Total sleep deprivation reduces the table tennis anticipation performance of young men: A functional magnetic resonance imaging study.

This study explored whether and how sleep deprivation (SD) affects sport-related anticipation. Twenty table tennis players and 28 non-athletes completed a table tennis anticipation task before and after 36 h SD. Functional magnetic resonance imaging (fMRI) data were acquired simultaneously. The results showed that, compared with the non-athletes, table tennis players had higher neural efficiency, manifested by their higher anticipation accuracy and lower frontal lobe activation. SD impaired anticipation performance, accompanied by decreased activation of the occipital and temporal lobes. Compensatory activation occurred in the left hippocampus and orbital part of the right inferior frontal gyrus (IFG) after SD in the table tennis player group, but not in the non-athlete group. The decreased accuracy of non-athletes was positively correlated with decreased activation of orbital part of the right IFG. This study's findings improve the understanding of the cognitive neuroscience mechanisms by which SD affects sport-related anticipation.

Total sleep deprivation impairs visual selective attention and triggers a compensatory effect: evidence from event-related potentials.

Many studies have demonstrated the impairment of sustained attention due to total sleep deprivation (TSD). However, it remains unclear whether and how TSD affects the processing of visual selective attention. In the current study, 24 volunteers performed a visual search task before and after TSD over a period of 36 h while undergoing spontaneous electroencephalography. Paired-sample t-tests of behavioral performance revealed that, compared with baseline values, the participants showed lower accuracy and higher variance in response time in visual search tasks performed after TSD. Analysis of the event-related potentials (ERPs) showed that the mean amplitude of the N2-posterior-contralateral (N2pc) difference wave after TSD was less negative than that at baseline and the mean amplitude of P3 after TSD was more positive than that at baseline. Our findings suggest that TSD significantly attenuates attentional direction/orientation processing and triggers a compensatory effect in the parietal brain to partially offset the impairments. These findings provide new evidence and improve our understanding of the effects of sleep loss.

Total sleep deprivation selectively impairs motor preparation sub-stages in visual search task: Evidence from lateralized readiness potentials.

Introduction: Many studies have provided evidence of a damage effect triggered by total sleep deprivation (TSD). However, it remains unclear whether the motor preparation processing is affected by TSD. Methods: In the current study, 23 volunteers performed a stimulus-response compatibility visual search task before and after TSD while undergoing spontaneous electroencephalography (EEG). Results: Repeated-measures analysis of variance revealed that: Compared with that at baseline, the visual search task's accuracy decreased after TSD, while the response time variance increased significantly. The peak amplitude of the stimulus-locked lateralized readiness potential (LRP) induced by a compatible stimulus was significantly more negative than that induced by an incompatible stimulus before TSD, whereas this difference was not significant after TSD. However, when taking sleep status into consideration, there were no significant main or interaction effects on response-locked LRPs. Discussion: Our findings suggest that TSD damages visual search behavior, selectively impairs the earlier sub-stages of motor preparation (sensory integration). These findings will provide a new perspective for understanding the effects of sleep loss.

Dynamic hippocampal functional connectivity responses to varying working memory loads following total sleep deprivation.

Sleep loss with work overload can impact human cognitive performance. However, the brain's response to an increased working memory load following total sleep deprivation (TSD) remains unclear. In the present study, we focussed on the dynamic response of the hippocampus to increased working memory load before and after total sleep deprivation of 36 h. A total of 16 male participants completed a verbal working memory task under functional magnetic resonance imaging. After whole-brain activation analysis and region of interest analysis of the hippocampus, the generalised form of context-dependent psychophysiological interactions (gPPI) was used to analyse the hippocampal functional connectivity with the whole brain. The results revealed that as the working memory load increased within a small range, from 0-back to 1-back task, the left hippocampal functional connectivity decreased with the left supplementary motor area, left pars opercularis, left rolandic operculum, right superior frontal gyrus, bilateral precentral gyrus, and left middle cingulate cortex following total sleep deprivation compared with that observed in resting wakefulness. When the working memory load further increased from 1-back to 2-back task, the connectivity increased between the left hippocampus and the left superior parietal lobule as well as between the left hippocampus and right lingual gyrus after total sleep deprivation compared with that observed in resting wakefulness. Moreover, the left hippocampus gPPI effect on the left middle cingulate cortex and left superior parietal lobule could predict the behavioural test accuracy in 1-back and 2-back task, respectively, following total sleep deprivation. These findings indicated that increased working memory load after total sleep deprivation disrupts working memory processes. The brain reacts to these disruptions in a dynamic and flexible manner, involving not only brain activation but also hippocampus-related functional network connections.

Altered insular functional connectivity correlates to impaired vigilant attention after sleep deprivation: A resting-state functional magnetic resonance imaging study.

Objectives: This study used resting-state functional magnetic resonance imaging (rs-fMRI) scans to assess the dominant effects of 36 h total sleep deprivation (TSD) on vigilant attention and changes in the resting-state network. Materials and methods: Twenty-two healthy college students were enrolled in this study. Participants underwent two rs-fMRI scans, once in rested wakefulness (RW) and once after 36 h of TSD. We used psychomotor vigilance tasks (PVT) to measure vigilant attention. The region-of-interest to region-of-interest correlation was employed to analyze the relationship within the salience network (SN) and between other networks after 36 h of TSD. Furthermore, Pearson's correlation analysis investigated the relationship between altered insular functional connectivity and PVT performance. Results: After 36 h of TSD, participants showed significantly decreased vigilant attention. Additionally, TSD induced decreased functional connectivity between the visual and parietal regions, whereas, a significant increase was observed between the anterior cingulate cortex and insula. Moreover, changes in functional connectivity in the anterior cingulate cortex and insula showed a significant positive correlation with the response time to PVT. Conclusion: Our results suggest that 36 h of TSD impaired vigilant visual attention, resulting in slower reaction times. The decrease in visual-parietal functional connectivity may be related to the decrease in the reception of information in the brain. Enhanced functional connectivity of the anterior cingulate cortex with the insula revealed that the brain network compensation occurs mainly in executive function.

Acute Sleep Deprivation Impairs Motor Inhibition in Table Tennis Athletes: An ERP Study.

Excellent response inhibition is the basis for outstanding competitive athletic performance, and sleep may be an important factor affecting athletes' response inhibition. This study investigates the effect of sleep deprivation on athletes' response inhibition, and its differentiating effect on non-athlete controls' performance, with the aim of helping athletes effectively improve their response inhibition ability through sleep pattern manipulation. Behavioral and event-related potential (ERP) data were collected from 36 participants (16 table tennis athletes and 20 general college students) after 36 h of sleep deprivation using ERP techniques and a stop-signal task. Sleep deprivation's different effects on response inhibition in the two groups were explored through repeated-measures ANOVA. Behavioral data showed that in a baseline state, stop-signal response time was significantly faster in table tennis athletes than in non-athlete controls, and appeared significantly longer after sleep deprivation in both groups. ERP results showed that at baseline state, N2, ERN, and P3 amplitudes were lower in table tennis athletes than in non-athlete controls, and corresponding significant decreases were observed in non-athlete controls after 36 h of sleep deprivation. Table tennis athletes showed a decrease in P3 amplitude and no significant difference in N2 and ERN amplitudes, after 36 h of sleep deprivation compared to the baseline state. Compared to non-athlete controls, table tennis athletes had better response inhibition, and the adverse effects of sleep deprivation on response inhibition occurred mainly in the later top-down motor inhibition process rather than in earlier automated conflict detection and monitoring.

Modafinil ameliorates the decline in pronunciation-related working memory caused by 36-h acute total sleep deprivation: An ERP study.

We aimed to explore whether modafinil mitigates the working memory decline induced by 36 h of acute total sleep deprivation (36-h TSD). Sixteen healthy male participants were enrolled in a randomized double-blind crossover control study involving three sleep-deprivation sessions. Participants were administered 400 mg of placebo, caffeine, or modafinil during these sessions. Behavior and EEG data were recorded while participants performed pronunciation-related working memory tasks. Behavioral indicators showed that, compared with placebo, modafinil improved the accuracy of pronunciation-related working memory tasks and reduced the response time. Compared with before sleep deprivation, the amplitudes of the event-related potentials (ERPs) increased in the N2 component and decreased in the P3 component after sleep deprivation in the placebo condition. In the caffeine condition, the amplitude of the P3 component decreased, the latency of the N2 component was prolonged, and the N2 amplitude remained unchanged. In the modafinil condition, the P3 latency was shortened, and no significant difference was found in the amplitude of the N2 or P3 ERPs; no significant difference was recorded in the N2 latency. Modafinil (400 mg) effectively ameliorated the decline in pronunciation-related working memory after 36-h TSD, suggesting that it may effectively counteract cognitive decline caused by acute sleep deprivation.

Total Sleep Deprivation Triggers Greater Activation in the Parietal Brain in the Visual Working Memory Updating Processes: An Event-Related Potentials Study.

Working memory functions are known to be altered after total sleep deprivation (TSD). However, few studies have explored the deficits of working memory updating (WMU) after TSD, or the underlying electrophysiological mechanisms of these alterations. In the current exploratory study, we enrolled 14 young male volunteers who performed two kinds of WMU tasks-spatial and object two-back tasks-with simultaneous electroencephalography recordings under two sleep conditions: a normal sleep baseline condition and after 36 h of TSD. Repeated-measures analysis of variance showed that compared with those at baseline, the rates of correct responses in the WMU tasks decreased significantly after TSD. Analysis of event-related potentials revealed that the average amplitude of P3 components decreased significantly in the frontal and central brain regions and increased significantly in the parietal brain regions. Our findings suggest that TSD damages WMU behavior, impairs cognitive functions in the frontal and central brain regions, and triggers greater activation in the parietal brain regions. This is the first study to report the existence of event-related compensatory neural activity. This event-related compensatory effect may provide a new perspective for understanding the mechanisms underlying the influences triggered by sleep loss.

Changes in ventromedial prefrontal cortex functional connectivity are correlated with increased risk-taking after total sleep deprivation.

There is evidence indicating that people are more likely to take risks when they are sleep-deprived than during resting wakefulness (RW). The ventromedial prefrontal cortex (vmPFC) could have a crucial psychophysiological role in this phenomenon. However, the intrinsic patterns of functional organization of the human vmPFC and their relationship with risk-taking during sleep deprivation (SD) are unclear. This study investigated the relationship between functional connectivity in the vmPFC and cerebral cortex and the risk-taking tendency after SD. The study participants were 21 healthy college students who underwent functional magnetic resonance imaging twice in the resting state, once during RW and once after 36 h of SD. The vmPFC was analyzed bilaterally for functional connectivity between the regions of interest. Correlation analysis was performed to evaluate changes in functional connectivity between the vmPFC and the cerebral cortex and risk-taking before and after SD. A single night of SD produced a definite deficit in functional connectivity between the vmPFC and thalamus bilaterally and an increase in functional connectivity between the vmPFC and dorsolateral prefrontal cortex (dlPFC) and the parietal lobe. We also found that the likelihood of risk-taking was positively correlated with increased functional connectivity between the vmPFC and dlPFC and negatively correlated with decreased functional connectivity between the vmPFC and thalamus bilaterally. These results demonstrate that lack of sleep substantially impairs functional connectivity between the vmPFC and the cerebral cortex, which in turn predicts the risk-taking behavior found after SD.

Altered Functional Connectivity in the Resting State Neostriatum After Complete Sleep Deprivation: Impairment of Motor Control and Regulatory Network.

Sleep loss not only compromises individual physiological functions but also induces a psychocognitive decline and even impairs the motor control and regulatory network. In this study, we analyzed whole-brain functional connectivity changes in the putamen and caudate nucleus as seed points in the neostriatum after 36 h of complete sleep deprivation in 30 healthy adult men by resting state functional magnetic resonance imaging to investigate the physiological mechanisms involved in impaired motor control and regulatory network in individuals in the sleep-deprived state. The functional connectivity between the putamen and the bilateral precentral, postcentral, superior temporal, and middle temporal gyrus, and the left caudate nucleus and the postcentral and inferior temporal gyrus were significantly reduced after 36 h of total sleep deprivation. This may contribute to impaired motor perception, fine motor control, and speech motor control in individuals. It may also provide some evidence for neurophysiological changes in the brain in the sleep-deprived state and shed new light on the study of the neostriatum in the basal ganglia.

Decreased Functional Connectivity in the Reward Network and Its Relationship With Negative Emotional Experience After Total Sleep Deprivation.

Sleep deprivation (SD) induces a negative emotional experience due to a prolonged time spent awake. However, few studies have focused on the mechanism underlying communication within brain networks or alterations during this emotional deterioration. We propose that negative reward judgment is important in poor emotional processing after SD, which will be reflected in functional connectivity in the reward network. We sought to analyze alterations in functional connectivity within the reward network and cerebral cortex. Furthermore, we analyzed changes in functional connectivity correlation with negative emotional experience after SD. Twenty-six healthy volunteers participated in this study. Two resting-state fMRI scans were obtained from the participants, once during resting wakefulness, and once after 36 h of total SD. The bilateral nucleus accumbens (NAc) was selected as a seed region for region of interest (ROI)-to-ROI functional connectivity analysis. Correlation analyses between functional connectivity alterations within the reward network and negative emotional experience were also performed. We found that SD decreased functional connectivity between the left NAc and anterior cingulate cortex (ACC) compared with resting wakefulness. There was a decreased functional connectivity with the ACC and right inferior frontal gyrus (IFG) after SD in the right NAc. Furthermore, decreased functional connectivity between the right NAc and right IFG, and NAc and ACC was negatively correlated with emotional experience scores. Sleep deprivation decreased functional connectivity within the reward network. This may be associated with the enhanced negative emotional experience that was found after total sleep deprivation.

Effects of Sleep Deprivation on Working Memory: Change in Functional Connectivity Between the Dorsal Attention, Default Mode, and Fronto-Parietal Networks.

Sleep deprivation (SD) is very common in modern society and has a profound effect on cognitive function, in particular on working memory (WM). This type of memory is required for completion of many tasks and is adversely affected by SD. However, the cognitive neural mechanism by which SD affects WM, remains unclear. In this study, we investigated the changes in the brain network involved in WM after SD. Twenty-two healthy subjects underwent functional magnetic resonance imaging scan while in a state of resting wakefulness and again after 36 h of total SD and performed a WM task before each scanning session. Nineteen main nodes of the default mode network (DMN), dorsal attention network (DAN), fronto-parietal network (FPN), salience network (SN), and other networks were selected for functional analysis of brain network connections. Functional connectivity measures were computed between seed areas for region of interest (ROI)-to-ROI analysis and to identify patterns of ROI-to-ROI connectivity. The relationship between the significant changes in functional connectivity in the brain network and WM performance were then examined by Pearson's correlation analysis. WM performance declined significantly after SD. Compared with the awake state, the functional connectivity between DAN and DMN significantly increased after SD while that between FPN and DMN significantly decreased. Correlation analysis showed that the enhanced functional connectivity between DAN and DMN was negatively correlated with the decline in WM performance and that the decline in functional connectivity between FPN and DMN was positively correlated with decreased WM performance. These findings suggested that SD may affect WM by altering the functional connectivity among DMN, DAN, and FPN.

Total Sleep Deprivation Impairs Lateralization of Spatial Working Memory in Young Men.

Total sleep deprivation (TSD) negatively affects cognitive function. Previous research has focused on individual variation in cognitive function following TSD, but we know less about how TSD influences the lateralization of spatial working memory. This study used event-related-potential techniques to explore asymmetry in spatial-working-memory impairment. Fourteen healthy male participants performed a two-back task with electroencephalogram (EEG) recordings conducted at baseline and after 36 h of TSD. We selected 12 EEG points corresponding to left and right sides of the brain and then observed changes in N2 and P3 components related to spatial working memory. Before TSD, P3 amplitude differed significantly between the left and right sides of the brain. This difference disappeared after TSD. Compared with baseline, P3 amplitude decreased for a duration as extended as the prolonged latency of N2 components. After 36 h of TSD, P3 amplitude decreased more in the right hemisphere than the left. We therefore conclude that TSD negatively affected spatial working memory, possibly through removing the right hemisphere advantage.

Effect of Sleep Deprivation on the Working Memory-Related N2-P3 Components of the Event-Related Potential Waveform.

Working memory is very sensitive to acute sleep deprivation, and many studies focus on the brain areas or network activities of working memory after sleep deprivation. However, little is known about event-related potential (ERP)-related changes in working memory after sleep loss. The purpose of this research was to explore the effects of 36 h of total sleep deprivation (TSD) on working memory through ERPs. Sixteen healthy college students performed working memory tasks while rested and after 36 h of TSD, and electroencephalography (EEG) data were simultaneously recorded while the subjects completed working memory tasks that included different types of stimulus materials. ERP data were statistically analyzed using repeated measurements analysis of variance to observe the changes in the working memory-related N2-P3 components. Compared with baseline before TSD, the amplitude of N2-P3 components related to working memory decreased, and the latency was prolonged after TSD. However, the increased amplitude of the P2 wave and the prolonged latency were found after 36 h of TSD. Thus, TSD can impair working memory capacity, which is characterized by lower amplitude and prolonged latency.