Optimising sounds for the driving of sleep oscillations by closed-loop auditory stimulation.

Recent studies have shown that slow oscillations (SOs) can be driven by rhythmic auditory stimulation, which deepens slow-wave sleep (SWS) and improves memory and the immune-supportive hormonal milieu related to this sleep stage. While different attempts have been made to optimise the driving of the SOs by changing the number of click stimulations, no study has yet investigated the impact of applying more than five clicks in a row. Likewise, the importance of the type of sounds in eliciting brain responses is presently unclear. In a study of 12 healthy young participants (10 females; aged 18-26 years), we applied an established closed-loop stimulation method, which delivered sequences of 10 pink noises, 10 pure sounds (B note of 247 Hz), 10 pronounced "a" vowels, 10 sham, 10 variable sounds, and 10 "oddball" sounds on the up phase of the endogenous SOs. By analysing area under the curve, amplitude, and event related potentials, we explored whether the nature of the sound had a differential effect on driving SOs. We showed that every stimulus in a 10-click sequence, induces a SO response. Interestingly, all three types of sounds that we tested triggered SOs. However, pink noise elicited a more pronounced response compared to the other sounds, which was explained by a broader topographical recruitment of brain areas. Our data further suggest that varying the sounds may partially counteract habituation.

Lengthening of the photoperiod influences sleep characteristics before and during total sleep deprivation in rat.

The photoperiod has been evidenced to influence sleep regulation in the rat. Nevertheless, lengthening of the photoperiod beyond 30 days seems to have little effect on the 24-hr baseline level of sleep and the response to total sleep deprivation. We studied the effects of 12:12 (habitual) and 16:8 (long) light-dark photoperiods on sleep, locomotor activity and body core temperature, before and after 24 hr of total sleep deprivation. Eight rats were submitted for 14 days to light-dark 12:12 (lights on: 08:00 hours-20:00 hours) followed by total sleep deprivation, and then for 14 days to light-dark 16:8 (light extended to 24:00 hours) followed by total sleep deprivation. Rats were simultaneously recorded for electroencephalogram, locomotor activity and body core temperature for 24 hr before and after total sleep deprivation. At baseline before total sleep deprivation, total sleep time and non-rapid eye movement sleep per 24 hr and during extended light hours (20:00 hours-24:00 hours) were higher (13% for total sleep time) after light-dark exposure compared with habitual photoperiod, while percentage delta power in non-rapid eye movements and rapid eye movements were unchanged. Locomotor activity and body core temperature were lower, particularly during extended light hours (20:00 hours-24:00 hours). Following total sleep deprivation, total sleep time and non-rapid eye movements were significantly lower after long photoperiod between 20:00 hours and 24:00 hours, and between 10:00 hours and 12:00 hours, and unchanged per 24 hr. The percentage delta power in non-rapid eye movements was lower between 08:00 hours and 11:00 hours. Total sleep deprivation decreased locomotor activity and body core temperature after habitual photoperiod exposure only. Fourteen days under long photoperiod (light-dark 16:8) increased non-rapid eye movements sleep, and decreased sleep rebound related to total sleep deprivation (lower non-rapid eye movements duration and delta power). This may create a model of sleep extension for the rat that has been found to favour anabolism in the brain and the periphery.

Effects of high-altitude exposure on supraspinal fatigue and corticospinal excitability and inhibition.

PURPOSE: While acute hypoxic exposure enhances exercise-induced central fatigue and can alter corticospinal excitability and inhibition, the effect of prolonged hypoxic exposure on these parameters remains to be clarified. We hypothesized that 5 days of altitude exposure would (i) normalize exercise-induced supraspinal fatigue during isolated muscle exercise to sea level (SL) values and (ii) increase corticospinal excitability and inhibition. METHODS: Eleven male subjects performed intermittent isometric elbow flexions at 50% of maximal voluntary contraction to task failure at SL and after 1 (D1) and 5 (D5) days at 4350 m. Transcranial magnetic stimulation and peripheral electrical stimulation were used to assess supraspinal and peripheral fatigues. Pre-frontal cortex and biceps brachii oxygenation was monitored by near-infrared spectroscopy. RESULTS: Exercise duration was not statistically different between SL (1095 ± 562 s), D1 (1132 ± 516 s), and D5 (1440 ± 689 s). No significant differences were found between the three experimental conditions in maximal voluntary activation declines at task failure (SL -16.8 ± 9.5%; D1 -25.5 ± 11.2%; D5 -21.8 ± 7.0%; p > 0.05). Exercise-induced peripheral fatigue was larger at D5 versus SL (100 Hz doublet at task failure: -58.8 ± 16.6 versus -41.8 ± 20.1%; p < 0.05). Corticospinal excitability at 50% maximal voluntary contraction was lower at D5 versus SL (brachioradialis p < 0.05, biceps brachii p = 0.055). Cortical silent periods were shorter at SL versus D1 and D5 (p < 0.05). CONCLUSIONS: The present results show similar patterns of supraspinal fatigue development during isometric elbow flexions at SL and after 1 and 5 days at high altitude, despite larger amount of peripheral fatigue at D5, lowered corticospinal excitability and enhanced corticospinal inhibition at altitude.

Changes of Cerebral and/or Peripheral Adenosine A1 Receptor and IGF-I Concentrations under Extended Sleep Duration in Rats.

Extended sleep improves sustained attention and reduces sleep pressure in humans. Downregulation of adenosine A1 receptor (A1R) and modulation of the neurotrophic factor insulin growth factor-1 (IGF-I) in brain structures controlling attentional capacities could be involved. In the frontal cortex and hippocampus of rats, we measured adenosine A1R and IGF-I protein concentrations after photoperiod-induced sleep extension. Two groups of twelve rats were adapted over 14 days to a habitual (CON) 12:12 light-dark (LD) schedule and an extended (EXT) 16:8 LD schedule. IGF-I content was also measured in plasma, liver, and skeletal muscle. In EXT, compared to CON rats, A1R content in the frontal cortex was significantly lower (p < 0.05), while IGF-I content was higher (p < 0.001), and no significant change was observed in the hippocampus. IGF-I content in plasma and muscle was higher (p < 0.001 and p < 0.01), while it was lower in liver (p < 0.001). The absolute weight and weight gain were higher in EXT rats (p < 0.01). These data suggest that 14 days under a 16:8 LD photoperiod respectively down- and upregulated cortical A1R and IGF-I levels. This photoperiod induced an anabolic profile with increased weight gain and circulating and muscular IGF-I levels. An extension of sleep duration might favor cerebral and peripheral anabolism, which may help attentional and physical capacities.

Achilles tendon vibration-induced changes in plantar flexor corticospinal excitability.

Daily Achilles tendon vibration has been shown to increase muscle force, likely via corticospinal neural adaptations. The aim of the present study was to determine the extent by which corticospinal excitability is influenced during direct Achilles tendon vibration. Motor-evoked potentials (MEPs) were elicited in the soleus (SOL), gastrocnemius medialis (GM) and tibialis anterior (TA) by transcranial magnetic stimulation of the motor cortical area of the leg with and without Achilles tendon vibration at various frequencies (50, 80 and 110 Hz). Contralateral homologues were also investigated. SOL and GM MEP amplitude significantly increased by 226 ± 188 and 66 ± 39%, respectively, during Achilles tendon vibration, without any difference between the tested frequencies. No MEP changes were reported for TA or contralateral homologues. Increased SOL and GM MEP amplitude suggests increased vibration-induced corticospinal excitability independent of vibration frequency.

Modulation of soleus corticospinal excitability during Achilles tendon vibration.

Soleus (SOL) corticospinal excitability has been reported to increase during Achilles tendon vibration. The aim of the present study was to further investigate SOL corticospinal excitability and elucidate the changes to intracortical mechanisms during Achilles tendon vibration. Motor-evoked potentials (MEPs) were elicited in the SOL by transcranial magnetic stimulation (TMS) of the corresponding motor cortical area of the leg with and without 50-Hz Achilles tendon vibration. SOL input-output curves were determined. Paired-pulse protocols were also performed to investigate short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) by conditioning test TMS pulses with sub-threshold TMS pulses at inter-stimulus intervals of 3 and 13 ms, respectively. During Achilles tendon vibration, motor threshold was lower than in the control condition (43 ± 13 vs. 49 ± 11 % of maximal stimulator output; p = 0.008). Input-output curves were also influenced by vibration, i.e. there was increased maximal MEP amplitude (0.694 ± 0.347 vs. 0.268 ± 0.167 mV; p < 0.001), decreased TMS intensity to elicit a MEP of half the maximal MEP amplitude (100 ± 13 vs. 109 ± 9 % motor threshold; p = 0.009) and a strong tendency for decreased slope constant (0.076 ± 0.04 vs. 0.117 ± 0.04; p = 0.068). Vibration reduced ICF (98 ± 61 vs. 170 ± 105 % of test MEP amplitude; p = 0.05), but had no effect on SICI (53 ± 26 vs. 48 ± 22 % of test MEP amplitude; p = 0.68). The present results further document the increased vibration-induced corticospinal excitability in the soleus muscle and suggest that this increase is not mediated by changes in SICI or ICF.

Impact reduction during running: efficiency of simple acute interventions in recreational runners.

Running-related stress fractures have been associated with the overall impact intensity, which has recently been described through the loading rate (LR). Our purpose was to evaluate the effects of four acute interventions with specific focus on LR: wearing racing shoes (RACE), increasing step frequency by 10 % (FREQ), adopting a midfoot strike pattern (MIDFOOT) and combining these three interventions (COMBI). Nine rearfoot-strike subjects performed five 5-min trials during which running kinetics, kinematics and spring-mass behavior were measured for ten consecutive steps on an instrumented treadmill. Electromyographic activity of gastrocnemius lateralis, tibialis anterior, biceps femoris and vastus lateralis muscles was quantified over different phases of the stride cycle. LR was significantly and similarly reduced in MIDFOOT (37.4 ± 7.20 BW s(-1), -56.9 ± 50.0 %) and COMBI (36.8 ± 7.15 BW s(-1), -55.6 ± 29.2 %) conditions compared to NORM (56.3 ± 11.5 BW s(-1), both P < 0.001). RACE (51.1 ± 9.81 BW s(-1)) and FREQ (52.7 ± 11.0 BW s(-1)) conditions had no significant effects on LR. Running with a midfoot strike pattern resulted in a significant increase in gastrocnemius lateralis pre-activation (208 ± 97.4 %, P < 0.05) and in a significant decrease in tibialis anterior EMG activity (56.2 ± 15.5 %, P < 0.05) averaged over the entire stride cycle. The acute attenuation of foot-ground impact seems to be mostly related to the use of a midfoot strike pattern and to a higher pre-activation of the gastrocnemius lateralis. Further studies are needed to test these results in prolonged running exercises and in the long term.

Strategies to Limit Cognitive Impairments under Sleep Restriction: Relationship to Stress Biomarkers.

Adding relaxation techniques during nap or auditory stimulation of EEG slow oscillation (SO) during nighttime sleep may limit cognitive impairments in sleep-deprived subjects, potentially through alleviating stress-releasing effects. We compared daytime sleepiness, cognitive performances, and salivary stress biomarker responses in 11 volunteers (aged 18-36) who underwent 5 days of sleep restriction (SR, 3 h per night, with 30 min of daily nap) under three successive conditions: control (SR-CT), relaxation techniques added to daily nap (SR-RT), and auditory stimulation of sleep slow oscillations (SO) during nighttime sleep (SR-NS). Test evaluation was performed at baseline (BASE), the fifth day of chronic SR (SR5), and the third and fifth days after sleep recovery (REC3, REC5, respectively). At SR5, less degradation was observed for percentage of commission errors in the executive Go-noGo inhibition task in SR-RT condition compared to SR-CT, and for sleepiness score in SR-NS condition compared both to SR-CT and SR-RT. Beneficial effects of SR-RT and SR-NS were additionally observed on these two parameters and on salivary α-amylase (sAA) at REC3 and REC5. Adding relaxation techniques to naps may help performance in inhibition response, and adding nocturnal auditory stimulation of SO sleep may benefit daytime sleepiness during sleep restriction with persistent effects during recovery. The two strategies activated the autonomic nervous system, as shown by the sAA response.

Acoustic stimulation time-locked to the beginning of sleep apnea events reduces oxygen desaturations: a pilot-study.

STUDY OBJECTIVES: We aimed to determine whether bone-conducted acoustic stimulation could prematurely terminate sleep apnea events, thereby decreasing amplitude and duration of subsequent oxygen desaturation. As oxygen desaturation has been linked to cardiovascular consequences, we postulate this could be a viable therapy in some cases. METHODS: Eight patients with severe Obstructive Sleep Apnea (2 women, 45 [20-68] y.o. Apnea-Hypopnea Index: 77.7 ± 22.3/h) underwent polysomnography at the Lausanne University Sleep Center. Short acoustic stimulations were administered by bone conduction every second event of sleep apnea. Sounds were remotely administered using a Dreem® headband worn by patients while undergoing nocturnal polysomnography. Amplitude (%) and duration(s) of oxygen desaturations following terminated apneas were compared to that of non-stimulated previous and subsequent events. RESULTS: 549 stimulations (68.6 ± 38 sounds per patient) in N1 (16.2%), N2 (69.9%), N3 (4.2%), and REM(9.6%) were conducted. Compared to the previous and subsequent non-stimulated apnea, stimulations reduced event duration by 21.4% (-3.4 ± 7.2 s, p < 0.0001) while oxygen desaturation amplitude and duration were reduced by 30.4% (mean absolute difference ± SD: -1.9 ± 2.8%, p < 0.0001), and 39.6% (-5.7 ± 9.2 s, p < 0.0001) respectively. For these variables, each patient showed a significant improvement following acoustic stimulation. Sound-associated discomfort was rated 1.14 ± 1.53 on an 8 points scale (8 = worst) and only 6.8% of emitted sounds were perceived by the patients, suggesting a well-tolerated intervention. CONCLUSIONS: Bone-conducted sound stimuli decreased apnea events duration as well as duration and amplitude of associated oxygen desaturations. Stimulations were well tolerated and rarely perceived by patients. This therapeutic approach deserves further investigation, with monitoring of effects on sleep quality, daytime function/sleepiness and cardiovascular parameters.

Greatest changes in objective sleep architecture during COVID-19 lockdown in night owls with increased REM sleep.

STUDY OBJECTIVES: The COVID-19 pandemic has had dramatic effects on society and people's daily habits. In this observational study, we recorded objective data on sleep macro- and microarchitecture repeatedly over several nights before and during the COVID-19 government-imposed lockdown. The main objective was to evaluate changes in patterns of sleep duration and architecture during home confinement using the pre-confinement period as a control. METHODS: Participants were regular users of a sleep-monitoring headband that records, stores, and automatically analyzes physiological data in real time, equivalent to polysomnography. We measured sleep onset duration, total sleep time, duration of sleep stages (N2, N3, and rapid eye movement [REM]), and sleep continuity. Via the user's smartphone application, participants filled in questionnaires on how lockdown changed working hours, eating behavior, and daily life at home. They also filled in the Insomnia Severity Index, reduced Morningness-Eveningness Questionnaire, and Hospital Anxiety and Depression Scale questionnaires, allowing us to create selected subgroups. RESULTS: The 599 participants were mainly men (71%) of median age 47 (interquartile range: 36-59). Compared to before lockdown, during lockdown individuals slept more overall (mean +3·83 min; SD: ±1.3), had less deep sleep (N3), more light sleep (N2), and longer REM sleep (mean +3·74 min; SD: ±0.8). They exhibited less weekend-specific changes, suggesting less sleep restriction during the week. Changes were most pronounced in individuals reporting eveningness preferences, suggesting relative sleep deprivation in this population and exacerbated sensitivity to societal changes. CONCLUSION: This unique dataset should help us understand the effects of lockdown on sleep architecture and on our health.

The Dreem Headband compared to polysomnography for electroencephalographic signal acquisition and sleep staging.

STUDY OBJECTIVES: The development of ambulatory technologies capable of monitoring brain activity during sleep longitudinally is critical for advancing sleep science. The aim of this study was to assess the signal acquisition and the performance of the automatic sleep staging algorithms of a reduced-montage dry-electroencephalographic (EEG) device (Dreem headband, DH) compared to the gold-standard polysomnography (PSG) scored by five sleep experts. METHODS: A total of 25 subjects who completed an overnight sleep study at a sleep center while wearing both a PSG and the DH simultaneously have been included in the analysis. We assessed (1) similarity of measured EEG brain waves between the DH and the PSG; (2) the heart rate, breathing frequency, and respiration rate variability (RRV) agreement between the DH and the PSG; and (3) the performance of the DH's automatic sleep staging according to American Academy of Sleep Medicine guidelines versus PSG sleep experts manual scoring. RESULTS: The mean percentage error between the EEG signals acquired by the DH and those from the PSG for the monitoring of α was 15 ± 3.5%, 16 ± 4.3% for ß, 16 ± 6.1% for λ, and 10 ± 1.4% for θ frequencies during sleep. The mean absolute error for heart rate, breathing frequency, and RRV was 1.2 ± 0.5 bpm, 0.3 ± 0.2 cpm, and 3.2 ± 0.6%, respectively. Automatic sleep staging reached an overall accuracy of 83.5 ± 6.4% (F1 score: 83.8 ± 6.3) for the DH to be compared with an average of 86.4 ± 8.0% (F1 score: 86.3 ± 7.4) for the 5 sleep experts. CONCLUSIONS: These results demonstrate the capacity of the DH to both monitor sleep-related physiological signals and process them accurately into sleep stages. This device paves the way for, large-scale, longitudinal sleep studies. CLINICAL TRIAL REGISTRATION: NCT03725943.

Beneficial effects of exercise training on cognitive performances during total sleep deprivation in healthy subjects.

OBJECTIVE: Exercise training has been shown to improve learning and memory, and to protect against the negative impact of sleep deprivation. The aim of this study was to investigate the effects of seven weeks of moderate- and high-intensity interval exercise training on vigilance/sustained attention, inhibition processes and working memory during 40-h total sleep deprivation (TSD) in 16 healthy young men. METHODS: The subjects were evaluated before (Baseline, BAS) and during TSD, and the day after a night of recovery sleep (Recovery, REC). RESULTS: Exercise training significantly decreased errors and increased speed assessed by the psychomotor vigilance task (PVT) during TSD and REC while no difference was found in executive inhibition (Go-noGo task) and working memory (2-Back task) performances. The multiple sleep latency test results were higher during BAS and REC at Post-exercise training, and no difference occurred in subjective sleepiness and daytime microsleeps over the 40-h TSD. The PVT speed was positively correlated with maximal oxygen consumption and maximal aerobic power measured before entry in the in-laboratory TSD protocol, and stage 3 sleep duration measured during the first night in the in-laboratory TSD protocol (N-1). Exercise training effects on sleep were found during the night recovery with lower stage-3 sleep and higher rapid eye movement (REM) sleep durations. An exercise training effect was also found on free insulin-like growth factor I levels with lower levels during TSD at Post-exercise training. CONCLUSIONS: In healthy young men, exercise training reduced sleep pressure at baseline and protected against sustained attention deficits induced by TSD with persistent effect after one night of recovery sleep. Nevertheless, exercise training was not effective in reducing deficits in executive inhibition and working memory induced by TSD.

AI vs Humans for the diagnosis of sleep apnea.

Polysomnography (PSG) is the gold standard for diagnosing sleep obstructive apnea (OSA). It allows monitoring of breathing events throughout the night. The detection of these events is usually done by trained sleep experts. However, this task is tedious, highly time-consuming and subject to important inter-scorer variability. In this study, we adapted our state-of-the-art deep learning method for sleep event detection, DOSED, to the detection of sleep breathing events in PSG for the diagnosis of OSA. We used a dataset of 52 PSG recordings with apnea-hypopnea event scoring from 5 trained sleep experts. We assessed the performance of the automatic approach and compared it to the inter-scorer performance for both the diagnosis of OSA severity and, at the microscale, for the detection of single breathing events. We observed that human sleep experts reached an average accuracy of 75% while the automatic approach reached 81% for sleep apnea severity diagnosis. The F1 score for individual event detection was 0.55 for experts and 0.57 for the automatic approach, on average. These results demonstrate that the automatic approach can perform at a sleep expert level for the diagnosis of OSA.

Limited Benefit of Sleep Extension on Cognitive Deficits During Total Sleep Deprivation: Illustration With Two Executive Processes.

Introduction: Sleep extension has been associated with better alertness and sustained attention capacities before, during and after sleep loss. However, less is known about such beneficial effect on executive functions (EFs). Our aim was to investigate such effects on two EFs (i.e., inhibition and working memory) for subjects submitted to total sleep deprivation and one-night of recovery. Methods: Fourteen healthy men (26-37 years old) participated in an experimental cross-over design with two conditions: extended sleep (EXT, 9.8 ± 0.1 h of Time In Bed, TIB) and habitual sleep (HAB, 8.2 ± 0.1 h TIB). During these two conditions subjects underwent two consecutive phases: Six nights of either EXT or HAB followed by 3 days in-laboratory: baseline (BASE), TSD (38 h) and after recovery (REC). EFs capacities were assessed through Go-NoGo (inhibition) and 2N-Back (working memory) tasks. Both EFs capacities were measured at different time (BASE/TSD/REC: 09:30, 13:00, 16:00; TSD: 21:00, 00:00, 03:00, 06:30). Results: In both conditions (HAB and EXT), TSD was associated with deficits in inhibition (higher errors and mean reaction time from TSD 09:30 until the end; p < 0.05) and working memory (lower corrects responses from TSD 06:30 or 09:30; p < 0.05). We observed no significant differences between HAB and EXT conditions on EFs capacities during BASE, TSD, and REC periods. Conclusion: Six nights of sleep extension is neither efficient to reduce core EFs deficits related to TSD nor to improve such capacities after a recovery night. These results highlight that sleep extension (six nights of 10 h of TIB) is not effective to limit EFs deficits related to TSD suggesting a disconnection inside cognition between executive and sustained attention processes. Clinical Trials: NCT02352272.

A Deep Learning Architecture for Temporal Sleep Stage Classification Using Multivariate and Multimodal Time Series.

Sleep stage classification constitutes an important preliminary exam in the diagnosis of sleep disorders. It is traditionally performed by a sleep expert who assigns to each 30 s of the signal of a sleep stage, based on the visual inspection of signals such as electroencephalograms (EEGs), electrooculograms (EOGs), electrocardiograms, and electromyograms (EMGs). We introduce here the first deep learning approach for sleep stage classification that learns end-to-end without computing spectrograms or extracting handcrafted features, that exploits all multivariate and multimodal polysomnography (PSG) signals (EEG, EMG, and EOG), and that can exploit the temporal context of each 30-s window of data. For each modality, the first layer learns linear spatial filters that exploit the array of sensors to increase the signal-to-noise ratio, and the last layer feeds the learnt representation to a softmax classifier. Our model is compared to alternative automatic approaches based on convolutional networks or decisions trees. Results obtained on 61 publicly available PSG records with up to 20 EEG channels demonstrate that our network architecture yields the state-of-the-art performance. Our study reveals a number of insights on the spatiotemporal distribution of the signal of interest: a good tradeoff for optimal classification performance measured with balanced accuracy is to use 6 EEG with 2 EOG (left and right) and 3 EMG chin channels. Also exploiting 1 min of data before and after each data segment offers the strongest improvement when a limited number of channels are available. As sleep experts, our system exploits the multivariate and multimodal nature of PSG signals in order to deliver the state-of-the-art classification performance with a small computational cost.

Sleep habits and strategies of ultramarathon runners.

Among factors impacting performance during an ultramarathon, sleep is an underappreciated factor that has received little attention. The aims of this study were to characterize habitual sleep behaviors in ultramarathon runners and to examine strategies they use to manage sleep before and during ultramarathons. Responses from 636 participants to a questionnaire were considered. This population was found to sleep more on weekends and holidays (7-8 h to 8-9 h) than during weekdays (6-7 h to 7-8 h; p < 0.001). Work was a mediator of napping habits since 19-25% reported napping on work days and 37-56% on non-work days. There were 24.5% of the participants reporting sleep disorders, with more women (38.9%) reporting sleep problems than men (22.0%; p < 0.005). Mean (±SD) sleepiness score on the Epworth Sleepiness Scale was 8.9 ± 4.3 with 37.6% of respondents scoring higher than 10, reflecting excessive daytime sleepiness. Most of the study participants (73.9%) had a strategy to manage sleep preceding an ultramarathon, with 54.7% trying to increase their opportunities for sleep. Only 21% of participants reported that they had a strategy to manage sleep during ultramarathons, with micronaps being the most common strategy specified. Sub-analyses from 221 responses indicated that sleep duration during an ultramarathon was correlated with finish time for races lasting 36-60 h (r = 0.48; p < 0.01) or > 60 h (r = 0.44; p < 0.001). We conclude that sleep duration among ultramarathon runners was comparable to the general population and other athletic populations, yet they reported a lower prevalence of sleep disorders. Daytime sleepiness was among the lowest rates encountered in athletic populations, which may be related to the high percentage of nappers in our population. Sleep extension, by increasing sleep time at night and daytime napping, was the main sleep strategy to prepare for ultramarathons.

Sprint Acceleration Mechanics in Fatigue Conditions: Compensatory Role of Gluteal Muscles in Horizontal Force Production and Potential Protection of Hamstring Muscles.

Aim: Hamstring muscle injury is the main injury related to sports requiring sprint acceleration. In addition, hamstring muscles have been reported to play a role in horizontal force production during sprint acceleration performance. The aim of the present study was to analyze (i) the determinants of horizontal force production and (ii) the role of hip extensors, and hamstring muscles in particular, for horizontal force production during repeated sprint-induced fatigue conditions. Method: In this experimental laboratory setting study including 14 sprint-trained male athletes, we analyzed (i) the changes in sprint mechanics, peak torque of the knee and hip extensors and flexors, muscle activity of the vastus lateralis, rectus femoris, biceps femoris, and gluteus, and sagittal plane lower limb motion, before and after twelve 6-s sprints separated by 44 s rest on an instrumented motorized treadmill, and (ii) the determinants of horizontal force production (FH ) during the sprint acceleration in a fatigue state (after 12 sprints). Results: The repeated-sprint protocol induced a decrease in maximal power output (Pmax) [-17.5 ± 8.9%; effect size (ES): 1.57, large] and in the contact-averaged horizontal force component (FH ) (-8.6 ± 8.4%; ES: 0.86, moderate) but not meaningful changes in the contact-averaged resultant (total) force (FTot ) (-3.4 ± 2.9%; ES: 0.55, small) and vertical force component (FV ) (-3.1 ± 3.2%; ES: 0.49, small). A decrease was found in concentric peak torque of the knee flexors and extensors and in gluteus and vastus lateralis muscle activity during entire swing and end-of-swing phase. An increase was found in contact time and swing time, while step frequency and knee speed before ground contact decreased. Muscular determinants associated with FH and its decrease after the repeated-sprint protocol were concentric peak torque of the hip extensors (p = 0.033) and a decrease in gluteus maximus activity at the end-of-swing (p = 0.007), respectively. Conclusion: Sprint-induced fatigue lead to changes in horizontal force production muscular determinants: hamstring muscle seems not to have the same role than in non-fatigue condition. Horizontal force production seems to be more dependent on the hip extensors and gluteus maximus function. Given the fatigue-induced decrease in hamstring muscle strength, we can hypothesize that muscle compensatory and kinematic strategies reported in a fatigued state could be an adaptation to allow/maintain performance and a protective adaptation to limit hamstring muscles constraints.

Performance of an Ambulatory Dry-EEG Device for Auditory Closed-Loop Stimulation of Sleep Slow Oscillations in the Home Environment.

Recent research has shown that auditory closed-loop stimulation can enhance sleep slow oscillations (SO) to improve N3 sleep quality and cognition. Previous studies have been conducted in lab environments. The present study aimed to validate and assess the performance of a novel ambulatory wireless dry-EEG device (WDD), for auditory closed-loop stimulation of SO during N3 sleep at home. The performance of the WDD to detect N3 sleep automatically and to send auditory closed-loop stimulation on SO were tested on 20 young healthy subjects who slept with both the WDD and a miniaturized polysomnography (part 1) in both stimulated and sham nights within a double blind, randomized and crossover design. The effects of auditory closed-loop stimulation on delta power increase were assessed after one and 10 nights of stimulation on an observational pilot study in the home environment including 90 middle-aged subjects (part 2).The first part, aimed at assessing the quality of the WDD as compared to a polysomnograph, showed that the sensitivity and specificity to automatically detect N3 sleep in real-time were 0.70 and 0.90, respectively. The stimulation accuracy of the SO ascending-phase targeting was 45 ± 52°. The second part of the study, conducted in the home environment, showed that the stimulation protocol induced an increase of 43.9% of delta power in the 4 s window following the first stimulation (including evoked potentials and SO entrainment effect). The increase of SO response to auditory stimulation remained at the same level after 10 consecutive nights. The WDD shows good performances to automatically detect in real-time N3 sleep and to send auditory closed-loop stimulation on SO accurately. These stimulation increased the SO amplitude during N3 sleep without any adaptation effect after 10 consecutive nights. This tool provides new perspectives to figure out novel sleep EEG biomarkers in longitudinal studies and can be interesting to conduct broad studies on the effects of auditory stimulation during sleep.

Leukocyte Expression of Type 1 and Type 2 Purinergic Receptors and Pro-Inflammatory Cytokines during Total Sleep Deprivation and/or Sleep Extension in Healthy Subjects.

The purinergic type P1 (adenosine A1 and A2A) receptors and the type P2 (X7) receptor have been suggested to mediate physiological effects of adenosine and adenosine triphosphate on sleep. We aimed to determine gene expression of A1R (receptor), A2AR, and P2RX7 in leukocytes of healthy subjects during total sleep deprivation followed by sleep recovery. Expression of the pro-inflammatory cytokines IL-1ß and TNF-α were also determined as they have been characterized as sleep regulatory substances, via P2RX7 activation. Blood sampling was performed on 14 young men (aged 31.9 ± 3.9) at baseline (B), after 24 h of sleep deprivation (24 h-SD), and after one night of sleep recovery (R). We compared gene expression levels after six nights of habitual (22.30-07.00) or extended (21.00-07.00) bedtimes. Using quantitative real-time PCR, the amount of mRNA for A1R, A2AR, P2RX7, TNF-α, and IL-1ß was analyzed. After 24 h-SD compared to B, whatever prior sleep condition, a significant increase of A2AR expression was observed that returned to basal level after sleep recovery [day main effect, F(2, 26) = 10.8, p < 0.001]. In both sleep condition, a day main effect on P2RX7 mRNA was observed [F(2, 26) = 6.7, p = 0.005] with significant increases after R compared with 24 h-SD. TNF-α and IL-1ß expressions were not significantly altered. Before 24 h-SD (baseline), the A2AR expression was negatively correlated with the latency of stage 3 sleep during the previous night, while that of the A1R positively. This was not observed after sleep recovery following 24 h-SD. This is the first study showing increased A2AR and not A1 gene expression after 24 h-SD in leukocytes of healthy subjects, and this even if bedtime was initially increased by 1.5 h per night for six nights. In conclusion, prolonged wakefulness induced an up-regulation of the A2A receptor gene expression in leukocytes from healthy subjects. Significant correlations between baseline expression of A1 and A2A receptors in peripheral cells and stage 3 sleep suggested their involvement in mediating the effects of adenosine on sleep.