Efficient attention depends on the temporal alignment between ongoing neural activity and task-relevant sensory events. Alpha-band dynamics, and particularly individual alpha frequency (IAF), have been proposed to regulate this alignment, yet direct causal evidence linking IAF to attentional timing remains limited. Here, we used neurofeedback (NF) to test whether experimentally induced changes in parieto-occipital IAF alter the neural and behavioral dynamics of visual attention. 108 healthy adults completed five sessions of EEG-based IAF neurofeedback or an active placebo control and performed the Attention Network Test (ANT) after each session. Participants were classified as learners or non-learners based on their ability to voluntarily increase IAF. Attentional performance was assessed using response times, efficiency scores, and cue-related facilitation. Neural measures included resting IAF and task-related alpha event-related desynchronization (α-ERD) amplitude and latency as an index of the timing of cortical engagement.Compared with non-learners and placebo participants, NF learners showed faster responses, higher attentional efficiency, and stronger facilitation effects following informative cues. At the neural level, learners exhibited shorter α-ERD latencies, indicating earlier task-related recruitment of visual–parietal networks. Crucially, repeated-measures mediation analyses revealed a partial sequential pathway whereby NF-related increases in IAF predicted faster response times through reductions in α-ERD latency. These findings provide causal evidence that IAF constrains the temporal dynamics of attentional deployment by regulating the speed of alpha-band desynchronization following task-relevant cues and identifying IAF as a key functional parameter governing attentional readiness and the temporal deployment of attention by shaping the dynamics of alpha-band desynchronization.

Atypical sensory experiences are highly prevalent in autistic children and include both hyper- and hypo-responsivity, often accompanied by sensory overload. Alpha oscillations (7-13 Hz), which dynamically regulate cortical excitability, represent a plausible neural mechanism underlying these phenomena: reduced alpha activity is associated with enhanced sensory responsiveness, whereas increased alpha supports suppression of external input. Although decreased alpha power has been repeatedly reported in autism, it remains unclear whether this reduction reflects lower oscillatory amplitude or reduced temporal stability of alpha rhythms, two mechanisms with distinct neurophysiological implications. To better characterize alpha activity in autism, we examined resting-state alpha dynamics in non-autistic children (NA; n = 39), autistic children (AU; n = 52), and siblings of autistic children (SIB; n = 26), aged 8-14 years. We combined traditional broadband measures of relative alpha power, parametric separation of periodic and aperiodic activity, and single-event analyses that quantify the temporal structure of alpha oscillations. Both broadband relative alpha power and periodic alpha power were reduced in autism over parietal regions, replicating prior findings. Importantly, ordinal analyses revealed an intermediate profile in siblings, supporting a liability-related gradient of alpha alterations. However, single-event analyses demonstrated that the average amplitude of individual alpha bursts did not differ between groups. Instead, autistic children showed significantly shorter alpha burst duration and reduced alpha abundance (i.e., proportion of time occupied by rhythmic alpha episodes), with siblings again exhibiting intermediate values. Linear regression analyses confirmed that reductions in relative and periodic alpha power were primarily driven by decreased alpha abundance rather than diminished burst amplitude. These findings indicate that altered alpha activity in autism reflects reduced temporal stability and density of alpha events rather than weaker oscillatory amplitude per se. Reduced persistence of alpha rhythms may therefore represent a neural marker of altered cortical excitability and sensory regulation in autism.

The aperiodic, 1/f-like component of electrophysiological activity is increasingly recognized as a meaningful feature of neural function, rather than background noise. In parallel, many EEG studies report transient changes in oscillatory power following stimulus onset and interpret these effects as signatures of attention, salience, or cognitive control. However, such conclusions usually rely on baseline normalization procedures that assume aperiodic activity remains stable from pre- to post-stimulus periods. Using high-density EEG recordings from typically developing children, we tested this assumption in two paradigms: an audiovisual simple reaction-time task (n = 36) and a visual oddball task (n = 38). For each task, conventional spectral analyses were compared with analyses that explicitly modeled and removed the aperiodic component in both pre- and post-stimulus windows. Across tasks, stimulus onset was associated with robust increases in aperiodic exponent and offset, indicating systematic changes in the 1/f component of the spectrum. In the audiovisual task, these changes were modality-specific, with central, parieto-occipital, or combined topographies depending on stimulus type. These effects were reduced but remained significant after ERP removal, indicating that they were not fully explained by phase-locked activity. Critically, once aperiodic activity was accounted for, the apparent poststimulus increase in theta power was largely abolished in both tasks, including the canonical fronto-central theta enhancement to infrequent targets in the oddball paradigm. The conventional method also overestimated the magnitude of beta desynchronization, particularly in the induced (ERP-removed) signal. The apparent gamma desynchronization detected by conventional analyses was reversed after aperiodic correction, revealing either synchronization or no change, indicating that it reflects a spurious consequence of spectral slope steepening rather than a true suppression of gamma oscillatory activity. In contrast, alpha desynchronization remained robust after aperiodic correction and was in fact enhanced, suggesting it reflects genuine oscillatory suppression. Together, these findings indicate that a substantial portion of conventional time-frequency effects, particularly apparent theta synchronization, may reflect changes in aperiodic activity in response to stimulation rather than genuine periodic oscillations, challenging core assumptions of conventional time-frequency analyses.

OBJECTIVE:This study aimed to examine the evolution of vigilance, sleepiness and electrophysiological markers of arousal in healthy subjects exposed to moderate hyperthermia, during habitual or restricted sleep conditions. METHODS:Twelve healthy males (30.4 ± 7.3 yr) completed two experimental crossover sessions in a bioclimatic chamber, consisting of sequential exposure to a thermoneutral condition (TCORE = 37.0 ± 0.2 °C) then an hyperthermic condition (TCORE = 38.3 ± 0.2 °C). Sessions followed either an habitual night of sleep (>6h time in bed, TIB) or sleep restriction (<3h TIB). A 10-minute psychomotor vigilance task (PVT) and a sleepiness scale were administered under thermoneutrality and hyperthermia conditions, immediately after recording a one-minute eyes-closed resting state electroencephalogram (EEG). This allowed for the calculation of individual alpha frequency (IAF), relative spectral powers (alpha, theta and beta bands) and theta-to-alpha ratio in frontal and parieto-occipital territories. RESULTS:Moderate hyperthermia induced an increase in PVT speed and a decrease in sleepiness. This arousal response was associated with an increase of IAF, a reduction in frontal theta power and an increase in frontal alpha power, leading to a decrease in the theta/alpha ratio. In contrast, sleep restriction induced the opposite effect on PVT performances and sleepiness, as well as for EEG parameters (without influence on IAF). No significant interaction was observed for all parameters. CONCLUSION:Sleep restriction and moderate hyperthermia induced opposite effects in our model with limited time exposure to heat. This confirms that heat can help with arousing under certain conditions, although this needs to be confirmed by further studies.

Intersensory switching (IS), the ability to shift attention between different sensory systems, is essential for cognitive flexibility, yet leads to slower responses compared to repeating the same sensory modality. The underlying neural mechanisms of IS remain largely unknown. In this study, high-density EEG was used to investigate these mechanisms in healthy adults (n = 53; mean age 26±7.39; 30 female) performing a speeded reaction time (RT) task involving visual and auditory stimuli. Trials were categorized as Repeat (same preceding modality) or Switch (different preceding modality). Switch trials showed slower RTs and delayed sensory responses (N1 and P2 components). Furthermore, across both Repeat and Switch trials, RT correlated with the latency of these neural responses. Additionally, lower alpha-band inter-trial phase coherence (ITPC) in primary sensory regions was noted for Switch compared to Repeat trials, suggesting reduced efficiency of sensory processing. Greater induced theta activity over fronto-central scalp regions in Switch trials suggested increased cognitive control demands. These findings support a model where the prior stimulus primes the sensory cortex for faster processing of Repeat trials, while Switch trials lead to heightened cognitive resources for adjustment, likely reflecting attentional reallocation mediated by the anterior cingulate cortex (ACC). The consistent effects across auditory and visual modalities indicate that IS relies on a core, modality-independent mechanism grounded in fundamental principles of sensory and attentional reorganization.

Sleep and muscle injury-related pain are in negative relationship, and sleep extension may be a favorable countermeasure. In response to muscle injury, an adaptive sleep response has been described in rats, characterized by an increase in total sleep time (TST) and nonrapid eye movement (NREM) sleep. This study examined the effects of photoperiod lengthening (a model of sleep prolongation in rats) on the sleep characteristics of muscle-injured rats and whether this lengthening could benefit injury-induced mechanical hyperalgesia using the Von Frey test. Switching from the conventional 12:12 light/dark (LD) photoperiod (light on: 08:00–20:00) to LD 16:8 (light extended to 24:00) gives rats an extra window of sleep. Our results show higher TST and NREM sleep times in LD 16:8 versus LD 12:12 injured rats during 4 h of light lengthening for 7 d postinjury, showing the efficiency of photoperiod lengthening to increase sleep time in injured rats. In addition, a cumulative effect with the adaptive sleep response to muscle injury occurred with higher TST and NREM sleep times in LD 16:8 injured versus noninjured rats during the dark period, reflecting the high need for sleep after the injury. Greater stability and higher relative delta power of NREM sleep during the extended light period were also observed in injured rats. Finally, the extended photoperiod limits the muscle injury-induced mechanical hyperalgesia for 13 d and allows faster recovery of the baseline mechanical threshold. This is associated with reduced pro-inflammatory cytokines levels in the hippocampus, a brain structure involved in pain processing.

STUDY OBJECTIVES:This study describes macro- and micro-sleep responses to a myotoxic skeletal muscle injury and investigates possible mechanisms.METHODS:We recorded the electroencephalogram (EEG)/electromyogram (EMG) of 24 Wistar rats before and after induction of tibialis anterior muscle injury (n = 8 per group: control, control + buprenorphine and injured). A top-down analysis of sleep characteristics was processed from total sleep time (TST), sleep stages, sleep stability, spectral analysis, and spindles. To further investigate the mechanisms involved, we analyzed the protein level of sleep regulatory molecules including tumor necrosis factor- α (TNF-α), interleukin-1β (IL-1β), insulin-like growth factor-1 (IGF-1), and brain and muscle ARNT-like 1 (BMAL1) in plasma, frontal cortex, hippocampus, and tibialis anterior, collected at day +2 after injury from non-EEG/EMG implanted rats.RESULTS:Muscle injury induces a significant increase in TST at 48 and 72 h post-injury, specific to non-rapid eye movement (NREM) sleep. These increases occur during the dark period and are associated with the higher stability of sleep over 24 h, without change in the different power/frequency spectral bands of NREM/REM sleep. There was no corresponding sleep increase in slow-wave activity or spindle density, nor were there changes in brain levels of the sleep-regulating proinflammatory cytokine IL-1β, which is otherwise involved in the local response to injury. Conversely, decreased protein levels of brain IGF-1 and muscle BMAL1, a core circadian clock gene, after injury may play a role in increased sleep time.CONCLUSION:Muscle injury induces an increase in total sleep time at 48- and 72-h post-injury, specific to NREM sleep during the dark period in rats and is associated with higher sleep stability over 24 h.

Identifier les périodes d’éveil et de sommeil à l’aide d’une nouvelle méthode non-invasive : le système piézo-électrique. Nous avons enregistré simultanément les animaux en EEG/EMG et avec le système piézo-électrique. Afin de s’assurer de la robustesse du système nous avons soumis les animaux à deux photopériodes différentes (12/12 et 16/8) conduisant à un changement de temps total de sommeil (n = 7 par groupe). Le temps total de sommeil (%/24 h) sur les 7 jours d’enregistrement et le temps de sommeil (%/h) sur les dernières 24 heures d’enregistrements n’étaient pas différents entre les méthodes et cela pour les deux photopériodes. Les deux méthodes ont détecté un temps de sommeil total plus élevé pour la photopériode 16/8 comparée à la photopériode 12/12 (p < .05), et significativement corrélée (p < .001) aux périodes de lumière et d’obscurité au cours de chaque photopériode. La précision pour l’identification des périodes de veille-sommeil entre les méthodes est de 81,9 % pour la photopériode 12/12 et de 84,9 % pour la photopériode 16/8. De plus, l’analyse spectrale du signal respiratoire enregistré avec le système piézo-électrique correspondant au période de sommeil lent et de sommeil paradoxal identifié par électroencéphalogramme/électromyogramme a abouti à la sélection de 36 caractéristiques que nous avons utilisées pour classifier les périodes de sommeil lent et de sommeil paradoxal grâce à un algorithme d’apprentissage supervisé et nous avons obtenu une précision de 90 %. Le système piézo-électrique est une méthode non-invasive fiable pour étudier le sommeil du rat.

Summary The piezoelectric cage‐floor sensors have been used to successfully dissect sleep patterns in mice based on signal features related to respiration and body movements. We studied performance of the piezoelectric system to quantify the sleep–wake pattern in the rat over 7 days of recording compared with a visual electroencephalogram/electromyogram scoring, and under two light/dark (LD12:12 and LD16:8) photoperiods leading to change in the 24‐hr sleep characteristics ( N = 7 per group). The total sleep time (%/24 hr) over the 7 days recording and hourly sleep time over the last 24‐hr recording were not statistically different between methods under the two photoperiods. Both methods detected higher total sleep time with the LD16:8 photoperiod compared with LD12:12 ( p < .05), and correlated significantly ( p < .001) at light and dark periods during each photoperiod. The accuracies for discrimination of sleep–wake patterns between methods were 81.9% and 84.9% for LD12:12 and LD16:8, respectively. In addition, spectral analysis of the respiratory signal given by piezo during all 10‐s periods of the corresponding non‐rapid eye movement and rapid eye movement sleep periods recorded by electroencephalogram/electromyogram resulted in selection of 36 features that could be inserted in an automated non‐rapid eye movement sleep and rapid eye movement sleep classification, with 90% accuracy with the electroencephalogram/electromyogram visual scoring. The piezo system proved to be a reliable non‐invasive alternative to electroencephalogram recording to study total sleep time in rat, with feasibility to discriminate between non‐rapid eye movement and rapid eye movement sleep stages. This will be interesting in pharmacological or bio‐behavioural studies evaluating sleep patterns or the restorative functions of sleep in the body and the brain.

Objectives: Athletes and military personnel may experience sleep disturbances due to conditions of training and competitions or military missions/field operations. The risk of muscle injuries is greater for them when sleep duration decreases, and training load increases simultaneously, which can be exacerbated by fatigue. Accumulating evidence demonstrates that sleep extension improved performance, pain sensitivity and GH/IGF-I anabolic responses, which may be beneficial in accelerating recovery from muscle injuries. Design & Methods: This narrative review describes the importance of sleep for the recovery/prevention of exercise-induced muscle injuries and provides perspectives on the transferability of currently available scientific evidence to the field. Results: The first part presents the role of sleep and its interaction with the circadian system for the regulation of hormonal and immune responses, and provides information on sleep in athletes and soldiers and its relationship to injury risk. The second part is an overview of muscle injuries in sport and presents the different phases of muscle regeneration and repair, i.e. degeneration, inflammation, regeneration, remodeling and maturation. Part three provides information on the deleterious effects of sleep deprivation on muscle tissue and biological responses, and on the benefits of sleep interventions. Sleep extension could potentially help and/or prevent recovery from exercise-induced muscle-injuries through increasing local IGF-I and controlling local inflammation. Conclusions: Although the science of sleep applied to sport is still an emerging field, the current scientific literature shows many potential physiological pathways between sleep and exercise-related muscle injuries. More direct studies are needed to establish clear guidelines for medical personnel and coaches. (c) 2021 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.