Journal of Sleep Research最新文献

Wind farm noise (WFN) exposure effects on sleep remain poorly understood. This study compared the probability of electroencephalographically (EEG) defined arousal from established sleep following WFN versus road traffic noise (RTN) onset. Sixty-eight adults were studied in a sleep laboratory on one night with repeated 20-s WFN and RTN exposures. Following ≥ 2 min of established sleep and ≥ 20-s between noise exposures, pre-recorded WFN or RTN samples were reproduced at sound pressure levels (SPLs) of 30, 40, and 50 dBA in random order. The primary outcome was the probability of EEG-defined arousal events (> 3 s EEG shifts to faster frequencies) following the onset of each noise exposure. Awakening responses (> 15 s EEG frequency shifts) were also evaluated. Noise type, SPL, and sleep stage effects on arousal and awakening response probabilities were evaluated using mixed effects logistic regression analyses. Of 68 participants, 62 (mean ± SD aged 49 ± 20 years, 35 females) had sufficient replicates of noise exposure data for analysis. Arousal response probabilities were low, particularly in deep sleep, but showed a significant noise type-by-SPL interaction (χ² = 13, p = 0.001), with marginally but significantly lower WFN compared to RTN arousal probabilities at 40 dBA (mean [95% CI]: 2.1 [1.5, 2.9] vs. 3.2 [2.4, 4.2]%, p = 0.016) and 50 dBA (5.0 [4.0, 6.2] vs. 8.6 [6.9, 10.6]%, p < 0.001). Awakenings were infrequent (< 4% at 50 dBA) but showed similar effects. These findings show that acute WFN onset is marginally less sleep disruptive than road traffic noise events of equivalent SPL ≥ 40 dBA.

Sleep profiles, including chronotype, sleep duration and sleep-wake time, may affect glycaemic outcomes. However, their associations with plasma glycaemic outcomes and 24-h interstitial glucose levels in individuals with prediabetes remains ambiguous. This study aimed to examine the association between sleep profiles and glycaemic outcomes in adults with prediabetes. Chronotype was assessed using the Malay-translated Munich Chronotype Questionnaire. Glycaemic outcomes, including fasting plasma glucose (FPG), 2-h postprandial glucose (2hPPG), glycated haemoglobin (HbA1c) levels and 24-h glucose profiles derived from seven-day continuous glucose monitoring (CGM). Generalised linear models and generalised estimating equations were used and adjusting for potential confounders. A total of 120 participants (mean age: 54 ± 15 years) were categorised as morning (18.4%), intermediate (60.8%) or evening (20.8%) chronotypes. Evening chronotypes demonstrated greater weekday-weekend discrepancy in awake time (0.7 h [±1.1 h]), indicating higher social jet lag. Each additional hour of jet lag in awake time was associated with a 0.28 mmol/L reduction in 2hPPG levels (95% CI: -0.49, -0.08), reflecting compensatory catch-up sleep on weekends. Longer sleep time was positively associated more time spent within the target glucose range (3.9-7.8 mmol/L) (β: 0.58, 95% CI: 0.06, 1.10), while evening chronotype showed higher 24-h mean glucose levels (β: 0.65 mmol/L, 95% CI: 0.22, 1.12). Evening chronotype and shorter sleep duration were associated with adverse glycaemic outcomes, while the unexpected inverse association between awake-time jet lag and 2hPPG may reflect short-term catch-up sleep rather than a protective effect. These findings highlight the importance of addressing sleep regularity in lifestyle interventions for prediabetes management.

This longitudinal study of Arctic residents investigates how physical activity and sleep, known to be affected by extreme Arctic photoperiods, are linked to blood lipid profiles and thus cardiovascular disease risk in this particularly vulnerable population. We analyzed parametric and non-parametric actigraphy data of physical activity (PA) and sleep measures across three distinct photoperiods (winter solstice, spring equinox, and summer solstice) in a cohort of Arctic residents. Multiple regression models, adjusted for photoperiod, were employed to determine independent associations of PA and sleep parameters with total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG). Robust circadian rhythms in PA were significantly associated with improved lipid profiles. Specifically, lower intra-daily variability IV (β = 0.423, p < 0.001) and higher inter-daily stability IS (β = -0.263, p = 0.019) of PA, indicating stable and predictable daily activity patterns, were associated with lower TG and TG/HDL-C ratios. A greater amplitude of PA rhythms was also associated with lower TG (β = -0.345, p = 0.002). An earlier timing of daily activity (acrophase) was associated with higher TC and LDL-C (β = -0.492, p < 0.001), while earlier wake times (β = -0.309, p = 0.009) and higher sleep efficiency (β = 0.237, p = 0.011) were associated with higher HDL-C. These findings highlight the relevance of circadian rhythmicity in dyslipidemia management, particularly in extreme photoperiods, suggesting that lifestyle interventions promoting stable daily activity and sleep patterns may be associated with improved metabolic health and reduced cardiovascular risk.

Sleep reactivity-an individual's susceptibility to sleep disruptions due to stress-has been linked to increased insomnia risk. Investigating how sleep reactivity moderates the 'stress → pre-sleep arousal → sleep' pathway may help mitigate sleep disturbances and enhance treatment outcomes. In the present study, full-time university students without sleep disorders completed the Ford Insomnia Response to Stress Test (FIRST), which assesses sleep reactivity. From 264 students, 30 students with the lowest and 30 with the highest FIRST scores were selected for further study. They provided daily actigraphy, Pre-sleep Arousal Scale ratings, pre-sleep heart rate (via an ŌURA ring), and perceived stress scores over 2 weeks. Multilevel moderated mediation analyses were conducted using 800 nights of data to examine within- and between-individual associations. At the within-individual level, days with higher-than-usual perceived stress were associated with reduced total sleep time and increased sleep onset latency (p's < 0.05). These effects were mediated by heightened pre-sleep cognitive arousal (p's < 0.05) but not moderated by the FIRST group. In contrast, between-individual analyses revealed a significant moderation by the FIRST group (p < 0.05). High sleep-reactive individuals reported significantly greater average levels of perceived stress and pre-sleep cognitive arousal, leading to prolonged wakefulness after sleep onset (b = 0.123, Monte Carlo confidence interval [MCCI] = 0.006-0.292), compared to low-reactive sleepers. Overall, on a day-to-day basis, both groups showed increased pre-sleep cognitive arousal and sleep disruptions in response to elevated daily stress. However, between individuals, high sleep reactivity significantly amplified the effect of pre-sleep cognitive (but not physiological) arousal, leading to more pronounced sleep disturbances compared to low-reactive sleepers.

PSG, a cornerstone diagnostic instrument in sleep medicine, is recommended for the diagnosis of numerous sleep disorders and might be used as a benchmark for evaluating therapeutical effectiveness. However, PSG has its limitations, and its usefulness in the future warrants reappraisal. First, it is a complex test that requires highly-trained personnel to correctly place the electrodes, monitor the patient, and manually analyse the data. This constitutes a significant economic burden for both society and healthcare systems. PSG also presents few technical limitations: variability of data between nights and variable reliability of scoring between readers. The results given to patients are also limited to the macrostructure of sleep, risking the loss of important information that escapes detection when relying solely on polysomnographic evaluation based on macro sleep stages. The current sleep scoring guidelines raise some doubts about their ability to capture the dynamic and complex nature of human sleep in both clinical and physiological contexts. On the other hand, advanced PSG analysis can provide key information for diagnosis particularly through the microstructural analysis of NREM oscillatory pattern, characterisation of spindles and slow waves, eye movement density, spectrum analysis with hypnodensity and sleep propensity with odd ratio products (ORP). These elements provide a better understanding of the differences between insomnia and poor sleep perception. Furthermore, these methods take into account the dynamics of sleep states, going beyond the mere distinction of sleep into macro stages, which poorly reflects the dynamic nature of sleep itself and including in the assessment of sleep function all the complex associations that sleep itself has with autonomic and cardiorespiratory variables. These insights will transform the role of technicians and clinicians in PSG analysis, with a shift towards training in digital data analysis and algorithms to better inform patients about their PSG results.

Sleep is essential for normal physiological functioning, and sleep deprivation is typically compensated by increasing subsequent sleep duration and/or intensity. However, a recent study showed that barnacle geese (Branta leucopsis) exhibit seasonal variation in sleep homeostasis, with full recovery of sleep after sleep deprivation in summer but no sleep rebound after similar deprivation in winter based on electroencephalography (EEG). This lack of sleep rebound could suggest that geese in winter do not build up sleep pressure during wakefulness or that accumulated sleep need is not reflected in EEG-based sleep measures. The current study investigated whether geese in winter accumulate sleep pressure during extended wakefulness, using behavioural activity and reactivity to stimulation as alternative indicators of sleep drive. If sleep deprivation increases sleep pressure, we expected geese to adopt more sleep postures and show elevated arousal thresholds in response to stimulation. Fifteen barnacle geese were implanted with epidural electrodes for EEG recordings and housed in a semi-natural enclosure during winter. We carefully observed and approached the geese at 10-min intervals during the night for 8-h following sunset. Although sleep was suppressed during this period, it did not lead to significant EEG changes and most of the lost sleep was not recovered. However, the behavioural observations revealed that geese exhibited increased sleep postures and diminished responsiveness to being approached. Our findings suggest that prolonged wakefulness in barnacle geese increases behavioural indicators of sleep pressure, also in winter, even though this rise in sleep drive is not clearly reflected in EEG-based sleep measures.

This overview with re-analysis of systematic reviews (SRs) aims to assess the effectiveness of orofacial myofunctional therapy (MT) for Obstructive Sleep Apnea (OSA) patients. We searched PubMed, Embase, and the Cochrane Library up to July 2024. SRs with meta-analyses on OSA in adults or children who underwent MT intervention compared to any control were included. Primary outcomes were severity of sleep apnea, oxygen saturation, sleep efficiency, and daytime sleepiness, while secondary outcomes included snoring intensity, frequency, and sleep quality. We included nine SRs, encompassing 21 unique primary studies (13 RCTs, 8 pre-post studies; n = 716 participants). The methodological quality of the SRs was generally critically low (5/9 SRs). After re-analyzing outcome data (primary studies overlap: 13.44%), MT seems to be more effective than control in reducing severity of sleep apnea (MD -9.54; CIs 95% -14.04, -5.04), daytime sleepiness (MD -3.62; CIs 95% -6.61, -0.63), sleep quality (MD -2.23; CIs 95% -2.93, -1.53), and in improving minimum oxygen saturation (MD 3.19; CIs 95% 1.47, 4.91) in adults. No differences were found in mean oxygen saturation and sleep efficiency. Meta-analyses comparing pre-MT to post-MT showed improvements post-MT. Sparse evidence was found for other outcomes and for children. MT may improve multiple clinical outcomes in OSA. Results should be interpreted cautiously, as most primary studies are at high risk of bias. More research is needed on the pediatric population.

This study aimed to assess the associations between the frequency of episodes of disorders of arousal (sleepwalking and sleep terrors) and emotional-behavioural problems in a longitudinal cohort of healthy children aged 4 and 5 years. Mother-child dyads (N = 345) were recruited during pregnancy for a longitudinal cohort study. Mothers completed validated questionnaires when children were 4 and 5 years old. Linear regressions assessed (1) the concurrent association between the frequency of disorders of arousal episodes (i.e., sleepwalking and sleep terrors) and emotional-behavioural problems in children at 4 and 5; and (2) the association between the frequency of disorders of arousal episodes at 4 and emotional-behavioural problems at 5. Models included the following covariates: child's sex, child's nighttime sleep duration, socioeconomic status and maternal depressive symptoms. More frequent episodes of disorders of arousal at age 4 were significantly associated with more concurrent internalising (B = 2.659, p = 0.001), and externalising problems (B = 2.740, p = 0.006). At age 5, the frequency of episodes was not associated with concurrent internalising and externalising problems (p > 0.05). More frequent episodes at age 4 were associated with more externalising problems at 5 (B = 2.462, p = 0.039). Although sleep terrors and sleepwalking are often benign, our results show that even in a non-clinical cohort, these sleep phenomena can be associated with emotional-behavioural problems in children as young as 4. While the mere presence of sleep terrors or sleepwalking is not alarming, screening for emotional-behavioural problems seems appropriate for children with frequent episodes.

Recent studies have shown that acoustic stimulation, a common neuromodulation technique, can enhance slow-wave activity (SWA), which is associated with immune, autonomic nervous system activity and cognitive health benefits. Despite some disagreement, many studies suggest that maximising tone-evoked SWA depends on the timing of the acoustic stimulus in relation to ongoing cortical slow oscillations. Given the close connection between the central and peripheral systems during sleep, particularly at the cortico-cardiac level, we here aimed to examine the overlooked relationship between the timing of stimulation and the dominant cortical and cardiac rhythms. We evaluated the effect of acoustic stimulation in different phases of the EEG slow oscillation (SO; ~0.8 Hz) component of SWA (0.5-4 Hz) and heart rate (HR) low-frequency (LF) (0.04-0.15 Hz) and high-frequency (HF) (0.15-0.4 Hz) oscillations on tone-evoked EEG slow activity and HR profiles. One hundred thirty-three adolescents underwent overnight polysomnography where acoustic tones (80 dB at 1000 Hz for 50 msec) were played with a random 15-30 s interstimulus interval. The analysis was limited to artefact and arousal-free episodes of NREM sleep. Playing acoustic tones in the upstate phases of EEG SOs, upstate phases of HR LF oscillations and downstate phases of HR HF oscillations induced significantly higher peak-to-peak amplitude EEG SOs (110%, 16% and 7%, respectively) (p < 0.001) and HR oscillations (16%, 56% and 25%, respectively) (p < 0.001), produced a greater number of EEG SOs (22%, 12% and 5%, respectively) and increased the SWA (3%, 14% and 3%, respectively) (p < 0.05) in contrast to playing tones in the other phase (downstate phases of EEG SOs, downstate phases of LF oscillations and upstate phases of HR HF oscillations). Our findings reveal complex interactions between the central and peripheral nervous systems in processing external stimuli, leading to significant variations in postcortical and cardiac oscillations. These results have potential implications for developing deep sleep enhancement technologies using adaptive interventions based on multidimensional oscillations.