Sleep Restriction Group Research Articles

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

BackgroundSleep loss is a common public health problem that causes hyperalgesia, especially that after surgery, which reduces the quality of life seriously.MethodsThe 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.ResultsThe 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.ConclusionsAffected 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.

Acute and chronic sleep restriction differentially modify maternal behavior and milk macronutrient composition in the postpartum rat

BackgroundsSleep restriction is considered a stressful condition itself, causing a wide variety of physiological alterations, from cognitive and hormonal to immunological status. In addition, it is established that stress in mother rats can modify milk ejection, milk composition, and maternal care of the pups. Also, sleep disturbances during the early stages of motherhood are a common feature of all studied species. In this context, while the impacts of sleep disruption in non-lactating animals were extensively investigated, its repercussions during the initial phases of motherhood have been poorly explored. Therefore, we wonder if maternal behavior, milk ejection and its macronutrient composition would be disrupted when mother rats are subjected to an additional acute or chronic sleep restriction to the already existing sleep disturbances. MethodsLactating rats were implanted with unilateral electrodes for polysomnographic recordings and for deep brain electrical stimulation into mesopontine waking-promoting area (for sleep deprivation). During the early postpartum period (postpartum day 5–9), mother rats were randomly assigned into one of three groups: chronic sleep restriction group (CSR; 6 h of sleep deprivation/day for five consecutive days), acute sleep restriction group (ASR; 6 h of sleep deprivation only for one day), or undisturbed group (control group). Active maternal behaviors (retrievals of the pups into the nest, mouthing, lickings [corporal and anogenital] and sniffing the pups) and passive maternal behaviors (kyphotic and supine nursing postures) were evaluated during a 30 min period without sleep restriction immediately after the sleep restriction or control period. The litter weight gain was assessed every day, and on the last experimental session mothers were milked for posterior macronutrients analysis (protein, carbohydrates and fat). ResultsWhen compared to control group, CSR decreased the amount of milk ejected in the middle days of the sleep restriction period, while ASR did not affect this parameter. Moreover, ASR reduced milk protein content compared to control and CSR groups. Finally, compared to the control group, CSR reduced active maternal behaviors towards the end of the treatment days. ConclusionsWe demonstrated that not only acute but also chronic sleep restriction impacts on the postpartum period, each one affecting different aspects of maternal behavior and lactation. Our results suggest the existence of a homeostatic recovery mechanism in breastfeeding during CSR, possibly ensuring the survival of the litter, while the decline in active maternal behaviors appears to be cumulative.

0211 Experimental Sleep Restriction, Moral Absolutism, and Religiosity

Abstract Introduction Moral absolutism is the notion that “rights” and “wrongs” are independent of situational circumstances, and it is a core philosophy of many religious traditions. We tested whether active church members and Christian pastors showed resiliency to mild sleep restriction when reporting religious beliefs/cognitions, when logging spiritual behaviors, and when judging the deserved-punishments for moral mistakes. Methods We recruited 92 adults who identified as active in Christian churches (members and pastors). On a Monday, participants completed baseline religiosity, mood, and cognitive functioning measures and were then randomly assigned to adhere to early (10:30pm) or late (1:30am) bedtimes for four nights, with 7:30am waketimes, while wearing actigraphy and keeping a daily diary of spiritual behaviors. On Friday, participants repeated the baseline assessments, responded whether a series of biblical stories were literal versus figurative, and rated a series of vignettes about moral mistakes that were committed by in-group leaders (pastors) and out-group leaders (imams; vignettes counterbalanced). Results The late bedtime condition reduced actigraphy-defined sleep by 85 min/night (p&amp;lt;.001). Despite spending more time awake, this sleep restricted group reported engaging in fewer spiritual behaviors during the week (e.g., prayer time; p&amp;lt;.01). On Friday, the sleep restricted group had worse mood disturbances (p&amp;lt;.001), worse subjective sleepiness (p&amp;lt;.001), and altered perceptions of the meaning of the Garden of Eden and Noah’s ark biblical stories (p&amp;lt;.05). Fluid intelligence was unaffected (p=.78). When evaluating religious leaders who made moral mistakes, the sleep restricted participants were significantly less forgiving (p&amp;lt;.01); for example, well-rested participants thought such leaders were still “somewhat likely” to get into Heaven, but sleep-restricted participants rated the leaders as “not very likely” to get into Heaven (p&amp;lt;.01). The effects of sleep restriction were most prominent in participants who most frequently attended religious services and when rating out-group religious leaders (r = -.49; opposite patterns were noted when participants were well-rested). Conclusion In contrast to moral absolutism philosophies, very mild sleep restriction produced significant changes to religious cognitions (story interpretation), spiritual behaviors, and expressions of beliefs (likeliness of getting into Heaven), and expressions of virtues (decreased forgiveness). Support (if any) URSA Grant and National Science Foundation (1920730, 1943323).

The Effect of Sleep Restriction, With or Without Exercise, on Skeletal Muscle Transcriptomic Profiles in Healthy Young Males.

BackgroundInadequate sleep is associated with many detrimental health effects, including increased risk of developing insulin resistance and type 2 diabetes. These effects have been associated with changes to the skeletal muscle transcriptome, although this has not been characterised in response to a period of sleep restriction. Exercise induces a beneficial transcriptional response within skeletal muscle that may counteract some of the negative effects associated with sleep restriction. We hypothesised that sleep restriction would down-regulate transcriptional pathways associated with glucose metabolism, but that performing exercise would mitigate these effects.Methods20 healthy young males were allocated to one of three experimental groups: a Normal Sleep (NS) group (8 h time in bed per night (TIB), for five nights (11 pm – 7 am)), a Sleep Restriction (SR) group (4 h TIB, for five nights (3 am – 7 am)), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB, for five nights (3 am – 7 am) and three high-intensity interval exercise (HIIE) sessions (performed at 10 am)). RNA sequencing was performed on muscle samples collected pre- and post-intervention. Our data was then compared to skeletal muscle transcriptomic data previously reported following sleep deprivation (24 h without sleep).ResultsGene set enrichment analysis (GSEA) indicated there was an increased enrichment of inflammatory and immune response related pathways in the SR group post-intervention. However, in the SR+EX group the direction of enrichment in these same pathways occurred in the opposite directions. Despite this, there were no significant changes at the individual gene level from pre- to post-intervention. A set of genes previously shown to be decreased with sleep deprivation was also decreased in the SR group, but increased in the SR+EX group.ConclusionThe alterations to inflammatory and immune related pathways in skeletal muscle, following five nights of sleep restriction, provide insight regarding the transcriptional changes that underpin the detrimental effects associated with sleep loss. Performing three sessions of HIIE during sleep restriction attenuated some of these transcriptional changes. Overall, the transcriptional alterations observed with a moderate period of sleep restriction were less evident than previously reported changes following a period of sleep deprivation.

Childhood adversity is associated with heightened inflammation after sleep loss

ObjectivesTo investigate whether childhood adversity exacerbates the relationship between sleep restriction and inflammation. MethodsParticipants (N = 46) were randomly assigned to an experimental sleep restriction group (n = 25) or a night of typical sleep (n = 21). Participants provided a dried blood spot sample the morning before and after the experimental night. ResultsA significant interaction emerged between childhood adversity and group assignment on C-reactive protein (CRP) after the experimental night (Beta = −0.02, SE = 0.01, P = .03, 95% CI: −0.05, −0.002). Sleep restriction resulted in an increase in CRP at high levels of childhood adversity (+1 SD; Effect = −0.57, SE = 0.15, P< .001; 95% CI: −0.87, −0.26) but not low levels of childhood adversity (Effect = −0.08, SE = 0.10, P = .40; 95% CI: −0.29, 0.12). ConclusionChildhood adversity may amplify the effect of sleep loss on markers of inflammation.

Effect of Sleep Restriction on Cardiometabolic and Haemoinflammatory Parameters in Adult Male Wistar Rats

Background and Objective: While insufficient sleep remains an under-recognized public health issue across the globe, there is paucity and heterogeneity of data regarding its cardiometabolic and haemoinflammatory implications. We, therefore, aimed to evaluate the impact of chronic sleep restriction on cardiometabolic and haemoinflammatory parameters in rats. Materials and Methods: 16 male Wistar rats (aged 8-10 weeks) were randomly assigned into equal control or sleep restriction groups. Gentle handling was used to induce sleep restriction for six weeks. Fasting weight and blood sugar were obtained and lipids were analyzed using their respective Randox kits. Malondialdehyde (MDA) levels and catalase (CAT) and superoxide dismutase (SOD) activities were assayed. Full blood count and CD4+ T cell count were determined using automated analyzer. Data were analyzed using Student’s t-test, with level of significance set at P ≤ 0.05, via SPSS software. Results: Chronic sleep restriction caused significant initial weight loss, increase in feed consumption, and percentage increase in fasting blood sugar (FBS) (32% vs. 15%). We also noted the triglyceride-glucose (TyG) index of sleep-restricted rats to be significantly higher (6.22) than that of controls (5.62). In addition, a significant reduction in monocyte count, monocyte-lymphocyte ratio (MLR), and absolute CD4+ cell count among the sleep-restricted rats was observed. Conclusion: Our findings have provided objective evidence that, over the course of 6 weeks, 5 hours of sleep restriction had caused body weight gain, hyperglycaemia, insulin resistance, and impairment in immunoinflammatory status; hence, it could be a risk factor for developing cardiometabolic syndrome and immune-related disorders.

Bone turnover marker responses to sleep restriction and weekend recovery sleep.

Prior data demonstrated three weeks of sleep restriction and concurrent circadian disruption uncoupled bone turnover markers (BTMs), indicating decreased bone formation and no change or increased bone resorption. The effect of insufficient sleep with or without ad libitum weekend recovery sleep on BTMs is unknown. BTMs were measured in stored serum from 20 healthy adults randomized to one of three study groups consisting of a control group (N=3 men; 9h/night) or one of two nocturnal sleep restriction groups in an inpatient laboratory environment. One Sleep Restriction group ("SR"; N=9; 4 women) had 5h sleep opportunity per night for nine nights. The other sleep restriction group had an opportunity for ad libitum Weekend Recovery sleep ("WR"; N=8; 4 women) after four nights of 5h sleep opportunity per night. Food intake was energy balanced at baseline and ad libitum thereafter. Fasted morning BTM levels and hourly 24h melatonin levels were obtained on study days 3 (baseline), 5 (after 1 night of sleep restriction for WR and SR), and 11 (after a sleep restricted workweek with weekend recovery sleep in WR or 7 nights of sleep restriction in SR). Linear mixed-effects modeling was used to examine the effect of study duration (e.g., change over time), study condition, age, and sex on BTMs. Pearson correlations were used to determine associations between changes in BTMs and changes in weight and morning circadian misalignment (i.e., duration of high melatonin levels after wake time). There was no significant difference between the three study groups in change over time (p ≥ 0.4 for interaction between assigned group and time for all BTMs), adjusted for age and sex. There was no significant change in N-terminal propeptide of procollagen type I (P1NP), osteocalcin, or C-telopeptide of type I collagen (CTX) from baseline to day 11 (all p ≥ 0.3). In women <25years old, there was a non-significant decline in P1NP from day 3 to day 5 (= -15.74±7.80ng/mL; p=0.06). Change in weight and morning circadian misalignment from baseline to day 11 were correlated with statistically non-significant changes in BTMs (all p ≤ 0.05). In this small secondary analysis, we showed that nine nights of prescribed sleep restriction with or without weekend recovery sleep and ad libitum food intake did not alter BTMs. It is possible that age, sex, weight change and morning circadian misalignment modify the effects of sleep restriction on bone metabolism.

Unethical Decision Making and Sleep Restriction: Experimental Evidence

Recent examinations into the cognitive underpinnings of ethical decision making has focused on understanding whether honesty is more likely to result from deliberative or unconscious decision processes. We randomly assigned participants to a multi-night sleep manipulation, after which they completed 3 tasks of interest: imperfectly identifiable dishonesty (the Coin Flip task), identifiable dishonesty (the Matrix task), and anti-social allocation choices (the Money Burning game). We document the validity of the sleep protocol via significantly reduced nightly sleep levels (objectively measured using validated instrumentation) and significantly higher sleepiness ratings in the sleep-restricted (SR) group compared to the wellrested (WR) group. We report that money burning decisions are not statistically different between SR and WR participants. However, regarding honesty, we find significant and robust effects of SR on honesty. In total, given the connection between sleepiness and deliberation, these results add to the literature that has identified conditions under which deliberation impacts ethical choice. When dishonesty harms an abstract “other” person (e.g., the researcher’s budget), reduced deliberation more likely increases dishonesty compared to when harm is done to someone at closer social distance (e.g., another subject). Key Words: Ethical choice, dishonesty, antisocial behavior, sleep.

Adverse interaction effects of chronic and acute sleep deficits on spatial working memory but not on verbal working memory or declarative memory.

The accumulation of chronic sleep deficits combined with acute sleep loss is common in shift workers and increases the risk of errors and accidents. We investigated single and combined effects of chronic and acute sleep loss and recovery sleep on working memory performance (N-back task) and on overnight declarative memory recall (paired-associate lists) in 36 healthy participants. After baseline measurements, the chronic sleep restriction group (n=21; mean [SD] age 26[4]years) underwent 5nights of sleep restriction (5-hr time in bed [TIB]), whereas the control group (n=15; mean [SD] age 28[6]years) had 8-hr TIB during those nights. Afterwards, both groups spent 1night with 8-hr TIB prior to acute sleep deprivation for 38hr, and a final recovery night (10-hr TIB). Chronic sleep restriction decreased spatial N-back performance compared to baseline (omissions: p = .001; sensitivity: p = .012), but not letter N-back performance or word-pair recall. Acute sleep deprivation impaired spatial N-back performance more in the chronic sleep restriction group than in the control group (interaction between group and time awake: p ≤ .02). No group differences during acute sleep loss appeared in letter N-back performance or word recall. It is concluded that chronic sleep loss, even when followed by a night of recovery sleep, increases the vulnerability to impairments in spatial working memory during subsequent acute sleep loss. Verbal working memory and declarative memory were not affected by restricted sleep.

Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms

ObjectiveSleep loss has emerged as a risk factor for the development of impaired glucose tolerance. The mechanisms underpinning this observation are unknown; however, both mitochondrial dysfunction and circadian misalignment have been proposed. Because exercise improves glucose tolerance and mitochondrial function, and alters circadian rhythms, we investigated whether exercise may counteract the effects induced by inadequate sleep. MethodsTo minimize between-group differences of baseline characteristics, 24 healthy young males were allocated into one of the three experimental groups: a Normal Sleep (NS) group (8 h time in bed (TIB) per night, for five nights), a Sleep Restriction (SR) group (4 h TIB per night, for five nights), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB per night, for five nights and three high-intensity interval exercise (HIIE) sessions). Glucose tolerance, mitochondrial respiratory function, sarcoplasmic protein synthesis (SarcPS), and diurnal measures of peripheral skin temperature were assessed pre- and post-intervention. ResultsWe report that the SR group had reduced glucose tolerance post-intervention (mean change ± SD, P value, SR glucose AUC: 149 ± 115 A.U., P = 0.002), which was also associated with reductions in mitochondrial respiratory function (SR: -15.9 ± 12.4 pmol O2.s−1.mg−1, P = 0.001), a lower rate of SarcPS (FSR%/day SR: 1.11 ± 0.25%, P < 0.001), and reduced amplitude of diurnal rhythms. These effects were not observed when incorporating three sessions of HIIE during this period (SR+EX: glucose AUC 67 ± 57, P = 0.239, mitochondrial respiratory function: 0.6 ± 11.8 pmol O2.s−1.mg−1, P = 0.997, and SarcPS (FSR%/day): 1.77 ± 0.22%, P = 0.971). ConclusionsA five-night period of sleep restriction leads to reductions in mitochondrial respiratory function, SarcPS, and amplitude of skin temperature diurnal rhythms, with a concurrent reduction in glucose tolerance. We provide novel data demonstrating that these same detrimental effects are not observed when HIIE is performed during the period of sleep restriction. These data therefore provide evidence in support of the use of HIIE as an intervention to mitigate the detrimental physiological effects of sleep loss.

Chronic Timed Sleep Restriction Attenuates LepRb-Mediated Signaling Pathways and Circadian Clock Gene Expression in the Rat Hypothalamus.

The sleep duration of adolescents has continued to decline over the past 20 years. Sleep insufficiency is one of the most important risk factors for obesity, but the mechanisms underlying the association are unclear. Therefore, the hypothalamic-regulated mechanisms of appetite and the circadian clock gene expression were examined in sleep-restricted rats. Rats aged 7 weeks were randomly divided into two groups: the control group and sleep restriction group (7 rats/group) rats were sleep-restricted for 4 weeks. Body weight gain and amount of food/water consumption were quantified. The expression of genes or proteins which regulated appetite and energy metabolism via leptin receptor signaling and the circadian clock in the hypothalamus were assessed. Chronic sleep restriction induced increased food intake and weight gain in adolescent and young adult rats from the second week of initiation of sleep restriction. Phosphorylation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) was decreased, although levels of circulating leptin or leptin receptor expression were unaltered. Furthermore, insulin receptor substrate (IRS)/phosphoinositide 3-kinase (PI3K)/AKT/mTOR and forkhead box O1 (FoxO1) signaling pathways were also compromised. Moreover, core circadian clock genes were also decreased in the sleep restriction group compared with the control. Chronic timed sleep restriction induced hyperphagic behaviors, attenuated leptin receptor-mediated signaling pathways, and depleted the expression of circadian clock gene in the hypothalamus of adolescent and young adult rats.

Effects of sleep restriction during pregnancy on postpartum maternal behavior in female rats

Preclinical studies evaluating the effects of gestational sleep restriction on maternal behavior are needed in order to provide information on the background mechanisms underlying this relationship. In this study, 32 female 90 days-old Wistar-Hannover rats were distributed in two groups: Control group (CTRL – n = 13), not subjected to any manipulation during pregnancy; and sleep restriction group (SR – n = 19) – subjected to sleep restriction during the whole pregnancy (21 days). Maternal behavioral analysis was conducted from postpartum day 1 (PPD1) to PPD7, based on observational ethograms. On PPD11 the animals were subjected to the grooming analysis algorithm, followed by the elevated plus maze. Results from an ethogram-based analysis indicated a decrease in self-grooming among sleep-deprived rats (denoting reduced anxiety-like behavior), but no significant differences were found in maternal behavior (except for a slight increase in high arched-back nursing). Controlled analysis detected an impairment in high-arched back nursing in sleep-deprived animals. The grooming microstructure analysis showed an increased frequency of incorrect transitions among sleep restricted animals, indicating increased anxiety-like behavior. No significant differences were observed in the elevated-plus maze. In conclusion, sleep-restricted pregnant rats display an equivalent or slightly increased maternal behavior during the postpartum period, when compared to control animals.

Chronic REM sleep restriction in young rats increases energy expenditure with no change in food intake.

What is the central question of this study? What are the effects of different periods of REM sleep restriction (7, 14 and 21days) on metabolic parameters in young rats? What is the main finding and its importance? Animals submitted to each period of REM sleep deprivation showed a negative energy balance, with reduced body weight gain, body energy gain and gross food efficiency, less body fat content, and increased energy expenditure. There was no increase in food intake after any of the REM sleep restriction periods. In young rats, negative energy balance is not compensated by increased dietary intake as observed in adult rats. Reduced sleep is associated with metabolic alterations, not only in adults, but also in children and adolescents. Several studies have shown that sleep restricted (SR) adult rats exhibit metabolic changes, followed by increased food intake, but few have evaluated these functions in young animals. The aim of the present study was to establish the metabolic parameters of young rats subjected to different periods of REM sleep restriction and to propose a correction factor for the correct measurement of food intake. Young male Wistar rats were distributed in control and SR groups for 7, 14 or 21days. Sleep restriction was performed by the single platform method for 18 h. Regardless of the length of sleep restriction, all SR rats had a negative energy balance, evidenced by reduction in body weight gain, body energy gain and gross food efficiency, accompanied by increased energy expenditure. In addition, sleep restriction reduced body fat content throughout the entire period. Discounting food spillage, there was no increase in food intake by SR rats. In conclusion, the present study revealed metabolic changes in SR young rats after different lengths of REM sleep restriction and that weight loss and increased energy expenditure were not compensated by increased dietary intake as occurs in adult rats, indicating that young rats use other mechanisms to cope with the negative energy balance caused by sleep restriction. In addition, we propose a correction factor for food intake, to prevent overestimation of this parameter, due to food spillage in the water containers.

The effect of sleep restriction, with or without high-intensity interval exercise, on myofibrillar protein synthesis in healthy young men.

Key points Sleep restriction has previously been associated with the loss of muscle mass in both human and animal models.The rate of myofibrillar protein synthesis (MyoPS) is a key variable in regulating skeletal muscle mass and can be increased by performing high‐intensity interval exercise (HIIE), although the effect of sleep restriction on MyoPS is unknown.In the present study, we demonstrate that participants undergoing a sleep restriction protocol (five nights, with 4 h in bed each night) had lower rates of skeletal muscle MyoPS; however, rates of MyoPS were maintained at control levels by performing HIIE during this period.Our data suggest that the lower rates of MyoPS in the sleep restriction group may contribute to the detrimental effects of sleep loss on muscle mass and that HIIE may be used as an intervention to counteract these effects. The present study aimed to investigate the effect of sleep restriction, with or without high‐intensity interval exercise (HIIE), on the potential mechanisms underpinning previously‐reported sleep‐loss‐induced reductions to muscle mass. Twenty‐four healthy, young men underwent a protocol consisting of two nights of controlled baseline sleep and a five‐night intervention period. Participants were allocated into one of three parallel groups, matched for age, V˙O2peak, body mass index and habitual sleep duration; a normal sleep (NS) group [8 h time in bed (TIB) each night], a sleep restriction (SR) group (4 h TIB each night), and a sleep restriction and exercise group (SR+EX, 4 h TIB each night, with three sessions of HIIE). Deuterium oxide was ingested prior to commencing the study and muscle biopsies obtained pre‐ and post‐intervention were used to assess myofibrillar protein synthesis (MyoPS) and molecular markers of protein synthesis and degradation signalling pathways. MyoPS was lower in the SR group [fractional synthetic rate (% day–1), mean ± SD, 1.24 ± 0.21] compared to both the NS (1.53 ± 0.09) and SR+EX groups (1.61 ± 0.14) (P < 0.05). However, there were no changes in the purported regulators of protein synthesis (i.e. p‐AKTser473 and p‐mTORser2448) and degradation (i.e. Foxo1/3 mRNA and LC3 protein) in any group. These data suggest that MyoPS is acutely reduced by sleep restriction, although MyoPS can be maintained by performing HIIE. These findings may explain the sleep‐loss‐induced reductions in muscle mass previously reported and also highlight the potential therapeutic benefit of HIIE to maintain myofibrillar remodelling in this context.

Weakly encoded memories due to acute sleep restriction can be rescued after one night of recovery sleep

Sleep is thought to play a complementary role in human memory processing: sleep loss impairs the formation of new memories during the following awake period and, conversely, normal sleep promotes the strengthening of the already encoded memories. However, whether sleep can strengthen deteriorated memories caused by insufficient sleep remains unknown. Here, we showed that sleep restriction in a group of participants caused a reduction in the stability of EEG activity patterns across multiple encoding of the same event during awake, compared with a group of participants that got a full night’s sleep. The decrease of neural stability patterns in the sleep-restricted group was associated with higher slow oscillation-spindle coupling during a subsequent night of normal sleep duration, thereby suggesting the instantiation of restorative neural mechanisms adaptively supporting cognition and memory. Importantly, upon awaking, the two groups of participants showed equivalent retrieval accuracy supported by subtle differences in the reinstatement of encoding-related activity: it was longer lasting in sleep-restricted individuals than in controls. In addition, sustained reinstatement over time was associated with increased coupling between spindles and slow oscillations. Taken together, these results suggest that the strength of prior encoding might be an important moderator of memory consolidation during sleep. Supporting this view, spindles nesting in the slow oscillation increased the probability of correct recognition only for weakly encoded memories. Current results demonstrate the benefit that a full night’s sleep can induce to impaired memory traces caused by an inadequate amount of sleep.

Protective effects of Hydrocotyle umbellata var. bonariensis Lam. (Araliaceae) on memory in sleep-impaired female mice

Ethnopharmacological relevanceHydrocotyle umbellata var.bonariensis Lam. (Hb), popularly known in Brazil as acariçoba and outside Brazil Hb by a number of names including marsh-pennywort, and many-flower, has traditionally been used in Ayurvedic medicine in the retardation of aging (Rasayana effect). Aim of the studyThe present study evaluated the effect of Hb treatment before and during paradoxical sleep deprivation (PSD) and sleep restriction (SR) on learning, memory, and acetylcholinesterase (AChE) brain activity. Material and methodsAdult Swiss nulliparous female mice were randomly distributed among the experimental groups. The treated groups received the aqueous solution of Hb leaves orally at concentrations of 500 and 1.000 mg/kg. PSD and SR were induced by the multiple platform method, in which the animals remained for 3-days in PSD or 15-days in SR for 22 h per day. The collection of the vaginal epithelium occurred daily to determine the estrous cycle. Body mass gain was determined. The animals were submitted to the passive avoidance test and were then euthanized for the collection of brain tissue and the determination of cerebral cholinesterase activity. ResultsThe aqueous solution of Hb was associated with a significant reduction in cholinesterase activity at both doses in the SR model, and at the dose of 1.000 mg/kg in the PSD model. Regarding the learning and memory test, the PSD group treated with 1.000 mg/kg presented significant improvement, whereas in the SR experiment none of the treated-groups showed any improvement in learning and memory. In the analysis of SR/PSD interference and/or Hb treatment on the estrous cycle, it was possible to observe that the treatment acted as a protector in the SR group, maintaining a normal cycle. ConclusionsThe analyses showed that Hb was safe to use during periods of SR or PSD, acting as an adaptogen for these situations, in addition to being able to reduce cholinesterase activity, which suggests its neuroprotective action. In relation to the estrous cycle, Hb can act as a protector in SR situations.

Multi-Night Sleep Restriction Impairs Long-Term Retention of Factual Knowledge in Adolescents

PurposeSleep deprivation is associated with increased forgetting of declarative memories. Sleep restriction across multiple consecutive nights is prevalent in adolescents, but questions remain as to whether this pattern of sleep impairs memory for material typically learned in the classroom and the time course of retention beyond a few days. MethodsAdolescents aged 15–18 years (n = 29) were given 5 hours sleep opportunity each night for 5 consecutive nights (sleep restricted group; SR), simulating a school week containing insufficient sleep. After the fourth night of restriction, participants learned detailed facts about different species of arthropod across a 6-hour period. Retention was tested 30 minutes and 3 days after learning and contrasted with a control group (n = 30) who had 9 hours sleep opportunity every night of the study. A subset of participants (SR, n = 14; control, n = 22) completed a surprise test 42 days after learning. ResultsMemory was significantly impaired in the SR group relative to controls, with 26% increased forgetting at the 30-minute test (t(57) = 2.54, p = .014, d = .66), 34% at the Day 3 test (t(57) = 2.65, p = .010, d = .69), and 65% at the Day 42 test (t(34) = 3.22, p = .003, d = 1.17). Vigilance was also significantly impaired after 4 nights of restricted sleep (p < .05), but did not correlate significantly with memory (p > .05). ConclusionLong-term retention of classroom material is significantly compromised when adolescents learn after being sleep restricted, reinforcing the importance of keeping good sleep habits to optimize learning.

Differential effects of split and continuous sleep on neurobehavioral function and glucose tolerance in sleep-restricted adolescents.

Study ObjectivesMany adolescents are exposed to sleep restriction on school nights. We assessed how different apportionment of restricted sleep (continuous vs. split sleep) influences neurobehavioral function and glucose levels.MethodsAdolescents, aged 15–19 years, were evaluated in a dormitory setting using a parallel-group design. Following two baseline nights of 9-hour time-in-bed (TIB), participants underwent either 5 nights of continuous 6.5-h TIB (n = 29) or 5-hour nocturnal TIB with a 1.5-hour afternoon nap (n = 29). After two recovery nights of 9-hour TIB, participants were sleep restricted for another three nights. Sleep was assessed using polysomnography (PSG). Cognitive performance and mood were evaluated three times per day. Oral glucose tolerance tests (OGTT) were conducted on mornings after baseline sleep, recovery sleep, and the third day of each sleep restriction cycle.ResultsThe split sleep group had fewer vigilance lapses, better working memory and executive function, faster processing speed, lower level of subjective sleepiness, and more positive mood, even though PSG-verified total sleep time was less than the continuous sleep group. However, vigilance in both sleep-restricted groups was inferior to adolescents in a prior sample given 9-hour nocturnal TIB. During both cycles of sleep restriction, blood glucose during the OGTT increased by a greater amount in the split sleep schedule compared with persons receiving 6.5-hour continuous sleep.ConclusionsIn adolescents, modest multinight sleep restriction had divergent negative effects on cognitive performance and glucose levels depending on how the restricted sleep was apportioned. They are best advised to obtain the recommended amount of nocturnal sleep.Trial registration https://clinicaltrials.gov/ct2/show/NCT03333512

Trait-like characteristics of sleep EEG power spectra in adolescents across sleep opportunity manipulations.

The electroencephalographic power spectra of non‐rapid eye movement sleep in adults demonstrate trait‐like consistency within participants across multiple nights, even when prior sleep deprivation is present. Here, we examined the extent to which this finding applies to adolescents who are habitually sleep restricted on school‐days and sleep longer on weekends. We evaluated 78 adolescents across three sleep restriction groups who underwent different permutations of adequate sleep (9 hr time‐in‐bed), sleep restriction (5 hr time‐in‐bed), afternoon naps (1 hr afternoon) and recovery sleep (9 hr time‐in‐bed) that simulate behaviour on school‐days and weekends. The control group comprised a further 22 adolescents who had 9 hr of sleep opportunity each night. Intra‐class correlation coefficients showed moderate to almost perfect within‐subject stability in electroencephalographic power spectra across multiple nights in both sleep restriction and control groups, even when changes to sleep macrostructure were observed. While nocturnal intra‐class correlation metrics were lower in the low‐frequency and spindle frequency bins in the sleep restriction compared with the control group, hierarchical clustering measures could still identify multi‐night electroencephalographic spectra as originating from the same individual. The trait‐like characteristics of electroencephalographic spectra from an adolescent remain identifiable despite the disruptive effects of multi‐night sleep restriction to sleep architecture.

Acute Sleep Restriction Has Differential Effects on Components of Attention.

Inadequate nightly sleep duration can impair daytime functioning, including interfering with attentional and other cognitive processes. Current models posit that attention is a complex function regulated by several separate, but interacting, neural systems responsible for vigilance, orienting, and executive control. However, it is not clear to what extent each of these underlying component processes is affected by sleep loss. The purpose of this study was to evaluate the effects of acute sleep restriction on these attentional components using the Dalhousie Computerized Attention Battery (DalCAB). DalCAB tasks were administered to healthy women (aged 19–25 years) on two consecutive mornings: once after a night with 9 h time in bed (TIB), and once again after either another night with 9 h TIB (control condition, n = 19) or after a night with 3 h TIB (sleep restriction condition, n = 20). Self-ratings of sleepiness and mood were also obtained following each sleep condition. Participants showed increases in self-reported sleepiness and fatigue after the second night only in the sleep restriction group. Sleep restriction primarily affected processing speed on tasks measuring vigilance; however, performance deficits were also observed on some measures of executive function (e.g., go/no-go task, flanker task, working memory). Tasks assessing orienting of attention were largely unaffected. These results indicate that acute sleep restriction has differential effects on distinct components of attention, which should be considered in modeling the impacts of sleep loss on the underlying attentional networks.