Effects Of Acute Sleep Deprivation Research Articles

A global transcriptional atlas of the effect of acute sleep deprivation in the mouse frontal cortex

Sleep deprivation (SD) has negative effects on brain and body function. Sleep problems are prevalent in a variety of disorders, including neurodevelopmental and psychiatric conditions. Thus, understanding the molecular consequences of SD is of fundamental importance in biology. In this study, we present the first simultaneous bulk and single-nuclear RNA sequencing characterization of the effects of SD in the male mouse frontal cortex. We show that SD predominantly affects glutamatergic neurons, specifically in layers 4 and 5, and produces isoform switching of over 1500 genes, particularly those involved in splicing and RNA binding. At both the global and cell-type specific level, SD has a large repressive effect on transcription, downregulating thousands of genes and transcripts. As a resource we provide extensive characterizations of cell-types, genes, transcripts, and pathways affected by SD. We also provide publicly available tutorials aimed at allowing readers adapt analyses performed in this study to their own datasets.

Effects of Acute Sleep Deprivation on Sporting Performance in Athletes: A Comprehensive Systematic Review and Meta-Analysis.

Using meta-analysis to comprehensively and quantitatively evaluate the impact of acute sleep deprivation on different sports performance of athletes, this study aims to provide scientific guidance for coaches in optimizing and adjusting training and competition arrangements. Establishing literature inclusion and exclusion criteria, we conducted searches in both Chinese and English databases. Using stata 14.0, we analyzed 75 indicators from 27 included literature, focusing on three aspects: the impact of acute sleep deprivation on overall athletic performance, the impact on sporting performance across various athletic abilities, and the disparities in athletic performance between morning and afternoon following acute sleep deprivation. The effect size of acute sleep deprivation on overall athletic performance was -0.56 (P<0.05). Sub-analyses revealed effect sizes of -0.23 (P<0.05) for whole night sleep deprivation, -1.17 (P<0.05) for partial sleep deprivation at the end of the night, and -0.25 (P>0.05) for partial sleep deprivation in the beginning of the night. The effect sizes of acute sleep deprivation on high intensity intermittent exercise, skill control, speed, aerobic endurance, and explosive power indicators were -1.57, -1.06, -0.67, -0.54, and -0.39 respectively (P<0.05). The effect sizes of acute sleep deprivation on the overall athletic performance in the morning and afternoon were -0.30, and -1.11, respectively (P<0.05). Acute sleep deprivation significantly impairs the overall athletic performance of athletes, with a more pronounced negative impact observed with partial sleep deprivation at the end of the night. Various types of exercise performance are adversely affected by acute sleep deprivation, with magnitude of impact ranking high intensity intermittent, skill control, speed, aerobic endurance, and explosive power. Following acute sleep deprivation, athletes' overall sporting performance in the afternoon is inferior to that in the morning.

Effects of Acute Sleep Deprivation on the Physiological Response to Woodsmoke and Exercise.

To evaluate sleep deprivation effects on the acute physiological response to a combined stressor of woodsmoke and exercise. Ten participants completed two exercise trials (8 hours of sleep vs 4 hours) with woodsmoke. Trials were conducted in a crossover design. Key measures examined before and after each trial included heart rate variability, pulse wave velocity, blood pressure, pulmonary function testing, and oxidative stress. Acute sleep deprivation experienced before exercise and woodsmoke exposure did not impact metrics of heart rate variability, pulse wave velocity, pulmonary function testing, blood pressure, or oxidative stress. Acute sleep deprivation did not amplify physiologic metrics in response to moderate-intensity aerobic exercise with inhaled woodsmoke. Although findings do not eliminate the negative impacts of inhaling woodsmoke, more research is needed to understand the acute effects of woodsmoke exposure on the cardiovascular system. 1.

Effects of Acute Sleep Deprivation on the Sequential Rate of Torque Development throughout the Force-Time Curve.

Objective The impact of sleep deprivation on the physiological determinants of explosive torque production remains poorly understood. We aimed at determining the acute effects of 24 hours of sleep deprivation on the sequential rate of torque development (RTD) obtained during plantar flexion through maximum voluntary isometric contraction (MVIC). Materials and Methods The study included 14 healthy-young adults (8 men and 6 women). The participants visited the laboratory on 2 different occasions: without and with 24 hours of sleep deprivation. In each session, the subjects were tested for RTD of the plantar flexors with concomitant recordings of the electromyographic (EMG) amplitude of the soleus over the following time intervals: 0 to 30, 30 to 50, 50 to 100, and 100 to 150 ms. Results Sleep deprivation did not affect peak RTD (without sleep deprivation: 283.3 ± 111.6 N.m.s -1 versus with sleep deprivation: 294.9 ± 99.2 N.m.s -1 ; p > 0.05) of plantar flexion. The sequential values of RTD, as well as the normalized amplitude of the soleus EMG, remained similar between both conditions (p > 0.05). Discussion In conclusion, we found that 24 hours of sleep deprivation do not affect muscle activation, nor explosive torque production throughout the torque-time curve. Thus, exercise performance and daily functionality in tasks involving rapid torque development might remain well preserved after 24 hours of acute sleep deprivation.

Antidepressant effects of acute sleep deprivation are reduced in highly controlled environments

BackgroundNumerous studies summarized in a recent meta-analysis have shown sleep deprivation rapidly improves depressive symptoms in approximately 50 % of individuals with major depressive disorder (MDD), however those studies were typically conducted in clinical settings. Here we investigated the effects of sleep deprivation utilizing a highly controlled experimental approach. Methods36 antidepressant-free individuals with MDD and 10 healthy controls (HC) completed a 5 day/4-night protocol consisting of adaptation, baseline, total sleep deprivation (TSD), and recovery phases. Light was kept consistently dim (≤50 lx), meals were regulated, and activity was restricted. In-the-moment mood was assessed using a modified Hamilton Rating Scale for Depression (HRSD) at screening and each morning following the experimental nights. ResultsDay of study had a significant effect on mood in both groups. Post-hoc analyses revealed that significant effects were attributed to mood improvement in the MDD group following study initiation prior to beginning TSD, and in the HC group following recovery sleep, but were not due to mood improvement in the MDD group during TSD. No further improvement in mood occurred during 36 h of TSD. LimitationsStrict eligibility requirements may limit generalizability. The requirement to be medication free may have biased toward a less severely depressed sample. ConclusionsResults revealed that individuals with moderate MDD can experience a significant reduction in depressive symptoms upon entering a highly controlled laboratory environment. Environmental effects on mood can be substantial and need to be considered.

0199 Effects of acute sleep deprivation on cognitive performance in depressed individuals

Abstract Introduction Acute sleep deprivation (SD) is an effective, rapid antidepressant treatment. However, SD has adverse effects on cognitive performance. The effects of SD on cognitive performance in depression remain underexplored. This study investigated relationships between depression and performance on Cognition – a neurocognitive battery of 10 tests that cover a range of cognitive domains – during acute SD. Methods Thirty-six individuals with current depression (69.4% female; 33±9.5 yrs) and 10 euthymic controls (40% female; 35±9.5 yrs) underwent a baseline night of sleep followed by 36 hours SD in the laboratory. Participants completed the Cognition battery twice after each protocol night. Each of the 10 Cognition tests has two separate metrics of performance: speed and accuracy. Multivariable linear regressions were used to assess effects of depression status, age, and gender on each performance metric at baseline. Mixed effects models were used to assess effects of depression status, sleep deprivation, and their interaction on performance metrics. All models included a random effect over participants and were adjusted for age, gender, and time of day. Results At baseline, depressed individuals were significantly faster than controls on three tests of working memory (β=-72.6; p=0.03), spatial orientation (β=-2944.7; p=0.01), and emotion recognition (β=-537.5; p=0.005) respectively, although these effects did not survive correction for multiple comparisons. Mixed effects model results revealed a significant effect of depression status on the speed metric from the spatial orientation test, whereby depressed individuals were faster across the protocol (β=-2579.6; p=0.04) and a significant interaction effect between depression status and study day on the speed metric from a risk-taking behavior test, whereby depressed individuals were slower after SD (β=480.9, p=0.01); neither effect survived correction for multiple comparisons. However, sleep deprivation was significantly associated with reductions in performance in models for 10 out of 20 metrics (all adjusted ps &amp;lt; 0.05). Conclusion These results suggest that currently depressed individuals exhibit the same decrements in cognitive performance after acute SD as non-depressed individuals. Future analyses will examine whether baseline depression severity predicts cognitive performance and whether differences in performance exist between SD responders versus non-responders. Support (if any) This work was supported by the National Institute of Mental Health (R01MH107571).

Acute sleep deprivation: impairment of biventricular function assesed by speckle tracking echocardiography in healthy subjects.

Sleep deprivation (SD) has been found to be associated with an increased incidence of adverse cardiovascular disease (CVD) events. The aim of this study was to investigate whetheror not acute SD has a pathological effect on the geometry and the systolic and diastolic functions of the right and left heart chambers by standard transthoracic echocardiography (TTE) and speckle tracking echocardiography (STE) in healthy individuals with acute SD. Nurses with no history of acute or chronic diseases underwent TTE and STE after working a night shift, a sleepless period of 24h and 7days of normal sleep after the night shift. Measurements of TTE and STE taken in the rested state were compared with those taken after 24h of sleep deprivation. The study included 52 nurses (38 women, 73%). The mean age of the study population was 27.9 ± 7.4years and mean BMI was 24.1 ± 4.8. Left atrial reservoir (51.5 ± 13.5 vs. 45.4 ± 10; p = 0.004), conduit (- 37.3 ± 11.3 vs. - 33.6 ± 7.9; p = 0.01), left ventricular global longitudinal strain(LVGLS, - 22.6 ± 2.4 vs. - 21.3 ± 2.4; p = 0.001), right ventricular global longitudinal strain (RVGLS, - 25.3 ± 3.7 vs. - 23.5 ± 3.9; p = 0.005) and right ventricular free wall longitudinal strain (RVFWSL, - 29.1 ± 4.2 vs. - 27 ± 4.5; p = 0.001) were impaired significantly after SD. This study is the first to investigate the negative effects of acute sleep deprivation on LV and RV strain in healthy adults using echocardiography. The findings showed that acute sleep deprivation leads to deterioration in function of both ventricles and left atrium. Speckle tracking echocardiography demonstrated subclinical diminished heart function.

Sleep and memory: The impact of sleep deprivation on transcription, translational control, and protein synthesis in the brain.

In countries around the world, sleep deprivation represents a widespread problem affecting school-age children, teenagers, and adults. Acute sleep deprivation and more chronic sleep restriction adversely affect individual health, impairing memory and cognitive performance as well as increasing the risk and progression of numerous diseases. In mammals, the hippocampus and hippocampus-dependent memory are vulnerable to the effects of acute sleep deprivation. Sleep deprivation induces changes in molecular signaling, gene expression and may cause changes in dendritic structure in neurons. Genome wide studies have shown that acute sleep deprivation alters gene transcription, although the pool of genes affected varies between brain regions. More recently, advances in research have drawn attention to differences in gene regulation between the level of the transcriptome compared with the pool of mRNA associated with ribosomes for protein translation following sleep deprivation. Thus, in addition to transcriptional changes, sleep deprivation also affects downstream processes to alter protein translation. In this review, we focus on the multiple levels through which acute sleep deprivation impacts gene regulation, highlighting potential post-transcriptional and translational processes that may be affected by sleep deprivation. Understanding the multiple levels of gene regulation impacted by sleep deprivation is essential for future development of therapeutics that may mitigate the effects of sleep loss.

Associations between resting state brain activity and A1 adenosine receptor availability in the healthy brain: Effects of acute sleep deprivation.

Previous resting-state fMRI (Rs-fMRI) and positron emission tomography (PET) studies have shown that sleep deprivation (SD) affects both spontaneous brain activity and A1 adenosine receptor (A1AR) availability. Nevertheless, the hypothesis that the neuromodulatory adenosinergic system acts as regulator of the individual neuronal activity remains unexplored. Therefore, fourteen young men underwent Rs-fMRI, A1AR PET scans, and neuropsychological tests after 52 h of SD and after 14 h of recovery sleep. Our findings suggested higher oscillations or regional homogeneity in multiple temporal and visual cortices, whereas decreased oscillations in cerebellum after sleep loss. At the same time, we found that connectivity strengths increased in sensorimotor areas and decreased in subcortical areas and cerebellum. Moreover, negative correlations between A1AR availability and rs-fMRI metrics of BOLD activity in the left superior/middle temporal gyrus and left postcentral gyrus of the human brain provide new insights into the molecular basis of neuronal responses induced by high homeostatic sleep pressure.

Acute sleep deprivation aggravates nitroglycerin-evoked hyperalgesia in mice.

Sleep deprivation can trigger migraine, and migraineurs often choose to sleep to relieve headaches during acute migraine. This study aimed to explore the effect of acute sleep deprivation on hyperalgesia induced by nitroglycerin in mice. In part one, after either 6-h sleep deprivation or 6-h normal sleep, mice were intraperitoneally injected with nitroglycerin or saline. The mechanical pain threshold and withdrawal latency of the hindpaw were measured every 30min for 6h. Next, the same sleep deprivation and injection procedure was performed with new mice, and mice were sacrificed 4.5h after injection. The trigeminal nucleus caudalis and upper cervical spinal segments were taken for immunofluorescence Fos staining. In part two, after injection of saline or nitroglycerin, the mice were either deprived of sleep for 6h or allowed to sleep without interference. The mechanical and thermal pain threshold were measured after 6h. In part three, we compared the sleep time of mice after intraperitoneal injection of saline or nitroglycerin without interference. Sleep deprivation for 6h did not cause any changes in the baseline pain thresholds in mice. However, pretreatment with 6-h sleep deprivation significantly prolonged the duration of hyperalgesia induced by nitroglycerin. Additionally, the expression of Fos at 4.5h was significantly higher in the 6-h sleep deprivation and nitroglycerin group than in the other three groups. When intraperitoneal injection was given first, the mechanical pain threshold of the hind paw was significantly lower in the group that received nitroglycerin with 6-h sleep deprivation than in the other groups. Compared to the saline injection, one-time nitroglycerin injection would result in a significant increase in sleep latency and decrease in sleep duration for the normal mice. Acute sleep deprivation significantly aggravated the hyperalgesia induced by nitroglycerin in mice, which highlights the importance of sleep disorders for migraine.

Sleep and circadian rhythm disruption alters the lung transcriptome to predispose to viral infection

Sleep and circadian rhythm disruption (SCRD), as encountered during shift work,increases the risk of respiratory viral infection including SARS-CoV-2. However, the mechanism(s) underpinning higher rates of respiratory viral infection following SCRD remain poorly characterized. To address this, we investigated the effects of acute sleep deprivation on the mouse lung transcriptome. Here we show that sleep deprivation profoundly alters the transcriptional landscape of the lung, causing the suppression of both innate and adaptive immune systems, disrupting the circadian clock, and activating genes implicated in SARS-CoV-2 replication, thereby generating a lung environment that could promote viral infection and associated disease pathogenesis. Our study provides a mechanistic explanation of how SCRD increases the risk of respiratory viral infections including SARS-CoV-2 and highlights possible therapeutic avenues for the prevention and treatment of respiratory viral infection.

The sleep homeostatic response to sleep deprivation in humans is heritable.

Following sleep deprivation, increases in delta power have historically been used to index increases in sleep pressure. Research in mice has demonstrated that the homeostatic delta power response to sleep deprivation is heritable. Whether this is true in humans is unknown. In the present study, we used delta power and ORP, a novel measure of sleep depth, to investigate the effects of acute sleep deprivation on sleep depth and to assess the heritability of sleep homeostasis in humans. ORP and delta power were examined during baseline and recovery sleep following 38 h of sleep deprivation in 57 monozygotic and 38 dizygotic same-sex twin pairs. Two complementary methods were used to estimate the trait heritability of sleep homeostasis. During recovery sleep, ORP was lower and delta power was higher than at baseline, indicating deeper sleep. However, at the end of the recovery night, delta power reached baseline levels but ORP demonstrated incomplete recovery. Both ORP and delta power showed a broad sense heritability of sleep homeostasis following sleep deprivation. The classical approach demonstrated an h2 estimate of 0.43 for ORP and 0.73 for delta power. Mixed-effect multilevel models showed that the proportion of variance attributable to additive genetic transmission was 0.499 (95% CI = 0.316-0.682; p < .0001) for ORP and 0.565 (95% CI = 0.403-0.726; p < .0001 for delta power. These results demonstrate that the homeostatic response to sleep deprivation is a heritable trait in humans and confirm ORP as a robust measure of sleep depth.

An experimental test of the effects of acute sleep deprivation on affect and avoidance

Background and objectivesAvoidance and sleep have been identified as mechanisms involved in the development and maintenance of many mental health disorders. However, there has been little research into the relation between sleep and avoidance. MethodsTo address this, a randomized controlled experiment using behavioral and self-report measures of affect and avoidance was conducted. Compared to a control group, we hypothesized that sleep-deprived individuals would demonstrate increased negative, and decreased positive, affectivity, more avoidance behavior toward a negatively valenced stimulus, as well as increased self-reported avoidance. Fifty-two healthy individuals ages 18–30 years old were randomly assigned to a full night of sleep deprivation or normal sleep. They completed a baseline and post-manipulation behavioral avoidance task (BAT) using a disgusting stimulus and self-reports of avoidance and state affect. ResultsRepeated measures ANOVAs demonstrated negative affectivity and self-reported avoidance increased, and positive affectivity decreased, from pre-to post-manipulation in the sleep loss condition as expected. However, there were no effects of sleep deprivation on avoidance behaviors. LimitationsThis study emphasized internal validity over generalizability. Additionally, the at-home sleep deprivation limited researcher control over the overnight activities of participants. ConclusionsResults replicate prior work on the affective consequences of sleep deprivation and highlight a discrepancy between the effect of sleep deprivation on behavioral avoidance toward a specific stimulus compared to self-reported cognitive and social avoidance behaviors.

TH-292. The effects of acute sleep deprivation on working memory: An investigation of EEG event-related oscillations

TH-292. The effects of acute sleep deprivation on working memory: An investigation of EEG event-related oscillations

Five Hours Total Sleep Deprivation Does Not Affect CA1 Dendritic Length or Spine Density.

Sleep is essential for long term memory function. However, the neuroanatomical consequences of sleep loss are disputed. Sleep deprivation has been reported to cause both decreases and increases of dendritic spine density. Here we use Thy1-GFP expressing transgenic mice to investigate the effects of acute sleep deprivation on the dendritic architecture of hippocampal CA1 pyramidal neurons. We found that 5 h of sleep deprivation had no effect on either dendritic length or dendritic spine density. Our work suggests that no major neuroanatomical changes result from a single episode of sleep deprivation.

Altered hippocampal transcriptome dynamics following sleep deprivation

Widespread sleep deprivation is a continuing public health problem in the United States and worldwide affecting adolescents and adults. Acute sleep deprivation results in decrements in spatial memory and cognitive impairments. The hippocampus is vulnerable to acute sleep deprivation with changes in gene expression, cell signaling, and protein synthesis. Sleep deprivation also has long lasting effects on memory and performance that persist after recovery sleep, as seen in behavioral studies from invertebrates to humans. Although previous research has shown that acute sleep deprivation impacts gene expression, the extent to which sleep deprivation affects gene regulation remains unknown. Using an unbiased deep RNA sequencing approach, we investigated the effects of acute sleep deprivation on gene expression in the hippocampus. We identified 1,146 genes that were significantly dysregulated following sleep deprivation with 507 genes upregulated and 639 genes downregulated, including protein coding genes and long non-coding RNAs not previously identified as impacted by sleep deprivation. Notably, genes significantly upregulated after sleep deprivation were associated with RNA splicing and the nucleus. In contrast, downregulated genes were associated with cell adhesion, dendritic localization, the synapse, and postsynaptic membrane. Furthermore, we found through independent experiments analyzing a subset of genes that three hours of recovery sleep following acute sleep deprivation was sufficient to normalize mRNA abundance for most genes, although exceptions occurred for some genes that may affect RNA splicing or transcription. These results clearly demonstrate that sleep deprivation differentially regulates gene expression on multiple transcriptomic levels to impact hippocampal function.

Effects of Acute Sleep Deprivation on Working Memory Capacity in Undergraduate Students

Sleep is a necessary staple in our everyday lives but with advancements in society and an increase in day to day commitments it feels as though there is not enough time in the day. One of the first things to be forsaken in the hopes of maintaining a work schedule or routine is sleep. While the lack of sleep is disproportionate in most demographics, in university students in particular, a lack of sleep is a common, consistent, and necessary plague. Students can be under the impression that the effects of sleep deprivation have mostly long-term repercussions; however, prior literature has indicated that sleep deprivation impacts not just long-term consolidation but also significantly affects memory in the short-term, specifically the working memory (Xie et al. 2019; Chee et al., 2006). In this investigation, we seek to understand the effects that acute sleep deprivation has on the working memory capacity of individuals using a 2-back spatial test. A sample of convenience of upper-class undergraduate students was chosen and the participants were asked to take a specific 2-back spatial test - twice on a day that they subjectively felt as having a regular sleep schedule and twice on a day that they subjectively felt as having sleep deprivation. The team predicted that working memory 2-back task scores will be adversely affected by sleep deprivation. While there was a statistically significant difference in the working memory scores on the full sample level, this was not reflected on the individual level. This indicates that the effects of sleep deprivation are not generalizable to a full population and that they must be reviewed on a case-by-case basis. Furthermore, since greater variation was observed in the sleep deprived scores in all individuals, it implies that sleep deprivation may indirectly affect the consistency of working memory by affecting attention span and concentration.

113 Effects of Sleep on Intrusive Symptoms and Emotion Reactivity in a Laboratory-Based Film Analogue Study

Abstract Introduction Recent literature highlights the need to focus on the impact of intrusive symptoms as a possible risk factor for the development and maintenance of PTSD. Cognitive and sleep models also contribute to the further understanding of intrusive symptoms. Further emotion work emphasizes that disgust is an emotion closely associated with the emergence of posttraumatic stress symptomology following traumatic events. Methods This study utilized a film eliciting disgust to examine the effects of acute sleep deprivation on the intensity of intrusive symptoms and emotion reactivity. Forty-nine college students were randomly assigned to sleep as usual or an acute sleep deprivation after watching a disturbing film. It was hypothesized that, relative to the control group, participants who were acutely sleep deprived would report higher frequency of intrusive symptoms and higher negative valence. Results Findings were partially consistent with hypotheses. There were no group or interaction effects on intrusive symptoms, although participants across both groups reported significant decreases in negative valence and intrusive symptoms across the study (F(1, 47) = 10.30, p &amp;lt; 0.01). There was a significant interaction effect between sleep group and self-reported negative valence, where individuals in the sleep deprived group reported significantly higher valence than individuals in the control group, despite significant decreases in negative valence over time (F(1, 48) = 7.869, p &amp;lt; 0.01). Conclusion Possible mechanisms that may contribute to the significant difference in valence may be due to higher order emotion regulation strategies that are compromised due to sleep loss. However, the significant decreases in negative valence and intrusive symptoms over time may be due to methodological factors or the type of sleep manipulation. Further work can address these challenges by using a larger sample size or examining the effects of chronic, partial sleep deprivation. Support (if any):

123 Detrimental effects of acute sleep deprivation on perceptual metacognition

Abstract Introduction Sleep deprivation (SD) impairs cognitive performance but its impact on metacognition – i.e. the ability to introspect about cognitive performance – is less clear. A few studies have assessed metacognitive accuracy after acute sleep deprivation in tasks of executive functions and found no impairments. However, whether SD has no influence on metacognition of other cognitive domains such as perception has not been investigated. In this study, we examined how metacognitive accuracy in perceptual decision tasks is affected by 32 hours of sustained wakefulness. Methods 14 participants (3 males, aged 20-32) repeated four visual psychophysical tasks (orientation discrimination, two-flicker fusion, vernier acuity and a novel face/house discrimination in noise) at regular intervals during 32 hours of sustained wakefulness and once after 8 hours recovery sleep. In each task, we concurrently measured quantitative indices of perceptual threshold, confidence rating and metacognitive accuracy (i.e. how well confidence ratings discriminate correct vs incorrect perceptual judgements). Results We observed a gradual increase of perceptual threshold in all tasks with increased time awake. Furthermore, metacognitive accuracy gradually decreased during sustained wakefulness in all tasks. Specifically, the decrease in metacognitive accuracy was driven by over-estimated confidence in trials when participants made incorrect perceptual judgements. After recovery sleep, perceptual thresholds were reset to baseline for all tasks, while metacognitive accuracy was reset to baseline for the orientation discrimination and two-flicker fusion tasks only. Conclusion We showed that sustained wakefulness up to 32 hours increasingly impairs metacognitive accuracy in perceptual decision tasks. These results are consistent across different perceptual tasks, but are in contrast to previous studies showing preserved metacognition of executive functions after SD. Overall, this suggests that the fundamental mechanisms of perceptual metacognition may be similarly affected by sleep deprivation, but that SD selectively impacts different domains of metacognition, such as perceptual metacognition and metacognition of executive functions. Support (if any) MB - Cardiff University PhD Funding CS - Wellcome Trust 209192/Z/17/Z

Mild regular treadmill exercise ameliorated the detrimental effects of acute sleep deprivation on spatial memory

Vulnerable areas like the hippocampus are sensitive to insults such as sleep deprivation (SD); they are also susceptible to environmental enrichment. Much evidence is accumulating that chronic sleep deprivation causes alterations in the hippocampus that responsible for spatial memory. However, there is conflicting about the differences between acute and chronic SD results. The purpose of this study was to determine the protective effects of mild treadmill exercise on acute SD rats.Four groups were created as control, exercise, sleep deprivation, exercise + sleep deprivation. Multiple platforms method was used to induce REM sleep deprivation (RD) for 48 h. The exercise was applied fivedaysperweekforfour weeks(5 × 4). For the first and second weeks, the length of the exercise was 15 min in two sessions (5 min interval) followed by 15 min in three, 15 min in four sessions. Morris water maze (MWM) was used as a spatial memory test. Gene level was determined by using the qPCR technique. Malondialdehyde (MDA) content in the hippocampus was measured as an extent of peroxidative damage to lipids by using the ELISA method.48 h RD impaired long-term spatial memory significantly. Mild, regular treadmill exercise ameliorated the detrimental effects of acute sleep deprivation on memory. There was no significant difference in MDA between groups. Hippocampal gene expression did not show any changes in all groups.Lack of correlation between memory impairment and levels of genes in the hippocampus is likely to be related to the differences in behavioral and genetic mechanisms.