Total sleep deprivation (TSD) leads to cognitive decline; however, the neurophysiological mechanisms underlying resting-state electroencephalogram (EEG) changes after TSD remain unclear. In this study, 42 healthy adult participants were subjected to 36 h of sleep deprivation (36 h TSD), and resting-state EEG data were recorded at baseline, after 24 h of sleep deprivation (24 h TSD), and after 36 h TSD. The analysis of resting-state EEG at baseline, after 24 h TSD, and after 36 h TSD using source localization analysis, power spectrum analysis, and functional connectivity analysis revealed a decrease in alpha-band power and a significant increase in delta-band power after TSD and impaired functional connectivity in the default mode network, precuneus, and inferior parietal lobule. The cortical activities of the precuneus, inferior parietal lobule, and superior parietal lobule were significantly reduced, but no difference was found between the 24 h and 36 h TSD groups. This may indicate that TSD caused some damage to the participants, but this damage temporarily slowed during the 24 h to 36 h TSD period.

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.

Background: Previous studies revealed that sleep deprivation (SD) impairs risk perception and leads to poor decision-making efficiency. However, how risk perception is related to brain regions’ communication after SD has not been elucidated. In this study, we investigated the neuropsychological mechanisms of SD-impaired risk perception. Methods: Nineteen healthy male adults were recruited and underwent resting-state functional magnetic resonance imaging during a state of rested wakefulness and after nearly 36 h of total SD. They then completed the balloon analog risk task, which was used to measure the risk perception ability of risky decision-making. Regional homogeneity (ReHo) and voxel-wise functional connectivity were used to investigate neurobiological changes caused by SD. Correlation analysis was used to investigate the relationship between changes in ReHo, function, and risk perception. Results: At the behavioral level, risk perception decreased after 36 h of SD. At the neural level, SD induced a significant increase in ReHo in the right postcentral gyrus and was positively correlated with risk perception changes. The functional connectivity between the right postcentral gyrus, left medial temporal gyrus, and right inferior temporal gyrus was enhanced. Critically, increased right postcentral gyrus and right inferior temporal gyrus connectivity positively correlated with changes in risk perception. Conclusions: SD impairs the risk perception associated with altered postcentral connectivity. The brain requires more energy to process and integrate sensory and perceptual information after SD, which may be one possible reason for decreased risk perception ability after SD.

Spatial cognition facilitates the successful completion of specific cognitive tasks through lateral processing and neuroplasticity. Long-term training in table tennis induces neural processing efficiency in the visuospatial cognitive processing cortex of athletes. However, the lateralization characteristics and neural mechanisms of visual–spatial cognitive processing in table tennis players in non-sport domains are unclear. This study utilized event-related potentials to investigate differences in the spatial cognition abilities of regular college students (controls) and table tennis players. A total of 48 participants (28 controls; 20 s-level national table tennis players) completed spatial cognitive tasks while electroencephalography data were recorded. Task performance was better in the table tennis group than in the control group (reaction time: P < 0.001; correct number/sec: P = 0.043), P3 amplitude was greater in the table tennis group (P = 0.040), spatial cognition showed obvious lateralization characteristics (P < 0.001), table tennis players showed a more obvious right-hemisphere advantage, and the P3 amplitude in the right hemisphere was significantly greater in table tennis athletes than in the control group. (P = 0.044). Our findings demonstrate a right-hemisphere advantage in spatial cognition. Long-term training strengthened the visual–spatial processing ability of table tennis players, and this advantage effect was reflected in the neuroplasticity of the right hemisphere (the dominant hemisphere for spatial processing).

Purpose: The function of working memory (WM) is impaired by total sleep deprivation (TSD) and cognitive load. However, it is unclear whether the load modulates the effect of TSD on WM. We conducted a pilot study to investigate the effects of 36 h of TSD on WM under different load levels. Materials and methods: Twenty-two male students aged 18–25 years were enrolled, who underwent two types of sleep conditions (baseline and 36 h TSD), where they performed two N-back WM tasks (one-back task and two-back task) with simultaneous electroencephalography recordings. Results: Repeated measures analysis of variance (ANOVA) indicated that, with the increasing load, the reaction time increased and the accuracy decreased. After TSD, the correct number per unit time decreased. The significant interaction effect of the P3 amplitudes between the load level and the sleep condition showed that the reduction in the amplitude of P3 in the two-back task due to TSD was more obvious than that in the one-back task. Conclusions: Our results provided evidence for the moderation of load on the impairment of TSD on WM. The degree of TSD-induced impairment for a higher load was greater than that for a lower load. The current study provides new insights into the mechanisms by which sleep deprivation affects cognitive function.