Self-reported sleep quantity, quality and sleep hygiene in elite athletes.

Sleep is essential for recovery and performance in elite athletes. While actigraphy-based studies revealed suboptimal sleep in athletes, information on their subjective experience of sleep is scarce. Relatively unexplored is also the extent to which athletes' sleep is adversely affected by environmental conditions and daytime behaviours, that is sleep hygiene. This study aimed to provide insight in sleep quantity, quality and its putative association with sleep hygiene. Participants were 98 elite (youth) athletes competing at the highest (inter-)national level. Sleep quantity, quality and sleep hygiene were assessed once covering a 1-month period by using established (sub)clinical questionnaires, and repeatedly during 7 consecutive days. Sleep quality was generally healthy, although 41% of all athletes could be classified as 'poor sleeper', and 12% were identified as having a sleep disorder. Daily self-monitoring revealed sleep durations of 8:11 ± 0:45 h, but elevated wake after sleep onset of 13 ± 19 min. Sleep quality, feeling refreshed, and morning vigor were moderate at best. Regarding sleep hygiene, general measures revealed irregular sleep-wake patterns, psychological strain and activating pre-sleep behaviours. At the daily level, blue-light exposure and late-evening consumption of heavy meals were frequently reported. General sleep hygiene revealed significant associations with sleep quality (0.45 < r > 0.50; P < 0.001). Results indicate that there is ample room for optimization, specifically in onset latency and in wake after sleep onset. Subtle improvements in sleep seem possible, and optimizing sleep hygiene, such as regular sleep-wake patterns and reducing psychological strain, may facilitate this sleep upgrading process.

Effects of Natural Between-Days Variation in Sleep on Elite Athletes' Psychomotor Vigilance and Sport-Specific Measures of Performance.

Performance capacity in athletes depends on the ability to recover from past exercise. While evidence suggests that athletic performance decreases following (partial) sleep deprivation and increases following sleep extension, it is unclear to which extent natural variation in sleep impacts performance. Sleep quantity and, for the first time, sleep stages were assessed among 98 elite athletes on three non-consecutive nights within a 7-day monitoring period, along with performance tests that were taken on standardized times each following morning. Performance assessment included psychomotor performance (10-minute psychomotor vigilance task) and sport-specific tests of fine (e.g., accuracy) and gross motor skills (e.g., endurance, power). Mixed-effects models were employed to assess the effect of sleep quantity (total sleep time (TST), sleep onset latency (SOL), wake after sleep onset, sleep efficiency) and sleep stage duration (light, deep, REM) on performance. Average TST was 7:30 ± 1:05 hours, with a mean variation of 57 minutes across days. Longer TSTs were associated with faster reaction times (p = 0.04). Analyses indicated small and inconsistent effects of sleep quantity (TST, SOL) and sleep staging (light sleep) on gross motor performance, and no effects on fine motor skill performance. Results indicate that natural variation in sleep quantity impacts psychomotor vigilance to a greater extent than athletic performance. Small or absent effects can be a consequence of the rather small variation in non-manipulated sleep. It is suggested that one night of compromised sleep may not be immediately problematic, but that more extreme sleep loss or accumulated sleep debt may have more severe consequences.

Sleep disturbances are associated with reduced health-related quality of life in patients with substance use disorders.

BACKGROUND AND OBJECTIVES: Sleep problems and substance use are strongly linked. Sleep problems play a role in the etiology of substance use, but also may be a result of it. After detoxification, sleep problems may worsen leading to relapse. Nowadays, most substance dependence treatment programs aim at recovery rather than total abstinence, and in that view health-related quality of life (HRQL) is a relevant construct. This article describes the association between self-perceived sleep problems and HRQL in a naturalistic population of polydrug-using inpatients. METHODS: At the start of treatment, 388 polydrug-using inpatients completed questionnaires concerning their sleep quality and HRQL. Three categories were established based on reported sleep problems: patients without sleep problems (21.6%), those with clinically relevant sleep problems (34.5%), and patients with sleep disorders (43.8%). RESULTS: Mean grades for quality of sleep were M = 7.3 (sd 1.7), M = 6.6 (sd 1.7) and M = 5.3 (sd 1.9) for the three categories, respectively. In addition, patients in the disorder category perceived a lower HRQL than those in the other categories. In the explanation of HRQL, both sleep problems and sleep disorders added significantly to the model when controlling for baseline characteristics. DISCUSSION AND CONCLUSIONS: Our findings stress the need for clinicians to pay attention to the quality of sleep of recovering polydrug users, since this may play an important role in the recovery process. Monitoring sleep during treatment is advocated. This study adds to the knowledge about the way HRQL and sleep are related in a naturalistic sample of substance-dependent patients.

Dim light, sleep tight, and wake up bright - Sleep optimization in athletes by means of light regulation.

Despite an elevated recovery need, research indicates that athletes often exhibit relatively poor sleep. Timing and consolidation of sleep is driven by the circadian system, which requires periodic light-dark exposure for stable entrainment to the 24-hour day, but is often disturbed due to underexposure to light in the morning (e.g. low-level indoor lighting) and overexposure to light in the evening (e.g. environmental and screen-light). This study examined whether combining fixed sleep schedules with light regulation leads to more consolidated sleep. Morning light exposure was increased using light-emitting goggles, whereas evening light exposure was reduced using amber-lens glasses. Using a within-subject crossover design, twenty-six athletes (14 female, 12 male) were randomly assigned to start the intervention with the light-regulation-week or the no light-regulation-week. Sleep was monitored by means of sleep diaries and actigraphy. Due to low protocol adherence regarding the fixed sleep-wake schedules, two datasets were constructed; one including athletes who kept a strict sleep-wake schedule (N = 8), and one that also included athletes with a more lenient sleep-wake schedule (N = 25). In case of a lenient sleep-wake schedule, light regulation improved self-reported sleep onset latency (Δ SOL = 8 min). This effect was stronger (Δ SOL = 17 min) and complemented by enhanced subjective sleep quality in case of a strict sleep-wake schedule. None of the actigraphy-based estimates differed significantly between conditions. To conclude, light regulation may be considered a potentially effective strategy to improve subjective sleep, but less obtrusive methods should be explored to increase protocol compliance.

Influence of emotional arousal on the N150 of the Auditory Evoked Potential from the rat amygdala.

This study tested whether a general increase in emotional arousal is a sufficient determinant for the evocation of the N150, a negative wave in amygdalar Auditory Evoked Potentials (AEPs). Rats received one of three conditioning protocols: either conditioned stimulus (CS) presentations alone (Control) CS-shock pairings (Paired) or unpaired presentations of the CS and shock (Unpaired). Amygdalar AEPs were recorded in response to the CS. It was hypothesized that if a state of emotional arousal is a sufficient condition for the manifestation of the N150, its amplitude should be enhanced in the Paired and Unpaired conditions relative to the Control condition, which was indeed found. In addition, it was found that the N150 had a larger amplitude in the Paired than in the Unpaired condition. This suggests that an additional N150 increase is established when animals learn the CS-US association. The results are discussed in relation to literature on amygdala function.

The auditory P3 from passive and active three-stimulus oddball paradigm.

The aim of this study was the comparison of basic characteristics of the P3 subcomponents elicited in passive and active versions of the auditory oddball paradigm. A 3-stimulus oddball paradigm was employed in which subjects were presented with random sequence of tones while they performed a discrimination task in visual modality with no response to the tone (passive task) or responded to an infrequently occurring target stimulus inserted into sequence of frequent standard and rare non-target stimuli (active task). Results show that the magnitude of the frontal P3 response is determined by the relative perceptual distinctiveness among stimuli. The amplitude of frontal component is larger for the stimuli more deviated from the standard in both passive and active tasks. In all cases however, a maximum over central or fronto-central scalp regions was demonstrated. Moreover, amplitude of this component was influenced by the strength of attentional focus--a significantly larger response was obtained in the active session than in its passive counterpart. The apparent parietal P3 responses were obtained only in the active condition. The amplitude of this component is larger for the target than the non-target across all electrode sites, but both demonstrated a parietal maxima. This findings suggest that generation of early frontal P3 could be related to alerting activity of frontal cortex irrespective of stimulus context, while generation of later parietal P3 is related to temporo-parietal network activated when neuronal model of perceived stimulation and attentional trace are comparing.

Train hard, sleep well? Perceived training load, sleep quantity and sleep stage distribution in elite level athletes.

OBJECTIVES: Sleep is essential for recovery and performance in elite athletes. While it is generally assumed that exercise benefits sleep, high training load may jeopardize sleep and hence limit adequate recovery. To examine this, the current study assessed objective sleep quantity and sleep stage distributions in elite athletes and calculated their association with perceived training load. DESIGN: Mixed-methods. METHODS: Perceived training load, actigraphy and one-channel EEG recordings were collected among 98 elite athletes during 7 consecutive days of regular training. RESULTS: Actigraphy revealed total sleep durations of 7:50±1:08h, sleep onset latencies of 13±15min, wake after sleep onset of 33±17min and sleep efficiencies of 88±5%. Distribution of sleep stages indicated 51±9% light sleep, 21±8% deep sleep, and 27±7% REM sleep. On average, perceived training load was 5.40±2.50 (scale 1-10), showing large daily variability. Mixed-effects models revealed no alteration in sleep quantity or sleep stage distributions as a function of day-to-day variation in preceding training load (all p's>.05). CONCLUSIONS: Results indicate healthy sleep durations, but elevated wake after sleep onset, suggesting a potential need for sleep optimization. Large proportions of deep sleep potentially reflect an elevated recovery need. With sleep quantity and sleep stage distributions remaining irresponsive to variations in perceived training load, it is questionable whether athletes' current sleep provides sufficient recovery after strenuous exercise.

The P3 produced by auditory stimuli presented in a passive and active condition: modulation by visual stimuli.

The aim of this study was to investigate how the processing of auditory stimuli is affected by the simultaneous presentation of visual stimuli. This was approached in an active and passive condition, during which a P3 was elicited in the human EEG by single auditory stimuli. Subjects were presented tones, either alone or accompanied by the simultaneous exposition of pictures. There were two different sessions. In the first, the presented tones demanded no further cognitive activity from the subjects (passive or 'ignore' session), while in the second session subjects were instructed to count the tones (active or 'count' session). The central question was whether inter-modal influences of visual stimulation in the active condition would modulate the auditory P3 in the same way as in the passive condition. Brain responses in the ignore session revealed only a small P3-like component over the parietal and frontal cortex, however, when the auditory stimuli co-occurred with the visual stimuli, an increased frontal activity in the window of 300-500 ms was observed. This could be interpreted as the reflection of a more intensive involuntary attention shift, provoked by the preceding visual stimulation. Moreover, it was found that cognitive load caused by the count instruction, resulted in an evident P3, with maximal amplitude over parietal locations. This effect was smaller when auditory stimuli were presented on the visual background. These findings might support the thesis that available resources were assigned to the analysis of visual stimulus, and thus were not available to analyze the subsequent auditory stimuli. This reduction in allocation of resources for attention was restricted to the active condition only, when the matching of a template with incoming information results in a distinct P3 component. It is discussed whether the putative source of this effect is a change in the activity of the frontal cortex.

Tracking pattern learning with single-trial event-related potentials.

OBJECTIVE: The main aim was to track the dynamics of pattern-learning using single-trial event-related potentials (ERPs). A new 'learning-oddball' paradigm was employed presenting eight random targets (the 'no-pattern') followed by eight regular targets (the 'pattern'). In total, six repetitions of the 'no-pattern' followed by the 'pattern' were presented. METHODS: We traced the dynamics of learning by measuring responses to 16 (eight random-eight regular) targets. Since this alternation of the 'no-pattern' followed by the 'pattern' was repeated six times, we extracted single-trial responses to all 96 targets to determine if learning occurred more rapidly with each repetition of the 'pattern.' RESULTS: Following random targets, ERPs contained a marked P3-N2 component that decreased to regular targets, whereas a contingent negative variation (CNV) appeared. ERP changes could be best described by sigmoid 'learning' curves. Single-trial analyses showed that learning occurred more rapidly over repetitions and suggested that the CNV developed prior to the decay of the N2-P3 component. CONCLUSIONS: We show a new paradigm-analysis methodology to track learning processes directly from brain signals. SIGNIFICANCE: Single-trial ERPs analyses open a wide range of applications. Tracking the dynamic structure of cognitive functions may prove crucial in the understanding of learning and in the study of different pathologies.

Cortical focus drives widespread corticothalamic networks during spontaneous absence seizures in rats.

Absence seizures are the most pure form of generalized epilepsy. They are characterized in the electroencephalogram by widespread bilaterally synchronous spike-wave discharges (SWDs), which are the reflections of highly synchronized oscillations in thalamocortical networks. To reveal network mechanisms responsible for the initiation and generalization of the discharges, we studied the interrelationships between multisite cortical and thalamic field potentials recorded during spontaneous SWDs in the freely moving WAG/Rij rat, a genetic model of absence epilepsy. Nonlinear association analysis revealed a consistent cortical "focus" within the peri-oral region of the somatosensory cortex. The SWDs recorded at other cortical sites consistently lagged this focal site, with time delays that increased with electrode distance (corresponding to a mean propagation velocity of 1.4 m/sec). Intra-thalamic relationships were more complex and could not account for the observed cortical propagation pattern. Cortical and thalamic sites interacted bi-directionally, whereas the direction of this coupling could vary throughout one seizure. However, during the first 500 msec, the cortical focus was consistently found to lead the thalamus. These findings argue against the existence of one common subcortical pacemaker for the generation of generalized spike-wave discharges characteristic for absence seizures in the rat. Instead, the results suggest that a cortical focus is the dominant factor in initiating the paroxysmal oscillation within the corticothalamic loops, and that the large-scale synchronization is mediated by ways of an extremely fast intracortical spread of seizure activity. Analogous mechanisms may underlie the pathophysiology of human absence epilepsy.

Morphometric Golgi study of cortical locations in WAG/Rij rats: the cortical focus theory.

Recently it was demonstrated that for the absence epilepsy characteristic spike-wave discharges initially emerge from the somatosensory cortex and quickly involve the rest of the cortex and cortico-thalamic network. This has led to the development of the focal theory of absence epilepsy. In this experiment, this theory was further investigated by studying the neuronal organization of the cortical focal zone, a non-focal zone in genetic epileptic WAG/Rij rats and functional related areas in non-epileptic age matched control rats. A classical Golgi staining technique was used to visualize whole cortical neurons with dendritic and axon arborisation. Apical dendrites of pyramidal cells in epileptic rats were often split, declined and were running in non-perpendicular directions. Quantitative differences between the strains were found for the length of neurons, between focal and control areas mainly for dendritic arborization. A significant "strain-zone" interaction was found for the maximal distance between two points of dendritic arborization, the mean length of a dendritic segment and the number of free terminations of apical dendrites. All this demonstrates that properties of dendrites in the cortical focal area of WAG/Rij rats were at variance with dendritic characteristics outside the focal area and with functional similar areas in non-epileptic controls. These features might reflect the hyperexcitability of somatosensory neurons, which underlie the initiation and spreading of spike-wave discharges in WAG/Rij rats. Finally, these results are in line with the cortical focus theory of absence epilepsy.

Mental and physical effort affect vigilance differently.

Both physical and mental effort are thought to affect vigilance. Mental effort is known for its vigilance declining effects, but the effects of physical effort are less clear. This study investigated whether these two forms of effort affect the EEG and subjective alertness differently. Participants performed a physical task and were subsequently presented with a mental task, or vice versa. Mental effort decreased subjective alertness and increased theta power in the EEG. Both results suggest a vigilance decline. Physical effort, however, increased subjective alertness and alpha and beta1 power in the EEG. These findings point towards an increase in vigilance. Beta2 power was reduced after physical effort, which may reflect a decrease in active cognitive processing. No transfer effects were found between the effort conditions, suggesting that the effects of mental and physical effort are distinct. It is concluded that mental effort decreases vigilance, whereas physical effort increases vigilance without improving subsequent task performance.

Mammalian sleep may have no adaptive advantage over simple activity-rest cycles.

The adaptive value of sleep remains unknown in spite of the intense research performed throughout the last decades. However, few sleep researchers are aware of the difficulties posed by the blind acceptance of an extreme adaptationist viewpoint. Under this philosophy, every anatomical and functional detail present in a living being should have a positive adaptive value, a position that has been considered as rather doubtful. In this report, it is proposed that most of the physiological changes used for mammalian sleep definition could be mere by-products of other true adaptations, such as the ontogenetic and phylogenetic development of the nervous system. As a result, complex mammalian sleep could have no adaptive value over that of the simplest forms of rest-activity cycles present in all living forms. In addition, it is proposed that the absence of adaptive value should, by default, be the first option regarding the function of sleep. Besides, the burden of the proof should be always charged over the proponents of every particular adaptive function. As this proof has not been reached, it is the absence of function for sleep which should be taken for granted.

Effects of diazepam and zolpidem on EEG beta frequencies are behavior-specific in rats.

A pharmacological dissociation of the relation between electroencephalographic (EEG) activity and behavior has been described for the benzodiazepines. While a decrease in high frequency EEG activity is associated with a decrease in arousal in drug-free conditions, sedative benzodiazepines increase beta activity. Non-benzodiazepine GABA(A) receptor modulators can increase beta activity as well. To further study the relationship between rat behavior and EEG under GABA(A) receptor modulation, EEG effects of diazepam (2.5 mg/kg) and zolpidem (2.5 mg/kg) were studied during different behaviors. Both drugs modulate the GABA(A) receptor, albeit that zolpidem shows alpha(1) subunit selectivity while diazepam is non-selective. A detailed analysis of rat open field behavior was made with a distinction of 25 behavioral elements. The EEG was segmented according to each behavioral element and a corresponding power spectrum calculated. Both diazepam and zolpidem increased EEG beta frequencies, characteristic for the benzodiazepines. However, the beta and gamma increase was specific for active behavior and not for inactivity. Interestingly, diazepam and zolpidem seemed to amplify, rather than dissociate, the relation between behavior and the EEG. It is hypothesized that the large increase in beta-3/gamma activity caused by diazepam and zolpidem is a compensatory mechanism that allows for behavioral activation, despite pharmacologically induced sedation.

Melatonin improves health status and sleep in children with idiopathic chronic sleep-onset insomnia: a randomized placebo-controlled trial.

OBJECTIVE: To investigate the effect of melatonin treatment on health status and sleep in children with idiopathic sleep-onset insomnia. METHOD: A randomized, double-blind, placebo-controlled trial was conducted in a Dutch sleep center, involving 62 children, 6 to 12 years of age, who suffered more than 1 year from idiopathic chronic sleep-onset insomnia. Patients received either 5 mg melatonin or placebo at 7 pm. The study consisted of a 1-week baseline period, followed by a 4-week treatment. Health status was measured with the RAND General Health Rating Index (RAND-GHRI) and Functional Status II (FS-II) questionnaires. Lights-off time, sleep onset, and wake-up time were recorded in a diary, and endogenous dim light melatonin onset was measured in saliva. RESULTS: The total scores of the RAND-GHRI and FS-II improved significantly more during melatonin treatment compared to placebo. The magnitude of change was much higher in the melatonin group than in the placebo group, with standardized response means for the RAND-GHRI of 0.69 versus 0.07 and for the FS-II of 1.61 versus 0.64. Melatonin treatment also significantly advanced sleep onset by 57 minutes, sleep offset by 9 minutes, and melatonin onset by 82 minutes, and decreased sleep latency by 17 minutes. Lights-off time and total sleep time did not change. CONCLUSIONS: Melatonin improves health status and advances the sleep-wake rhythm in children with idiopathic chronic sleep-onset insomnia.

Effects of stimulus repetitions on the event-related potential of humans and rats.

The present study compared the effects of repeated stimulus presentations on the event-related potential (ERP) of humans and rats. Both species were presented with a total of 100 auditory stimuli, divided into four blocks of 25 stimuli. By means of wavelet denoising, single-trial ERPs were established in both humans and rats. The auditory ERPs were characterized by the presence of two positive and two negative waves in both humans and rats, albeit with different latencies in the two species (P1, N1, P2, and N2). The results showed decreased amplitudes within blocks for the N1, P2, and N2 components in humans and for the N1 and P2 components in rats. Decreased amplitudes across blocks were found for the N2 component in humans and for the P2 and N2 components in rats. In both humans and rats, response decrements within a block were thus most prominent for the early ERP components, whereas the changes across blocks were most prominent for the later components. These results suggest a correspondence of the ERP correlates of elemental stimulus processing between humans and rats. It is further suggested that the observed amplitude reductions may reflect habituation and/or recovery cycle processes.

Mental effort affects vigilance enduringly: after-effects in EEG and behavior.

Vigilance is assumed to decline with sustained task performance. The EEG-effects during performance on mental tasks, however, cannot be ascribed indisputably to vigilance decline per se. During task performance itself, effects of information processing and vigilance decline may be confounded. In this study, effects of sustained mental effort were studied in the absence of specific information processing, after sustained information processing had taken place, namely after an effortful 70-min intelligence test. Vigilance was determined by means of EEG-measures in a rest condition. Furthermore, behavioral performance was assessed on two different tasks, the traditional Clock test and the SART. After mental effort, theta power in the EEG and errors on the SART were increased. Beta2 power, however, also appeared enhanced. We conclude that sustained mental effort produces an enduring decrease in vigilance, but that some active processing is enhanced at the same time. A second study replicated the EEG-results after mental effort.

Mental effort causes vigilance decrease due to resource depletion.

The resource view on vigilance performance was tested. First, a low demanding task was compared with a similar low demanding task in which stimulus presentation was less monotonous due to added, irrelevant, stimuli. The resource view, maintaining that vigilance is lowered by hard mental work, predicts that addition of irrelevant stimuli will not affect performance. The classic arousal theory, however, states that arousal drops due to monotonous stimulus presentation and predicts that decreasing monotony will enhance performance. Results showed that performance was unaffected by added stimuli. Second, we tested whether a high-demanding task (with identical stimulus presentation as the low demanding task, but different instruction) would cause a greater decline in performance than the low demanding task. Indeed, in the high-demanding task performance was affected most. In sum, it appears that vigilance decreases due to hard mental work, which requires many resources. Both overall performance and decrement in performance can be explained in terms of resources, and this suggests that vigilance tasks should be resource-demanding tasks, which do not have to be of long duration.

Correlation between long latency evoked potentials from amygdala and evoked cardiac response to fear conditioned stimulus in rats.

We investigated relation between activity of central nucleus of amygdala (CE) and phasic heart rate deceleration during differential fear conditioning. We found that P2 component of long-lasting event potential (EP) to CS+ but not to CS- correlated strongly with HR deceleration in the 1st second after stimulus onset. The obtained results are discussed in the light of LeDoux's and Kapp's findings showing crucial role of amygdala in processing of emotionally relevant stimulation and it's involvement in initiating autonomic responses.

Anxiolytic and antidepressive effects of electric stimulation of the paleocerebellar cortex in pentylenetetrazol kindled rats.

Anxiety and depression are component of interictal behavioral deteriorations that occur as a consequence of kindling, a procedure to induce chronic epilepsy. The aim of this study was to evaluate the possible effects of electrical stimulation (ES) of paleocerebellar cortex on anxiety and depressive-like behavior in a PTZ kindled epilepsy model. Kindling was induced via pentylenetetrazol (PTZ) (25.0 mg/kg IP daily) during three weeks. Locomotion in open field, elevated plus-maze (EPM) and Porsolt forced swimming test have been used for the assessment of anxiety and depression-like behavior. ES (100 Hz) has been delivered to V-VII lobules of vermal cortex of kindled rats. ES of paleocerebellum reversed kindling-induced reduction of crossings of central squares, increased rearings, and decreased the number of defecations in open field. The duration that kindled animals spent in the open arms of the EPM increased in post- ES period, and the number of enterings into the closed arms of the EPM decreased. The duration of the immobility response in the swimming test in kindled rats was reduced after ESs of paleocerebellum. In all: ES of paleocerebellar structures suppressed anxious and depressive-like behavior in PTZ-kindled rats.