Effects of Chronic Sleep Restriction on Transcriptional Sirtuin 1 Signaling Regulation in Male Mice White Adipose Tissue.

Chronic sleep restriction (CSR) is a prevalent issue in modern society that is associated with several pathological states, ranging from neuropsychiatric to metabolic diseases. Despite its known impact on metabolism, the specific effects of CSR on the molecular mechanisms involved in maintaining metabolic homeostasis at the level of white adipose tissue (WAT) remain poorly understood. Therefore, this study aimed to investigate the influence of CSR on sirtuin 1 (SIRT1) and the peroxisome proliferator-activated receptor γ (PPARγ) signaling pathway in the WAT of young male mice. Both genes interact with specific targets involved in multiple metabolic processes, including adipocyte differentiation, browning, and lipid metabolism. The quantitative PCR (qPCR) results demonstrated a significant upregulation of SIRT-1 and some of its target genes associated with the transcriptional regulation of lipid homeostasis (i.e., PPARα, PPARγ, PGC-1α, and SREBF) and adipose tissue development (i.e., leptin, adiponectin) in CSR mice. On the contrary, DNA-binding transcription factors (i.e., CEBP-ß and C-myc), which play a pivotal function during the adipogenesis process, were found to be down-regulated. Our results also suggest that the induction of SIRT1-dependent molecular pathways prevents weight gain. Overall, these findings offer new, valuable insights into the molecular adaptations of WAT to CSR, in order to support increased energy demand due to sleep loss.

Glucose competition between endothelial cells in the blood-spinal cord barrier and infiltrating regulatory T cells is linked to sleep restriction-induced hyperalgesia.

BACKGROUND: Sleep loss is a common public health problem that causes hyperalgesia, especially that after surgery, which reduces the quality of life seriously. METHODS: The 48-h sleep restriction (SR) mouse model was created using restriction chambers. In vivo imaging, transmission electron microscopy (TEM), immunofluorescence staining and Western blot were performed to detect the status of the blood-spinal cord barrier (BSCB). Paw withdrawal mechanical threshold (PWMT) was measured to track mouse pain behavior. The role of infiltrating regulatory T cells (Tregs) and endothelial cells (ECs) in mouse glycolysis and BSCB damage were analyzed using flow cytometry, Western blot, CCK-8 assay, colorimetric method and lactate administration. RESULTS: The 48-h SR made mice in sleep disruption status and caused an acute damage to the BSCB, resulting in hyperalgesia and neuroinflammation in the spinal cord. In SR mice, the levels of glycolysis and glycolysis enzymes of ECs in the BSCB were found significantly decreased [CON group vs. SR group: CD31+Glut1+ cells: p < 0.001], which could cause dysfunction of ECs and this was confirmed in vitro. Increased numbers of infiltrating T cells [p < 0.0001] and Treg population [p < 0.05] were detected in the mouse spinal cord after 48-h SR. In the co-cultured system of ECs and Tregs in vitro, the competition of Tregs for glucose resulted in the glycolysis disorder of ECs [Glut1: p < 0.01, ENO1: p < 0.05, LDHα: p < 0.05; complete tubular structures formed: p < 0.0001; CCK8 assay: p < 0.001 on 24h, p < 0.0001 on 48h; glycolysis level: p < 0.0001]. An administration of sodium lactate partially rescued the function of ECs and relieved SR-induced hyperalgesia. Furthermore, the mTOR signaling pathway was excessively activated in ECs after SR in vivo and those under the inhibition of glycolysis or co-cultured with Tregs in vitro. CONCLUSIONS: Affected by glycolysis disorders of ECs due to glucose competition with infiltrating Tregs through regulating the mTOR signaling pathway, hyperalgesia induced by 48-h SR is attributed to neuroinflammation and damages to the barriers, which can be relieved by lactate supplementation.

Sleep and subjective age: protect your sleep if you want to feel young.

The current studies examined the impact of insufficient sleep and sleepiness on the subjective experience of age. Study 1, a cross-sectional study of 429 participants (282 females (66%), 144 males, 3 other gender; age range 18-70), showed that for each additional day of insufficient sleep in the last 30 days, subjective age increased by 0.23 years. Study 2, an experimental crossover sleep restriction study (n = 186; 102 females (55%), 84 males; age range 18-46), showed that two nights of sleep restriction (4 h in bed per night) made people feel 4.44 years older compared to sleep saturation (9 h in bed per night). Additionally, moving from feeling extremely alert (Karolinska Sleepiness Scale (KSS) score of 1) to feeling extremely sleepy (KSS score of 9) was associated with feeling 10 years older in both studies. These findings provide compelling support for insufficient sleep and sleepiness to exert a substantial influence on how old we feel, and that safeguarding sleep is probably a key factor in feeling young.

Effects of low-dose acetylsalicylic acid on the inflammatory response to experimental sleep restriction in healthy humans.

BACKGROUND: Sleep deficiencies, such as manifested in short sleep duration or insomnia symptoms, are known to increase the risk for multiple disease conditions involving immunopathology. Inflammation is hypothesized to be a mechanism through which deficient sleep acts as a risk factor for these conditions. Thus, one potential way to mitigate negative health consequences associated with deficient sleep is to target inflammation. Few interventional sleep studies investigated whether improving sleep affects inflammatory processes, but results suggest that complementary approaches may be necessary to target inflammation associated with sleep deficiencies. We investigated whether targeting inflammation through low-dose acetylsalicylic acid (ASA, i.e., aspirin) is able to blunt the inflammatory response to experimental sleep restriction. METHODS: 46 healthy participants (19F/27M, age range 19-63 years) were studied in a double-blind randomized placebo-controlled crossover trial with three protocols each consisting of a 14-day at-home monitoring phase followed by an 11-day (10-night) in-laboratory stay (sleep restriction/ASA, sleep restriction/placebo, control sleep/placebo). In the sleep restriction/ASA condition, participants took low-dose ASA (81 mg/day) daily in the evening (22:00) during the at-home phase and the subsequent in-laboratory stay. In the sleep restriction/placebo and control sleep/placebo conditions, participants took placebo daily. Each in-laboratory stay started with 2 nights with a sleep opportunity of 8 h/night (23:00-07:00) for adaptation and baseline measurements. Under the two sleep restriction conditions, participants were exposed to 5 nights of sleep restricted to a sleep opportunity of 4 h/night (03:00-07:00) followed by 3 nights of recovery sleep with a sleep opportunity of 8 h/night. Under the control sleep condition, participants had a sleep opportunity of 8 h/night throughout the in-laboratory stay. During each in-laboratory stay, participants had 3 days of intensive monitoring (at baseline, 5th day of sleep restriction/control sleep, and 2nd day of recovery sleep). Variables, including pro-inflammatory immune cell function, C-reactive protein (CRP), and actigraphy-estimated measures of sleep, were analyzed using generalized linear mixed models. RESULTS: Low-dose ASA administration reduced the interleukin (IL)-6 expression in LPS-stimulated monocytes (p<0.05 for condition*day) and reduced serum CRP levels (p<0.01 for condition) after 5 nights of sleep restriction compared to placebo administration in the sleep restriction condition. Low-dose ASA also reduced the amount of cyclooxygenase (COX)-1/COX-2 double positive cells among LPS-stimulated monocytes after 2 nights of recovery sleep following 5 nights of sleep restriction compared to placebo (p<0.05 for condition). Low-dose ASA further decreased wake after sleep onset (WASO) and increased sleep efficiency (SE) during the first 2 nights of recovery sleep (p<0.001 for condition and condition*day). Baseline comparisons revealed no differences between conditions for all of the investigated variables (p>0.05 for condition). CONCLUSION: This study shows that inflammatory responses to sleep restriction can be reduced by preemptive administration of low-dose ASA. This finding may open new therapeutic approaches to prevent or control inflammation and its consequences in those experiencing sleep deficiencies. TRIAL REGISTRATION: ClinicalTrials.gov NCT03377543.

Acute partial sleep restriction does not impact arterial function in young and healthy humans.

Habitual short sleep durations are associated with several cardiovascular diseases. Experimental research generally supports these findings as metrics of arterial function are impaired after complete deprivation of sleep and after longer periods of partial sleep restriction. The acute influence of a single instance of partial sleep restriction (PSR), however, has not been defined. We evaluated arterial structure and function among 32 university-aged participants on two occasions: once after normal habitual sleep (NS), and again the morning after an acute partial sleep restriction (PSR) intervention involving only 3 h of sleep for a single night. Endothelial function was measured using ultrasonography at the brachial artery via flow-mediated dilatation (FMD), and a ramp peak oxygen uptake test was used to evaluate cardiorespiratory fitness. Blood samples were collected from a subset of participants to investigate the influence of circulatory factors on cellular mechanisms implicated in endothelial function. Sleep duration was lower after a night of PSR compared to NS (P < 0.001); however, there were no appreciable differences in any haemodynamic outcome between conditions. FMD was not different between NS and PSR (NS: 6.5 ± 2.9%; PSR: 6.3 ± 2.9%; P = 0.668), and cardiorespiratory fitness did not moderate the haemodynamic response to PSR (all P > 0.05). Ex vivo cell culture results aligned with in vivo data, showing that acute PSR does not alter intracellular processes involved in endothelial function. No differences in arterial structure or function were observed between NS and acute PSR in healthy and young participants, and cardiorespiratory fitness does not modulate the arterial response to acute sleep restriction.

The effects of partial sleep restriction and subsequent caffeine ingestion on neurovascular coupling.

Habitual poor sleep is associated with cerebrovascular disease. Acute sleep deprivation alters the ability to match brain blood flow to metabolism (neurovascular coupling [NVC]) but it is not known how partial sleep restriction affects NVC. When rested, caffeine disrupts NVC, but its effects in the sleep-restricted state are unknown. The purpose of this study was therefore to investigate the effects of partial sleep restriction and subsequent caffeine ingestion on NVC. A total of 17 adults (mean [standard deviation] age 27 [5] years, nine females) completed three separate overnight conditions with morning supplementation: habitual sleep plus placebo (Norm_Pl), habitual sleep plus caffeine (Norm_Caf), and partial (50% habitual sleep) restriction plus caffeine (PSR_Caf). NVC responses were quantified as blood velocity through the posterior (PCAv) and middle (MCAv) cerebral arteries using transcranial Doppler ultrasound during a visual search task and cognitive function tests, respectively. NVC was assessed the evening before and twice the morning after each sleep condition-before and 1-h after caffeine ingestion. NVC responses as a percentage increase in PCAv and MCAv from resting baseline were not different at any timepoint, across all conditions (p > 0.053). MCAv at baseline, and PCAv at baseline, peak, and total area under the curve were lower 1-h after caffeine in both Norm_Caf and PSR_Caf as compared to Norm_Pl (p < 0.05), with no difference between Norm_Caf and PSR_Caf (p > 0.14). In conclusion, NVC was unaltered after 50% sleep loss, and caffeine did not modify the magnitude of the response in the rested or sleep-deprived state. Future research should explore how habitual poor sleep affects cerebrovascular function.

The effect of single-component sleep restriction therapy on depressive symptoms: A systematic review and meta-analysis.

Sleep restriction therapy is a behavioural component within cognitive behavioural therapy for insomnia and is an effective standalone treatment for insomnia, but its effect on depressive symptoms remains unclear. This review aimed to synthesise and evaluate the impact of single-component sleep restriction therapy on depressive symptoms relative to a control intervention. We searched electronic databases and sleep-related journals for randomised controlled trials and uncontrolled clinical trials, published from 1 January 1986 until 19 August 2023, that delivered sleep restriction therapy to adults with insomnia. Random-effects meta-analysis of standardised mean differences and Cochrane risk of bias assessment were performed on randomised controlled trials, while uncontrolled clinical trials were discussed narratively. The meta-analysis was pre-registered on PROSPERO (ID: CRD42020191803). We identified seven randomised controlled trials (N = 1102) and two uncontrolled clinical trials (N = 22). Findings suggest that sleep restriction therapy is associated with a medium effect for improvement in depressive symptoms at post-treatment (Nc = 6, g = -0.45 [95% confidence interval = -0.70 to -0.21], p < 0.001) and a small effect at follow-up (Nc = 4, g = -0.31 [95% confidence interval = -0.45 to -0.16], p < 0.001). Five of the seven included randomised controlled trials were judged to have a high risk of bias. Standalone sleep restriction therapy appears to be efficacious for improving depressive symptoms at post-treatment and follow-up. However, conclusions are tentative due to the small number of trials and because none of the trials was performed in a population with clinically defined depression. Large-scale trials are needed to test the effect of sleep restriction therapy in patients experiencing depression and insomnia. Findings also highlight the need to improve the standardisation and reporting of sleep restriction therapy procedures, and to design studies with more rigorous control arms to reduce potential bias.

Concentration-effect relationships of plasma caffeine on EEG delta power and cardiac autonomic activity during human sleep.

Acute caffeine intake affects brain and cardiovascular physiology, yet the concentration-effect relationships on the electroencephalogram and cardiac autonomic activity during sleep are poorly understood. To tackle this question, we simultaneously quantified the plasma caffeine concentration with ultra-high-performance liquid chromatography, as well as the electroencephalogram, heart rate and high-frequency (0.15-0.4 Hz) spectral power in heart rate variability, representing parasympathetic activity, with standard polysomnography during undisturbed human sleep. Twenty-one healthy young men in randomized, double-blind, crossover fashion, ingested 160 mg caffeine or placebo in a delayed, pulsatile-release caffeine formula at their habitual bedtime, and initiated a 4-hr sleep opportunity 4.5 hr later. The mean caffeine levels during sleep exhibited high individual variability between 0.2 and 18.4 µmol L-1 . Across the first two non-rapid-eye-movement (NREM)-rapid-eye-movement sleep cycles, electroencephalogram delta (0.75-2.5 Hz) activity and heart rate were reliably modulated by waking and sleep states. Caffeine dose-dependently reduced delta activity and heart rate, and increased high-frequency heart rate variability in NREM sleep when compared with placebo. The average reduction in heart rate equalled 3.24 ± 0.77 beats per minute. Non-linear statistical models suggest that caffeine levels above ~7.4 µmol L-1 decreased electroencephalogram delta activity, whereas concentrations above ~4.3 µmol L-1 and ~ 4.9 µmol L-1 , respectively, reduced heart rate and increased high-frequency heart rate variability. These findings provide quantitative concentration-effect relationships of caffeine, electroencephalogram delta power and cardiac autonomic activity, and suggest increased parasympathetic activity during sleep after intake of caffeine.

Sleep restriction alters the integration of multiple information sources in probabilistic decision-making.

The detrimental effects of sleep loss on overall decision-making have been well described. Due to the complex nature of decisions, there remains a need for studies to identify specific mechanisms of decision-making vulnerable to sleep loss. Bayesian perspectives of decision-making posit judgement formation during decision-making occurs via a process of integrating knowledge gleaned from past experiences (priors) with new information from current observations (likelihoods). We investigated the effects of sleep loss on the ability to integrate multiple sources of information during decision-making by reporting results from two experiments: the first implementing both sleep restriction (SR) and total sleep deprivation (TSD) protocols, and the second implementing an SR protocol. In both experiments, participants were administered the Bayes Decisions Task on which optimal performance requires the integration of Bayesian prior and likelihood information. Participants in Experiment 1 showed reduced reliance on both information sources after SR, while no significant change was observed after TSD. Participants in Experiment 2 showed reduced reliance on likelihood after SR, especially during morning testing sessions. No accuracy-related impairments resulting from SR and TSD were observed in both experiments. Our findings show SR affects decision-making through altering the way individuals integrate available sources of information. Additionally, the ability to integrate information during SR may be influenced by time of day. Broadly, our findings carry implications for working professionals who are required to make high-stakes decisions on the job, yet consistently receive insufficient sleep due to work schedule demands.

Awareness of errors is reduced by sleep loss.

The ability to detect and subsequently correct errors is important in preventing the detrimental consequences of sleep loss. The Error Related Negativity (ERN), and the error positivity (Pe) are established neural correlates of error processing. Previous work has shown sleep loss reduces ERN and Pe, indicating sleep loss impairs error-monitoring processes. However, no previous work has examined behavioral error awareness, in conjunction with EEG measures, under sleep loss conditions, and studies of sleep restriction are lacking. Using combined behavioral and EEG measures, we report two studies investigating the impact of total sleep deprivation (TSD) and sleep restriction (SR) on error awareness. Fourteen healthy participants completed the Error Awareness Task under conditions of TSD and 27 completed the same task under conditions of SR. It was found that TSD did not influence behavioral error awareness or ERN or Pe amplitude, however, SR reduced behavioral error awareness, increased the time taken to detect errors, and reduced Pe amplitude. Findings indicate individuals who are chronically sleep restricted are at risk for reduced recognition of errors. Reduced error awareness may be one factor contributing to the increased accidents and injuries seen in contexts where sleep loss is prevalent.

Role of Thymoquinone on sleep restriction and its mitigating effect on leptin-mediated signaling pathway in rat brain.

BACKGROUND: Sleep and stress interact bidirectionally by acting on brain circuits that affect metabolism. Sleep and its alterations have impact on blood leptin levels, metabolic hormone that regulates appetite. Brain expresses the receptors for the peptide hormone leptin produced from adipocytes. The hypothalamic orexin neurons are low during sleep and active when awake, influenced by a complex interaction with leptin. Thymoquinone was found to be the major bioactive component of Nigella sativa. The aim of this study was to study the role of thymoquinone on sleep restriction and its mitigating effect on leptin-mediated signaling pathway in rat brain. METHODS AND RESULTS: 30 adult male Wistar rats were divided into 5 groups with 6 animals in each group: Control; Thymoquinone (TQ); Corn oil; Chronic Sleep restriction (CSR); and CSR + TQ. After 30 days, behavioral analysis, antioxidant, lipid profile, glucose level, liver and kidney function test, neurotransmitters, neuropeptides, and mRNA expression in in vivo studies were also assessed and pharmacokinetic and docking were done for thymoquinone. Thymoquinone has also shown good binding affinity to the target proteins. CSR has induced oxidative stress in the discrete brain regions and plasma. Current study has shown many evidences that sleep restriction has altered the neurobehavioral, antioxidant status, lipid profile, neurotransmitters, neuropeptide levels, and feeding behavior which damage the Orexin-leptin system which regulates the sleep and feeding that leads to metabolic dysfunction. CONCLUSION: The potentiality of Thymoquinone was revealed in in silico studies, and its action in in vivo studies has proved its effectiveness. The study concludes that Thymoquinone has exhibited its effect by diminishing the metabolic dysfunction by its neuroprotective, antioxidant, and hypolipidemic properties.

The association between proportion of night shifts and musculoskeletal pain and headaches in nurses: a cross-sectional study.

BACKGROUND AND PURPOSE: Shift work is associated with musculoskeletal pain and headaches, but little is known about how the intensity of shift work exposure is related to musculoskeletal pain and headaches. This study aimed to investigate whether a higher proportion of night shifts is associated with a higher occurrence of musculoskeletal pain and headaches. Furthermore, to investigate whether sleep duration can mediate this potential association. METHOD: The study included 684 nurses in rotating shift work who responded to a daily questionnaire about working hours, sleep, and pain for 28 consecutive days. The data were treated cross-sectionally. RESULTS: A negative binomial regression analysis adjusted for age and BMI revealed that working a higher proportion of night shifts is not associated with a higher occurrence of musculoskeletal pain and headaches. On the contrary, those working ≥ 50% night shifts had a significantly lower occurrence of pain in the lower extremities than those who worked < 25% night shifts (IRR 0.69 95% CI 0.51, 0.94). There was no indication of a mediation effect with total sleep time (TST). CONCLUSION: The results of this study indicate that working a higher proportion of night shifts is not associated with a higher occurrence of musculoskeletal pain and headaches.

The effect of a dynamic lighting schedule on neurobehavioral performance during a 45-day simulated space mission.

Study Objectives: We previously reported that during a 45-day simulated space mission, a dynamic lighting schedule (DLS) improved circadian phase alignment and performance assessed once on selected days. This study aimed to evaluate how DLS affected performance on a 5-minute psychomotor vigilance task (PVT) administered multiple times per day on selected days. Methods: Sixteen crewmembers (37.4 ±â€…6.7 years; 5F) underwent six cycles of 2 × 8-hour/night followed by 5 × 5-hour/night sleep opportunities. During the DLS (n = 8), daytime white light exposure was blue-enriched (~6000 K; Level 1: 1079, Level 2: 76 melanopic equivalent daytime illuminance (melEDI) lux) and blue-depleted (~3000-4000 K; L1: 21, L2: 2 melEDI lux) 3 hours before bed. In the standard lighting schedule (SLS; n = 8), lighting remained constant (~4500K; L1: 284, L2 62 melEDI lux). Effects of lighting condition (DLS/SLS), sleep condition (5/8 hours), time into mission, and their interactions, and time awake on PVT performance were analyzed using generalized linear mixed models. Results: The DLS was associated with fewer attentional lapses (reaction time [RT] > 500 milliseconds) compared to SLS. Lapses, mean RT, and 10% fastest/slowest RTs were worse following 5 compared to 8 hours of sleep but not between lighting conditions. There was an effect of time into mission on RTs, likely due to sleep loss. Overall performance differed by time of day, with longer RTs at the beginning and end of the day. There were more lapses and slower RTs in the afternoon in the SLS compared to the DLS condition. Conclusions: Future missions should incorporate DLS to enhance circadian alignment and performance. This paper is part of the Sleep and Circadian Rhythms: Management of Fatigue in Occupational Settings Collection.

Association Between EEG Microarousal During Nocturnal Sleep and Next-Day Selective Attention in Mild Sleep-Restricted Healthy Undergraduates.

Purpose: To explore whether sleep electroencephalogram (EEG) microarousals of different standard durations predict daytime mood and attention performance in healthy individuals after mild sleep restriction. Participants and Methods: Sixteen (nine female) healthy college students were recruited to examine the correlations between nocturnal EEG microarousals of different standard durations (≥3 s, ≥5 s, ≥7 s, ≥9 s) under mild sleep restriction (1.5 h) and the following morning's subjective alertness, mood, sustained attention, and selective attention task performance. Results: Results revealed that mild sleep restriction significantly reduced subjective alertness and positive mood, while having no significant effect on negative mood, sustained attention and selective attention performance. The number of microarousals (≥5 s) was negatively associated with positive mood at 6:30. The number of microarousals was significantly and positively correlated with the response time difference value of disengagement component of the selective attention task at around 7:30 (≥5 s and ≥7 s) and 9:00 (≥5 s). The number of microarousals (≥7 s) was significantly and positively correlated with the inaccuracy difference value of orientation component of the selective attention task at around 9:00. Conclusion: The number of EEG microarousals during sleep in healthy adults with mild sleep restriction was significantly and negatively related to their daytime positive affect while positively associated with the deterioration of disengagement and orientation of selective attention performance, but this link is dependent on the standard duration of microarousals, test time and the type of task.

The effects of sustained mild sleep restriction on stress and distress among healthy adults: Findings from two randomized crossover studies.

OBJECTIVE/BACKGROUND: Experimental studies suggest that sleep loss affects psychological outcomes. However, most studies focus on acute severe in-laboratory sleep restriction, with limited ecological validity. This study examines the impact of sustained mild sleep restriction (SR) on stress and distress among healthy adults in a naturalistic home environment. PATIENTS/METHODS: We analyzed data from two randomized crossover studies. Individuals who regularly slept 7-9 h/night completed two 6-wk intervention phases separated by a 6-wk washout: habitual sleep (HS: maintenance of habitual bed and wake times) and SR (delayed bedtime by 1.5 h/night and maintenance of habitual wake time). Adherence to sleep duration requirements was verified with wrist actigraphy and daily sleep diaries during each intervention phase. Measures of perceived stress, subjective anxiety, subjective depression, rumination, and cortisol were collected at baseline and endpoint of each intervention phase. RESULTS: Sixty-two participants (age 36.4 ± 14.0 y, 85.5 % women, 63.3 % racial/ethnic minority) were included in our analyses. Mean total sleep time was 7.4 ± 0.4 h/night during HS and 6.2 ± 0.4 h/night during SR (p < 0.001). Higher perceived stress (3.6 ± 1.0, p = 0.0007) and subjective anxiety (1.1 ± 0.5, p = 0.039) were observed after SR compared to HS. No effect of sleep condition was observed on subjective depression, rumination, and cortisol. CONCLUSIONS: Our findings suggest that prolonged mildly insufficient sleep, similar to what commonly experienced in the real world, can lead to increased perceived stress and subjective anxiety in healthy adults. Addressing sleep loss, even if mild, should be a key component of interventions aimed at promoting mental health in the general population.

The Impact of Sleep: From Ancient Rituals to Modern Challenges.

Although sleep is crucial for mental and physical health, insufficient sleep is a growing problem in our modern society. In general, adults need approximately eight hours of sleep per night, but this is often unfeasible nowadays. This sleep restriction has been observed, and it has worsened, throughout the past two centuries; therefore, it is more attributed to socioeconomic changes than to biological adaptations. The most important factors to contribute to this sleep restriction were the popularization of artificial light and industrialization. The present manuscript briefly overviews, from a socioanthropological perspective, the reasons why sleep has been impacted, disclosing its effects on individuals and on society.

In Males with Adequate Dietary Needs Who Present No Sleep Disturbances, Is an Acute Intake of Zinc Magnesium Aspartate, Following Either Two Consecutive Nights of 8 or 4 h of Sleep Deprivation, Beneficial for Sleep and Morning Stroop Interference Performance?

PURPOSE: Purpose: We examined whether supplementation of zinc magnesium aspartate (ZMA) in two groups of males, either partially sleep-restricted (4 h) or with habitual sleep (8 h) for 2 nights, was beneficial for sleep and subsequent morning Stroop performance. METHODS: Participants were randomly allocated to two independent groups who either had 4 h (33 males) or 8 h (36 males) sleep for two nights. Using a double-blinded, randomised counterbalanced design, they then completed five sessions, (i) two familiarisation sessions including 7 days of sleep and dietary intake, (ii) three conditions with 4 h or 8 h sleep and either NoPill control (NoPill), placebo (PLAC) or ZMA (ZMA). Sleep was assessed by actimetry and sleep questionnaires, and cognitive performance was assessed by the Stroop test. The data were analysed using a general linear model with repeated measures. RESULTS: A main effect for "sleep" (4 or 8 h) was found, where more opportunity to sleep resulted in better "sleep" metrics (both objective and subjective) as well as better Stroop scores (lower colour-interference and word-interference scores and lower error in words). No main effect for "Pill" was found other than the mood state depression, where subjective ratings for the PLAC group were lower than the other two conditions. Interactions were found in anger, ease to sleep and waking time. CONCLUSION: Having 8 h opportunity to sleep resulted in better "sleep" metrics as well as better Stroop scores compared to 4 h. Supplementation of ZMA for 4 or 8 h for 2 nights had no effect on subsequent morning cognitive performance but reduced sleep or total sleep time by ~0.46 h compared to the other conditions. An interaction was found where sleep time was reduced by ~0.94 h in the ZMA group in the 8 h condition compared to NoPill or PLAC.

Changes in higher order cognitive function between four watch keeping schedules.

Maritime industries utilize many different watch keeping schedules to maintain vigilance and crew safety around the clock. These schedules can be fatiguing, negatively impacting vigilant attention. This has led to the consideration of schedules that might allow for more sleep time, but how these schedules impact higher order cognitive function remains unclear. These schedules require assessment with tasks that are relevant to real-world operations on maritime vessels. This study investigated the effect of four schedules on higher order cognitive function. N = 27 (16 female) participants were recruited to a 10-day laboratory study, comparing four schedules. The schedules investigated were eight-on/eight-off/four-on/four-off (8/8/4/4) with sleep from 09:30 to 16:00 (condition A); six-on/six-off (6/6) with sleep from 08:30 to 12:30 and 21:30 to 00:00 (condition B); four-on/four-off (4/4/4/4/4/4) with sleep from 18:00 to 00:30 (condition C); and four-on/four-off (4/4/4/4/4/4) with sleep from 01:30 to 08:00 (condition D). Higher order cognitive function was assessed 2-3× daily whilst "on watch" using tests of visual scanning, learning, working memory, mental flexibility, and visuomotor control. Conditions were ranked and stability of performance on watch was compared between conditions using Kruskal-Wallis tests. Cognitive function within condition B was ranked the worst for most of the tasks. However, the stability of higher order cognitive function was poorest across the waking day within condition A. These findings highlight the variability in cognitive capacities during different watch keeping schedules.

Sleep deprivation and recovery: Endurance racing as a novel model.

The aim of this study was to investigate sleep-wake behavior and gain insights into perceived impairment (sleep, fatigue, and cognitive function) of athletes competing in two international multi-day adventure races. Twenty-four athletes took part across two independent adventure races: Queensland, Australia and Alaska, USA. Individual sleep periods were determined via actigraphy, and racers self-reported their perceived sleep disturbances, sleep impairment, fatigue and cognitive function. Each of these indices was calculated for pre-, during- and post-race periods. Sleep was severely restricted during the race period compared to pre-race (Queensland, 7:46 [0:29] vs. 2:50 [1:01]; Alaska, 7:39 [0:58] vs. 2:45 [2:05]; mean [SD], hh:mm). As a result, there was a large cumulative sleep debt at race completion, which was not 'reversed' in the post-race period (up to 1 week). The deterioration in all four self-reported scales of perceived impairment during the race period was largely restored in the post-race period. This is the first study to document objective sleep-wake behaviors and subjective impairment of adventure racers, in the context of two geographically diverse, multi-day, international adventure races. Measures of sleep deprivation indicate that sleep debt was extreme and did not recover to pre-race levels within 1 week following each race. Despite this objective debt continuing, perceived impairment returned to pre-race levels quickly post-race. Therefore, further examination of actual and perceived sleep recovery is warranted. Adventure racing presents a unique scenario to examine sleep, performance and recovery.

Effects of Supplementing Zinc Magnesium Aspartate on Sleep Quality and Submaximal Weightlifting Performance, following Two Consecutive Nights of Partial Sleep Deprivation.

Purpose: We examined whether supplementation of zinc magnesium aspartate (ZMA), while partially sleep deprived, was beneficial to sleep quality and subsequent morning (07:00 h) submaximal weightlifting. Methods: Using a double-blinded, randomized counterbalanced design, sixteen trained males were recruited and completed six sessions: (i) one repetition max (1 RM) for bench press and back squat; (ii) two familiarisation sessions; (iii) three conditions with 4 h sleep and either: ZMA, placebo (PLA), or NoPill control (NoPill). Submaximal exercise session consisted of three repetitions at 40, 60 and 80% of 1 RM for bench press and back squat. Average power (AP), average velocity (AV), peak velocity (PV), displacement (D) and time-to-peak velocity (tPV) were recorded using MuscleLab linear encoders. Data were analysed using a general linear model with repeated measures and linear correlation. Results: No significant main effect for condition was found for performance values or subjective ratings of fatigue. Main effect for "load" on the bar was found, where AP and tPV values increased with load (p < 0.05). No significant relationship between dose of zinc or magnesium ingested and change in performance for 80% 1 RM power-outputs was found. Conclusion: Supplementation of ZMA for two nights of partial sleep deprivation had no effect on sleep or subsequent morning performance.