 0.04–0.15 Hz), and High Frequency (HF; 0.15–0.40 Hz) components (10). Due to its questionable reliability in short-term recordings, VLF was not interpreted. HF power predominantly reflects parasympathetic activity, while the LF component (when normalized for total power) is indicative of sympathetic modulation. The LF-to-HF ratio serves as an index of sympathovagal balance. 4. Cognitive Stress (Stroop Test) The Stroop test, a well-established measure of cognitive interference and frontal lobe function, was utilized to induce mental stress and assess cognitive processes such as attention and processing speed (27). Administered via a computer program, participants were seated in front of a screen and instructed to press designated keys corresponding to the ink color of words displayed at a rate of one word per second. The stimulus set included words printed in congruent (matching) and incongruent (non-matching) ink colors. 5. Task Difficulty Immediately following the cognitive test, participants were asked to rate the perceived difficulty of the task. They provided their evaluations using a visual analog scale (VAS), which was anchored at one end with “very easy” (1) and at the opposite end with “very difficult” (10). Statistical analysis All statistical analyses were performed using IBM SPSS Statistics version 20.0 (IBM Corp., Armonk, NY). To evaluate the effects of sleep deprivation and subsequent interventions across repeated measurements, a Linear Mixed Model (LMM) framework was employed. This approach was selected due to its robustness in handling missing data and its ability to account for both fixed effects and random inter-individual variability, making it particularly suitable for repeated measures designs. Prior to analysis, an a priori power calculation was conducted using G*Power 3.1 to ensure sufficient statistical power. Assuming a medium effect size (F = 0.25), an alpha level of 0.05, and power (1-β) of 0.80, the total sample size (N = 30) was deemed adequate for detecting meaningful group, time, and interaction effects within the LMM framework. The dependent variables included subjective sleepiness (Modified Karolinska Sleepiness Scale, mKSS), perceived cognitive task difficulty, systolic and diastolic blood pressure (SBP and DBP), and HRV indices (SDNN, RMSSD, LF, HF, LF/HF ratio, and RR intervals). Fixed effects included Time (Baseline, Post-Deprivation, Post-Intervention), Group (Caffeine, Nap, Control), and Sex (Male, Female). To model intra-individual correlations, random intercepts were included for each participant. A variance components covariance structure was applied to residuals to appropriately model error terms. In the presence of multiple comparisons, Bonferroni correction was applied to maintain a conservative control over Type III error. Statistical significance was defined at p < .05 (two-tailed). Model fit was assessed using Akaike Information Criterion (AIC) and Bayesian Information Criterion (BIC), and assumptions related to normality and homoscedasticity were confirmed through residual diagnostics.

The sample comprised 30 healthy young adults (15 females and 15 males) with a mean age of 19.9 ± 1.5 years and a mean body mass index (BMI) of 23.8 ± 3.8 kg/m². Pittsburgh Sleep Quality Index scores confirmed normal sleep quality (mean ± SD = 3.5 ± 1.3). All participants maintained a regular sleep schedule during the week preceding the experiment, verified by sleep diaries. Modified Karolinska Sleepiness Scale (mKSS) and Cognitive Task Difficulty Subjective sleepiness and cognitive task difficultly measurement are given in Table 1. The level of sleepiness increased in response to sleep deprivation. The linear mix model analysis of subjective sleepiness and cognitive task difficultly are given in Table 2. A significant main effect of time was observed [F(2,48) = 73.812, p < .001], indicating a marked increase in sleepiness following sleep deprivation. Post-intervention values decreased slightly but did not return to baseline, suggesting persistent subjective fatigue. A significant main effect of gender was observed [F(1,24) = 21.400, p = .001], with females consistently reporting higher sleepiness than males Post-deprivation mKSS scores were markedly higher in females (mean ± SE = 8.3 ± 0.5) than in males (6.7 ± 0.4), indicating greater subjective fatigue. A significant interaction between time and gender [F(2,48) = 7.204, p = .002] indicated that the increase in sleepiness was more pronounced in females. Moreover, a significant time × group interaction [F(4,48) = 3.340, p = .017] revealed that the caffeine group demonstrated the most effective reduction in sleepiness post-intervention. Although the group main effect did not reach significance [F(2,24) = 2.844, p = .078], pairwise comparisons suggested that the caffeine group exhibited lower scores than control. Regarding perceived cognitive task difficulty, a significant time × gender interaction [F(2,48) = 3.558, p = .036] was identified. Females reported higher difficulty ratings following sleep deprivation compared to males (VAS: females = 6.4 ± 0.4 vs. males = 5.2 ± 0.3), highlighting potential gender differences in cognitive load vulnerability. Blood Pressure Measurements Analysis of systolic and diastolic blood pressure under resting and stress conditions indicated notable gender-based differences (Table 3). The linear mix model analysis resting and stress blood pressure are given in Table 4. A significant main effect of gender was found for resting SBP [F(1,24) = 4.331, p = .048] and DBP [F(1,24) = 4.259, p = .049], with males displaying higher values. Under cognitive stress, SBP increased significantly, with a significant main effect of gender [F(1,24) = 6.639, p = .017] and a significant group × gender interaction [F(2,24) = 4.794, p = .018]. In particular, the caffeine group showed attenuation of SBP increases under stress, most notably in male participants. HRV Measurements Table 5 displays means and standard errors for HRV parameters, and Table 6 summarizes linear mixed model results. HRV analyses indicated significant changes in autonomic balance in response to sleep deprivation and interventions, influenced by both time and gender. For the low-frequency (LF) component, a significant main effect of time was observed during rest [F(2,41) = 3.676, p = .034], reflecting increased sympathetic activity after deprivation. For the high-frequency (HF) component, significant group × gender [F(2,24) = 3.686, p = .040] and time × gender [F(2,48) = 3.670, p = .033] interactions were found. Male participants in the caffeine group showed higher HF values (mean = 3.6 ± 0.3 ln ms²), suggesting preserved parasympathetic activity. The LF/HF ratio revealed a significant group × gender interaction [F(2,24) = 10.143, p = .001] and a time × group interaction [F(4,47) = 2.685, p = .043]. The caffeine and nap groups demonstrated post-intervention reductions in LF/HF ratio compared to control, indicating sympathovagal rebalancing. A significant main effect of gender was noted for SDNN [F(1,24) = 4.427, p = .046], with higher values in males (mean = 47.8 ± 2.1 ms vs. 41.2 ± 2.5 ms in females), reflecting greater overall autonomic flexibility. Significant main effects of time were detected for RR intervals during rest [F(2,48) = 8.292, p = .001] and stress [F(2,48] = 5.715, p = .006). Increased RR intervals after deprivation followed by normalization post-intervention suggest transient parasympathetic compensation and recovery. This study investigated the psychophysiological consequences of 24-hour total sleep deprivation and the effectiveness of 200 mg caffeine and napping as recovery strategies. Key findings revealed that subjective sleepiness significantly increased post-deprivation, with females reporting higher levels than males. Caffeine appeared more effective than napping or no intervention in attenuating sleepiness. Additionally, women reported greater difficulty with cognitive tasks after deprivation. Hemodynamic and HRV parameters revealed gender-based differences and divergent effects of interventions, particularly in autonomic balance restoration. Overall, the findings support the hypothesis that acute sleep deprivation significantly disrupts autonomic and cardiovascular parameters, and that intervention strategies—particularly caffeine—may offer sex-dependent recovery benefits. Sleepiness and Cognitive Load Subjective sleepiness, as measured by the modified Karolinska Sleepiness Scale (mKSS), increased significantly after 24-hour sleep deprivation, consistent with prior findings indicating a strong correlation between prolonged wakefulness and heightened sleep propensity (28,29). Females reported significantly higher levels of sleepiness than males, echoing prior studies that attribute greater subjective sensitivity in females to circadian and hormonal differences (30,31). Caffeine intake reduced perceived sleepiness more effectively than the nap and control conditions, aligning with literature showing caffeine’s role in temporarily antagonizing adenosine receptors and enhancing alertness (32). Cognitive task difficulty was also affected, with a significant interaction between time and gender. Females rated the Stroop task as more difficult following sleep deprivation, consistent with literature suggesting that females may experience a greater cognitive burden under sleep-restricted conditions (33). This may be attributed to differential resource allocation strategies and possibly greater affective reactivity to fatigue in females (34). These findings extend previous research, highlighting a need for further examination of how hormonal cycles and individual chronotypes might influence cognitive fatigue under sleep restriction. Cardiovascular Responses and Gender Differences Resting and stress-induced blood pressure responses revealed clear gender effects, with males exhibiting higher systolic and diastolic blood pressure. These results are in line with prior work demonstrating baseline hemodynamic differences between both gender (35). Under mental stress, caffeine intake was associated with attenuated systolic blood pressure responses, especially among males, supporting previous studies indicating caffeine’s complex role in modulating cardiovascular reactivity (36, 37). Interestingly, while caffeine has been linked to enhanced sympathetic reactivity, in this study it appeared to have a buffering effect under stress. This may be due to its alertness-promoting effect minimizing the cognitive load experienced during stress exposure, particularly among males (38). Conversely, females demonstrated more pronounced increases in diastolic BP following sleep deprivation, indicating greater vascular sensitivity and potential autonomic dysregulation. These observations underscore the necessity of considering gender differences when evaluating cardiovascular responses to sleep deprivation and interventions. Autonomic Nervous System Modulation HRV analyses further elucidated the physiological impacts of sleep deprivation and intervention. LF power predominantly reflects sympathetic modulation, whereas HF power reflects parasympathetic (vagal) activity. The LF/HF ratio serves as an index of sympathovagal balance. A significant increase in LF power post-sleep deprivation indicated enhanced sympathetic activity, consistent with stress-related autonomic shifts observed in the literature (13, 39). Conversely, time × gender and group × gender interactions in HF power suggested that parasympathetic tone was better preserved in males, especially in the caffeine group. This resilience is also supported by prior reports on gender-specific autonomic recovery patterns (40). The significant group × gender and time × group interactions observed in the LF/HF ratio suggest that both caffeine and nap interventions effectively promote sympathovagal rebalancing following sleep deprivation, with caffeine exhibiting a more pronounced effect in males. Caffeine and nap interventions both reduced LF/HF ratios after deprivation, although caffeine was more effective in males. These outcomes are consistent with findings from prior research suggesting that naps restored parasympathetic activity, while caffeine primarily affected central alertness mechanisms (41,42). These findings are consistent with prior research indicating that daytime naps enhance parasympathetic activity, thereby improving autonomic function. For instance, Cellini et al. (43) demonstrated that naps can increase HF power, reflecting heightened parasympathetic modulation. Conversely, caffeine’s role in modulating autonomic balance appears to be multifaceted. While caffeine is known to antagonize adenosine receptors, leading to increased alertness, it also influences cardiovascular responses to stress. Notably, Farag et al. (36) found that caffeine consumption enhances hemodynamic responses during mental stress, with variations observed between genders; men tend to exhibit increased vascular resistance, whereas women display heightened cardiac output in response to caffeine intake during stress. This differential effect may account for the more substantial reduction in LF/HF ratio observed in males following caffeine intervention. Furthermore, gender differences in autonomic function have been documented, with studies indicating that females generally exhibit higher parasympathetic tone compared to males, potentially influencing the effectiveness of interventions aimed at restoring autonomic balance. For example, research has shown that females are more likely to exhibit bradycardia and a lowering of blood pressure under arterial occlusion, suggesting a cardioprotective response (44). Collectively, these findings underscore the importance of considering gender-specific responses when evaluating the efficacy of interventions designed to mitigate the autonomic disturbances associated with sleep deprivation. Higher SDNN values, typically associated with greater autonomic adaptability and reduced stress reactivity, were more prominent in males, suggesting enhanced cardiac autonomic flexibility in response to physiological strain. This pattern may reflect either inherent trait-level autonomic resilience or sex-specific reactivity to the challenges induced by sleep deprivation. For instance, Koenig and Thayer’s (45) meta-analysis indicates that females exhibit higher vagal activity despite a higher heart rate, highlighting the complexity of sex differences in autonomic regulation. The transient increase in RR intervals after deprivation suggests a short-term parasympathetic rebound, potentially reflecting a compensatory autonomic response before normalization through intervention. While both interventions offered partial recovery, the relative magnitude of improvement—especially in sympathovagal metrics—was more substantial in the caffeine group, primarily among male participants. Implications and Future Directions The differential effects of caffeine and napping underscore the importance of tailoring interventions to individual characteristics such as sex. While caffeine effectively reduced subjective sleepiness and partially restored autonomic function—especially in males—napping offered a milder but more balanced recovery. These findings may inform strategies for managing sleep deprivation in occupational settings, particularly in gender-diverse environments like healthcare and military operations. Future studies should examine hormonal influences, extend interventions beyond a single session, and incorporate chronic sleep restriction models to enhance ecological validity. Furthermore, using multimodal cognitive assessments and neuroimaging methods may clarify the central mechanisms underlying differential recovery trajectories.

This study has several limitations. First, the relatively small sample size (n = 30) may limit the generalizability of findings and reduce statistical power for detecting subtle effects, particularly in interaction terms. Second, only healthy young adults were included, restricting applicability to clinical or older populations. Third, the interventions (nap duration, caffeine dose) were fixed and not individualized. Future research should explore dose–response effects and assess longer-term impacts.

In conclusion, the findings underscore the multifaceted impact of acute sleep deprivation on subjective, cognitive, and physiological domains. Gender significantly modulates these effects, with females generally exhibiting greater vulnerability in subjective and autonomic measures. Caffeine and short naps offer partial recovery benefits, with caffeine proving more effective for alertness and naps supporting autonomic regulation. These insights highlight the importance of personalized fatigue management strategies in occupational and clinical settings, particularly where cognitive performance and cardiovascular health are critical. Author Contributions Nurcan Erdoğan Kurtaran: conceptualization, funding acquisition, formal analysis, investigation, methodology, project administration, writing – original draft, writing – review and editing. Gülnur Öztürk: project administration, data curation, visualization, writing – original draft. Samime Şarlı Gündüz: project administration, data curation, writing – original draft. Elif Ezgi Gürel: project administration, supervision, writing- review and editing. Ümmühan Erge : project administration, investigation, writing- review and editing. Levent Öztürk: supervision , conceptualization, project administration, formal analysis, writing- review and editing.

We thank the participants and student collaborators that made this study possible.

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Subjective Sleepiness and Cognitive Task Difficulty | Caffeine | Nap | Control | Caffeine | Nap | Control | Caffeine | Nap | Control | |||||||||| | F | M | F | M | F | M | F | M | F | M | F | M | F | M | F | M | F | M | | | mKSS | 2.8 ±0.7 | 2.2 ±0.7 | 2.6 ±0.7 | 3 ±0.7 | 4.4 ±0.7 | 2.2±0.7 | 8.4 ±0.7 | 6.4±0.7 | 8.6 ±0.7 | 7.4 ±0.7 | 8 ±0.7 | 6.6 ±0.7 | 5.9 ±0.8 | 3.2 ±0.7 | 8.2 ±0.7 | 3.2 ±0.7 | 9.4 ±0.7 | 6±0.7 | | CT D | 6.4 ±0.7 | 4 ±0.7 | 6 ±0.7 | 6.8±0.7 | 4.8 ±0.7 | 6.2 ±0.7 | 5.4 ±0.7 | 5.2 ±0.7 | 6.4 ±0.7 | 5.2 ±0.7 | 4.2 ±0.7 | 4.4 ±0.7 | 6 ±0.7 | 3.2 ±0.7 | 6.6 ±0.7 | 5.6 ±0.7 | 5.4±0.7 | 3.8±0.7 | mKSS: modified Karolinska Sleepiness Scale, CTD: Cognitive Task Difficulty, Mean±SE Table 2. Mixed Model ANOVA Results for Subjective Sleepiness and Cognitive Task Difficulty | mKSS | F(2, 48) = 73.812, p < .001 | F(2, 24) = 2.844, p = .078 | F(1, 24) = 21.400, p < .001 | F(4, 48) = 3.340, p = .017 | F(2, 48) = 7.204, p = .002 | F(2, 24) = .142, p = .868 | | CTD | F(2, 48) = 1.913, p = .159 | F(2, 24) = 2.521, p = .101 | F(1, 24) = 2.247, p = .147 | F(4, 48) = .791, p = .537 | F(2, 48) = 3.558, p = .036 | F(2, 24) = 1.145, p = .335 | mKSS: modified Karolinska Sleepiness Scale, CTD: Cognitive Task Difficulty Table 3. Resting and Mental Stress Blood Pressure Responses | Caffeine | Nap | Control | Caffeine | Nap | Control | Caffeine | Nap | Control | |||||||||| | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | | | SBP-R | 93 ±5.1 | 102±5.1 | 99.6±5.1 | 116±5.1 | 105.5±5.5 | 101±5.1 | 96±5.1 | 104.6±5.1 | 93±5.1 | 115±5.1 | 102.8±5.1 | 102±5.1 | 101.2±5.1 | 105±5.1 | 93±5.1 | 112.6±5.1 | 103.2 ±5.1 | 98±5.1 | | SBP-S | 100 ±5.7 | 105±5.7 | 96±5.7 | 125.6±5.7 | 104.2±5.7 | 104±5.7 | 94.2 ±5.7 | 106.6±5.7 | 94.4±5.7 | 121±5.7 | 110±5.7 | 104 ±5.7 | 102±5.7 | 109±5.7 | 97±5.7 | 124±5.7 | 107.6±5.7 | 103±5.7 | | DBP-R | 60±3.1 | 63.6±3.1 | 62±3.1 | 71.2±3.1 | 65.2±3.1 | 69±3.1 | 61±3.1 | 62±3.1 | 59±3.1 | 70±3.1 | 62±3.1 | 65±3.1 | 66.8±3.1 | 64±3.1 | 59.4±3.1 | 72±3.1 | 63.2±3.1 | 63.2±3.1 | | DBP-S | 63±3.1 | 64±3.1 | 61±3.1 | 75.8±3.1 | 64.8±3.1 | 68±3.1 | 64±3.1 | 64±3.1 | 60.8±3.1 | 71.4±3.1 | 63±3.1 | 66.3±3.1 | 65±3.1 | 65.6±3.1 | 59.6±3.1 | 70.6±3.3 | 64.8±3.1 | 65±3.1 | SBP-R: Resting Systolic Blood Pressure, Mental Stress Systolic Blood Pressure, Resting Diastolic Blood Pressure, Mental Stress Diastolic Blood Pressure Table 4. Mixed Model ANOVA Results for Resting and Mental Stress Blood Pressure Responses | SBP-R | F(2, 47) = .083, p = .920 | F(2, 24) = .524, p = .599 | F(1, 24) = 4.331, p = .048 | F(4, 47) = 1.603, p = .189 | F(2, 47) = .613, p = .546 | F(2, 24) = 3.217, p = .058 | | SBP-S | F(2, 48) = .657, p = .523 | F(2, 24) = .917, p = .413 | F(1, 24) = 6.639, p = .017 | F(4, 48) = .837, p = .509 | F(2, 48) = .111, p = .895 | F(2, 24) = 4.794, p = .018 | | DBP-R | F(2, 48) =1.817, p = .174 | F(2, 24) = .500, p = .613 | F(1, 24) = 4.259, p = .049 | F(4, 48) = 1.938, p = .119 | F(2, 48) = .570, p = .570 | F(2, 24) = 2.065, p = .149 | | DBP-S | F(2, 45) = .816, p = .449 | F(2, 23) = .314, p = .734 | F(1, 23) = 4.496, p = .045 | F(4, 45) = 1.135, p = .352 | F(2, 45) = .766, p = .471 | F(2, 23) = 2.375, p = .115 | SBP-R: Resting Systolic Blood Pressure, Mental Stress Systolic Blood Pressure, Resting Diastolic Blood Pressure, Mental Stress Diastolic Blood Pressure Table 5. Resting and Mental Stress Heart Rate Variability Responses | Caffeine | Nap | Control | Caffeine | Nap | Control | Caffeine | Nap | Control | |||||||||| | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | Female | Male | | | LF-R | 566 ± 168 | 768 ± 184 | 594 ± 184 | 611 ± 168 | 546 ± 168 | 888 ± 184 | 626 ± 168 | 1160 ± 168 | 825 ± 168 | 791 ± 168 | 628 ± 168 | 811 ± 168 | 701 ± 168 | 969 ± 184 | 841 ± 184 | 1035± 207 | 867 ± 168 | 878 ± 168 | | LF-S | 531 ± 187 | 552± 187 | 643 ± 201 | 424 ± 201 | 423 ± 187 | 524 ± 187 | 694 ± 187 | 1086± 187 | 555 ± 201 | 679± 187 | 345 ± 187 | 415 ± 187 | 468 ± 187 | 734 ± 187 | 610 ± 187 | 768± 187 | 548 ± 187 | 511± 187 | | HF-R | 301 ± 151 | 554 ± 151 | 526 ± 151 | 284± 151 | 475 ± 151 | 514 ± 151 | 434± 151 | 712± 151 | 838 ± 151 | 315± 151 | 499 ± 151 | 378± 151 | 365 ± 151 | 1042± 151 | 426 ± 151 | 398 ±151 | 627 ± 151 | 585± 151 | | HF-S | 385 ± 150 | 388 ± 150 | 394 ± 150 | 230± 150 | 346 ± 150 | 417 ± 150 | 444± 150 | 756 ± 150 | 695 ± 164 | 300± 150 | 368 ± 150 | 387± 150 | 340 ± 150 | 773± 150 | 409 ± 150 | 342 ± 150 | 457 ± 150 | 432 ± 150 | | RATIO-R | 6.9 ± 0.8 | 4.2 ± 0.8 | 3.1 ± 0.8 | 5.8 ± 0.9 | 3.5 ± 0.8 | 4.2 ± 0.8 | 5.2 ± 0.8 | 3.1 ± 0.8 | 2.9 ± 0.8 | 8 ± 0.8 | 3.3 ± 0.8 | 4.9 ± 0.8 | 5.1 ± 0.8 | 2.5 ± 0.8 | 4.9 ± 0.8 | 7.1 ± 0.9 | 3.5 ± 0.8 | 4 ± 0.8 | | RATIO-S | 4.8 ± 0.7 | 3.3 ± 0.7 | 2.9 ± 0.7 | 4.5 ± 0.7 | 2.3± 0.7 | 2.3 ± 0.7 | 4.8 ± 0.7 | 2.2 ± 0.7 | 1.9 ± 0.7 | 5.3 ± 0.8 | 1.7 ± 0.7 | 2.1 ± 0.7 | 3.4 ± 0.7 | 1.5 ± 0.7 | 3.1 ± 0.7 | 5.2 ± 0.8 | 2.5 ± 0.7 | 3.1 ± 0.7 | | SDNN-R | 53 ± 8.6 | 67.6 ± 8.6 | 50.2 ± 8.6 | 63.4± 8.6 | 60 ± 8.6 | 66.6 ± 8.6 | 55.4 ± 8.6 | 67 ± 8.6 | 64± 8.6 | 75.4 ± 8.6 | 58.2 ± 8.6 | 57.6 ± 8.6 | 54 ± 8.6 | 69± 8.6 | 59.6 ± 8.6 | 90.8 ± 8.6 | 58.2 ± 8.6 | 59.4± 8.6 | | SDNN-S | 47.4 ± 6.4 | 48 ± 6.4 | 45.8 ± 6.4 | 48.2 ± 6.4 | 47 ± 6.4 | 51.2± 6.4 | 54 ± 6.4 | 52.4 ± 6.4 | 55 ± 6.4 | 55.8 ± 6.4 | 40.4 ± 6.4 | 42.2 ± 6.4 | 44.2 ± 6.4 | 61.4 ± 6.4 | 44 ± 6.4 | 61.2 ± 6.4 | 48.8 ± 6.4 | 44 ± 6.4 | | RMSSD-R | 42.2 ± 7.5 | 50 ± 7.5 | 46 ± 7.5 | 40.8 ± 7.5 | 46.4 ± 7.5 | 57.6± 7.5 | 39 ± 7.5 | 56 ± 7.5 | 59.6± 7.5 | 41.8 ± 7.5 | 49.8± 7.5 | 46.8± 7.5 | 39.8 ± 7.5 | 56.6 ± 7.5 | 46.2 ± 7.5 | 49± 7.5 | 50 ± 7.5 | 46.4± 7.5 | | RMSSD-S | 35 ± 7.1 | 41.2 ± 7.1 | 44.8± 7.1 | 37.4 ± 7.1 | 39.4 ± 7.1 | 50.8± 7.1 | 38.6 ± 7.1 | 51 ± 7.1 | 53± 7.1 | 34.6 ± 7.1 | 50 ± 7.1 | 35.6± 7.1 | 35.4 ± 7.1 | 60.8 ± 7.1 | 43.8± 7.1 | 39.6 ± 7.1 | 45.2 ± 7.1 | 44.4 ± 7.1 | | RR-R | 700 ± 39 | 716 ± 39 | 704± 39 | 708 ± 39 | 689± 39 | 759± 39 | 754± 39 | 772 ± 39 | 760 ± 39 | 779± 39 | 772 ± 39 | 754± 39 | 757± 39 | 797± 39 | 677 ± 39 | 780 ± 39 | 762 ± 39 | 740 ± 39 | | RR-S | 676 ± 44 | 720 ± 44 | 669 ± 44 | 679 ± 44 | 694 ± 44 | 755 ± 44 | 734 ± 44 | 767 ± 44 | 756 ± 44 | 741 ± 44 | 774± 44 | 720 ± 44 | 717 ± 44 | 786 ± 44 | 654 ± 44 | 751 ± 44 | 754 ± 44 | 714 ± 44 | R-Resting, S-Mental Stress Table 6. Mixed Model ANOVA Results for Resting and Mental Stress Heart Rate Variability Measurement | LF-R | F(2,41) = 3.676, p = .034 | F(2, 22) = .023, p = .977 | F(1, 22) = 3.044, p = .095 | F(4, 41) = .671, p = .616 | F(2, 41) = .097, p = .907 | F(2, 22) = .528, p = .597 | | LF-S | F(2, 45) = 1.167, p = .320 | F(2, 24) = 1.034, p = .371 | F(1, 24) = .590, p = .450 | F(4, 45) = 2.138, p = .091 | F(2, 45) = 1.131, p = .332 | F(2, 24) = .262, p = .772 | | HF-R | F(2, 48) = 2.479, p = .095 | F(2, 24) = .344, p = .713 | F(1, 24) = .100, p = .755 | F(4, 48) = 2.070, p = .099 | F(2, 48) = 3.670, p = .033 | F(2, 24) = 3.686, p = .040 | | HF-S | F(2, 47) = 2.073, p = .137 | F(2, 24) = .653, p = 530 | F(1, 24) = .046, p = .832 | F(4, 47) = .651, p = .629 | F(2, 47) = .723, p = .491 | F(2, 24) = 1.878, p = .175 | | RATIO-R | F(2,47) = .008, p = .992 | F(2, 24) = 2.123, p = .142 | F(1, 24) = 1.189, p = .286 | F(4, 47) = 2.685, p = .043 | F(2, 47) = 1.700, p = .194 | F(2, 24) = 10.143, p = .001 | | RATIO-S | F(2, 47) = .451, p = .640 | F(2, 24) = 3.386, p = .051 | F(1, 24) = .291, p = .594 | F(4, 47) = 2.056, p = .102 | F(2, 47) = .158, p = .854 | F(2, 24) = 6.836, p = .004 | | SDNN-R | F(2, 48) = .852, p = .433 | F(2, 24) = .677, p = .518 | F(1, 24) = 4.427, p = .046 | F(4, 48) = 1.760, p = .152 | F(2, 48) = .581, p = .563 | F(2, 24) = .761, p = .478 | | SDNN-S | F(2, 48) = .451, p = .640 | F(2, 24) = .920, p = .412 | F(1, 24) = 1.063, p = 313 | F(4, 48) = 1.454, p = .231 | F(2, 48) = 1.460, p = .242 | F(2, 24) = .227, p = .798 | | RMSSD-R | F(2, 48) = .111, p = .895 | F(2, 24) = .105, p = .900 | F(1, 24) = .390, p = .538 | F(4, 48) = .457, p = .767 | F(2, 48) = .522, p = .597 | F(2, 24) = 1.676, p = .208 | | RMSSD-S | F(2, 48) = .584, p = .561 | F(2, 24) = .073, p = .930 | F(1, 24) = .064, p = .803 | F(4, 48) = .639, p = .637 | F(2, 48) = 2.369, p = .104 | F(2, 24) = 2.588, p = .096 | | RR-R | F(2, 48) = 8.292, p = .001 | F(2, 24) = .097, p = .907 | F(1, 24) = .766, p = .390 | F(4, 48) = 1.069, p = .382 | F(2, 48) = 1.091, p = .344 | F(2, 24) = .129, p = .879 | | RR-S | F(2, 48) = 5.715, p = .006 | F(2, 24) = .296, p = .747 | F(1, 24) = .513, p = .481 | F(4, 48) = .873, p = .487 | F(2, 48) = 2.059, p = .139 | F(2, 24) = .311, p = .736 | Information & Authors Information Version history Copyright This work is licensed under a Non Exclusive No Reuse License. Authors Metrics & Citations Metrics Article Usage 834views 140downloads Citations Download citation Nurcan Erdoğan Kurtaran, Gülnur Öztürk, Samime Şarlı Gündüz, et al. Physiological and Cognitive Effects of 24-Hour Sleep Deprivation: A Gender-Specific Comparison of Nap and Caffeine Interventions. Authorea. 21 April 2025. DOI: https://doi.org/10.22541/au.174525321.14454190/v1 DOI: https://doi.org/10.22541/au.174525321.14454190/v1 If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download. For more information or tips please see 'Downloading to a citation manager' in the Help menu.