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An acute bout of high‐intensity exercise affects nocturnal sleep and sleep‐dependent memory consolidation
Journal of Sleep Research
Abstract
Acute exercise has been shown to affect long‐term memory and sleep. However, it is unclear whether exercise‐induced changes in sleep architecture are associated with enhanced memory. Recently, it has been shown that exercise followed by a nap improved declarative memory. Whether these effects transfer to night sleep and other memory domains has not yet been studied. Here, we investigate the influence of exercise on nocturnal sleep architecture and associations with sleep‐dependent procedural and declarative memory consolidation. Nineteen subjects (23.68 ± 3.97 years) were tested in a balanced cross‐over design. In two evening sessions, participants either exercised (high‐intensity interval training) or rested immediately after encoding two memory tasks: (1) a finger tapping task and (2) a paired‐associate learning task. Subsequent nocturnal sleep was recorded by polysomnography. Retrieval was conducted the following morning. High‐intensity interval training lead to an increased declarative memory retention ( p = 0.047, d = 0.40) along with a decrease in REM sleep ( p = 0.012, d = 0.75). Neither procedural memory nor NREM sleep were significantly affected. Exercise‐induced changes in N2 showed a positive correlation with procedural memory retention which did not withstand multiple comparison correction. Exploratory analyses on sleep spindles and slow wave activity did not reveal significant effects. The present findings suggest an exercise‐induced enhancement of declarative memory which aligns with changes in nocturnal sleep architecture. This gives additional support for the idea of a potential link between exercise‐induced sleep modifications and memory formation which requires further investigation in larger scaled studies.
... It is made Recent evidence suggested that performing a single session of high-intensity interval exercise (HIIE), that alternates short periods of intense exercise with active recovery, may be a powerful approach for enhancing motor skill consolidation and promoting neuroplasticity 18 . While these benefits are well-documented for visuomotor tasks 19 , few studies have examined its effect on SML paradigms that depend more heavily on explicit memory components [20][21][22] . Findings from these behavioral studies did not reveal any additional gains in performance following HIIE, hence suggesting that physical exercise might not contribute to further improving consolidation of explicit SML acquired with PP. ...
... The major result of this study is that HIIE had a detrimental effect on accuracy at both early and late stages of consolidation regardless of the type of practice. This result contrast with findings from recent studies using modified explicit SML paradigms, which reported no impact of HIIE on motor performance during consolidation [20][21][22] . The main distinction with motor paradigms that may benefit from HIIE seems to lie in the implicit versus explicit nature of the motor skill practice. ...
... This hypothesis is partially supported by the fact that a large number of participants in Cristini's study 20 either failed to recall the sequence in the explicit groups or, discovered part of the sequence in the implicit group. Conversely, Frisch et al. 22 used a SML task with only 5-item paired with concurrent word list learning, a procedural and declarative learning overlap that is well-documented to interfere when performed in close temporal proximity, potentially explaining the absence of HIIE effects on SML consolidation 40 . Here, we hypothesize that the explicit bimanual 8-item SML task, which involves the prefrontal cortex during acquisition and consolidation tests 41 , may have been particularly susceptible to HIIE-induced disruption of brain networks supporting goal-directed components of SML, ultimately leading to greater performance deterioration after HIIE. ...
High-intensity interval exercise (HIIE) is known to enhance motor consolidation following physical practice (PP), but its effects on sequential motor learning (SML) through PP or motor imagery (MI) remain unclear. We examined whether HIIE modulates SML consolidation in 48 participants who learned an explicit SML task through PP or MI. Performance was assessed before and after acquisition, after HIIE or rest, and at 24 hours and 7 days. Both PP and MI improved performance, with greater gains for PP (p = 0.042), and both induced intracortical disinhibition (p = 0.03). HIIE increased BDNF (p = 0.044) and lactate levels (p < 0.001), markers typically linked to neuroplasticity, yet unexpectedly impaired SML at early (p < 0.01) and late consolidation (p < 0.05), without affecting excitability. These findings challenge the presumed coupling between exercise-induced biomarkers and behavioral gains, suggesting that HIIE may hinder consolidation when explicit components of motor learning are involved.
The effects of different intensities of evening exercise on subsequent sleep remain contradictory. Thus, this systematic review and network meta-analysis aimed to compare and rank the effects of different intensities of acute evening exercise on sleep in healthy adults with good sleep. Articles were systematically searched journals indexed in the PubMed, Web of Science, Cochrane Library, Embase, and Scopus databases from inception to the 5th of May, 2022. The basic search terms included exercise, sleep and timing, which were combined with AND. Of the 12,203 retrieved, twenty-eight studies with 325 participants met the inclusion criteria. Results revealed that there were no significant differences in terms of impacts on sleep caused by different intensities of acute evening exercise, except that when compared to no exercise, acute evening high-intensity exercise decreased rapid eye movement sleep (mean difference [MD] = −1.95%, 95% credible interval [CI] = −3.58 to −0.35). Compared to no exercise, acute evening moderate-intensity exercise was ranked as the most potential method to improve sleep, displaying a trend to improve wake time after sleep onset (MD = −2.50 min, 95% CI = −8.17 to 1.62), sleep efficiency (MD = +0.41%, 95% CI = −0.71 to 1.66), the proportion of stage N1 (MD = −0.72%, 95% CI = −2.08 to 0.71) and N3 sleep (slow-wave sleep) (MD = +0.84%, 95% CI = −1.17 to 2.78). Acute evening low-intensity exercise displayed the greatest tendency to shorten sleep onset latency (MD = −1.02 min, 95% CI = −4.39 to 2.50) compared to no exercise. Overall, regardless of intensity, acute evening exercise completed before bedtime does not disrupt subsequent sleep in healthy young and middle-aged adults.
An important step when designing an empirical study is to justify the sample size that will be collected. The key aim of a sample size justification for such studies is to explain how the collected data is expected to provide valuable information given the inferential goals of the researcher. In this overview article six approaches are discussed to justify the sample size in a quantitative empirical study: 1) collecting data from (almost) the entire population, 2) choosing a sample size based on resource constraints, 3) performing an a-priori power analysis, 4) planning for a desired accuracy, 5) using heuristics, or 6) explicitly acknowledging the absence of a justification. An important question to consider when justifying sample sizes is which effect sizes are deemed interesting, and the extent to which the data that is collected informs inferences about these effect sizes. Depending on the sample size justification chosen, researchers could consider 1) what the smallest effect size of interest is, 2) which minimal effect size will be statistically significant, 3) which effect sizes they expect (and what they base these expectations on), 4) which effect sizes would be rejected based on a confidence interval around the effect size, 5) which ranges of effects a study has sufficient power to detect based on a sensitivity power analysis, and 6) which effect sizes are expected in a specific research area. Researchers can use the guidelines presented in this article, for example by using the interactive form in the accompanying online Shiny app, to improve their sample size justification, and hopefully, align the informational value of a study with their inferential goals.
Sleep disorders affect a large portion of the global population and are strong predictors of morbidity and all-cause mortality. Sleep staging segments a period of sleep into a sequence of phases providing the basis for most clinical decisions in sleep medicine. Manual sleep staging is difficult and time-consuming as experts must evaluate hours of polysomnography (PSG) recordings with electroencephalography (EEG) and electrooculography (EOG) data for each patient. Here, we present U-Sleep, a publicly available, ready-to-use deep-learning-based system for automated sleep staging (sleep.ai.ku.dk). U-Sleep is a fully convolutional neural network, which was trained and evaluated on PSG recordings from 15,660 participants of 16 clinical studies. It provides accurate segmentations across a wide range of patient cohorts and PSG protocols not considered when building the system. U-Sleep works for arbitrary combinations of typical EEG and EOG channels, and its special deep learning architecture can label sleep stages at shorter intervals than the typical 30 s periods used during training. We show that these labels can provide additional diagnostic information and lead to new ways of analyzing sleep. U-Sleep performs on par with state-of-the-art automatic sleep staging systems on multiple clinical datasets, even if the other systems were built specifically for the particular data. A comparison with consensus-scores from a previously unseen clinic shows that U-Sleep performs as accurately as the best of the human experts. U-Sleep can support the sleep staging workflow of medical experts, which decreases healthcare costs, and can provide highly accurate segmentations when human expertize is lacking.
Exercise can improve sleep by reducing sleep latency and increasing slow-wave sleep (SWS). Some studies, however, report adverse effects of exercise on sleep architecture, possibly due to a wide variety of experimental conditions used. We examined the effect of exercise on quality of sleep using standardized exercise parameters and novel analytical methods. In a cross-over intervention study we examined the effect of 60 min of vigorous exercise at 60% V˙O2max on the metabolic state, assessed by core body temperature and indirect calorimetry, and on sleep quality during subsequent sleep, assessed by self-reported quality of sleep and polysomnography. In a novel approach, envelope analysis was performed to assess SWS stability. Exercise increased energy expenditure throughout the following sleep phase. The subjective assessment of sleep quality was not improved by exercise. Polysomnography revealed a shorter rapid eye movement latency and reduced time spent in SWS. Detailed analysis of the sleep electro-encephalogram showed significantly increased delta power in SWS (N3) together with increased SWS stability in early sleep phases, based on delta wave envelope analysis. Although vigorous exercise does not lead to a subjective improvement in sleep quality, sleep function is improved on the basis of its effect on objective EEG parameters.
Sleep strengthens memories by repeatedly reactivating associated neuron ensembles. Our studies show that although long-term memory for a medium number of word-pairs (160) benefits from sleep, a large number (320) does not. This suggests an upper limit to the amount of information that has access to sleep-dependent declarative memory consolidation, which is possibly linked to the availability of reactivation opportunities. Due to competing processes of global forgetting that are active during sleep, we hypothesized that even larger amounts of information would enhance the proportion of information that is actively forgotten during sleep. In the present study, we aimed to induce such forgetting by challenging the sleeping brain with vast amounts of to be remembered information. For this, 78 participants learned a very large number of 640 word-pairs interspersed with periods of quiet awake rest over the course of an entire day and then either slept or stayed awake during the night. Recall was tested after another night of regular sleep. Results revealed comparable retention rates between the sleep and wake groups. Although this null-effect can be reconciled with the concept of limited capacities available for sleep-dependent consolidation, it contradicts our hypothesis that sleep would increase forgetting compared to the wake group. Additional exploratory analyses relying on equivalence testing and Bayesian statistics reveal that there is evidence against sleep having a detrimental effect on the retention of declarative memory at high information loads. We argue that forgetting occurs in both wake and sleep states through different mechanisms, i.e., through increased interference and through global synaptic downscaling, respectively. Both of these processes might scale similarly with information load.
There is compelling evidence that sleep (N2, REM sleep, but also N3) supports the consolidation of motor memory in adults. Although children express higher levels of REM sleep and N3, it is still not understood why sleep does not benefit the consolidation of motor memory in children as in adults. Here, we aimed to manipulate sleep by daytime physical exercise in typically developing boys (N = 12; range 9-12 yrs) to test the impact on sleep and motor learning. The manipulation consisted of 1 h of intense ergometer exercise during the daytime before a night of restorative sleep. In a rest control condition, children were seated comfortably and listened to an audio drama. Motor learning was assessed with a visuomotor finger sequence tapping task; in both conditions learning took place before either exercise or rest. Prior to sleep in the sleep laboratory, motor memory was assessed as a baseline. Motor memory was again collected in the morning after a night of sleep in the lab. While there was no change in N3, we found prolonged REM sleep latency after physical activity compared to rest, corresponding to a prolonged first sleep cycle. With respect to motor learning, we found superior accuracy of motor performance after physical exercise compared to rest. Our findings suggest that physical exercise during the daytime stabilizes sleep-dependent motor learning.
Objective: To investigate the different effects of acute aerobic exercise on the formation of long-term declarative memory (DM) and procedural memory (PM). Methods: Twenty-two young men completed DM and PM tasks under three experimental conditions: pre-acquisition exercise, post-acquisition exercise, and no exercise (control). The DM task encompassed word learning, free recall tests both immediately and 1 h later, and a recognition test conducted 24 h after word learning. A serial reaction time task (SRTT) was utilized to assess exercise effects on PM. The SRTT included a sequence learning phase followed by sequence tests 1 h and 24 h later. The exercise program consisted of 30 min of moderate-intensity aerobic exercise. Results: In the DM task, compared to the control condition, pre-acquisition exercise, but not post-acquisition exercise, enhanced free recall performance significantly 1 h and 24 h later. The target word recognition rate and discriminative index (d′) of the recognition test were significantly enhanced in both exercise conditions compared to the control condition. In the PM task, we observed significantly reduced (improved) reaction times at the 24-h test in the post-acquisition exercise condition compared to in the control condition. Conclusion: Acute aerobic exercise may enhance long-term DM and PM via effects on different processing periods. For DM, exercise had a pronounced effect during the encoding period, whereas for PM, exercise was found to have an enhancing effect during the consolidation period.
Background
Physical exercise improves mental health and cognitive function. The purpose of this systematic review was to evaluate the current literature examining the acute effects of a single exercise workout on learning and memory functions in young adults.
Methods
The review was conducted in alignment with the PRISMA guidelines. Studies were included if they were indexed in PubMed, published between 2009 and 2019, used an experimental study design and conducted on young human adults. The MeSH terms “exercise”, “learning” and “young adults” were used together with the filters Publication dates ‐ 10 years; Human Species; and Article types ‐ Clinical Trial.
Results
Thirteen studies met the inclusion criteria and were evaluated. The types of exercise stimulus that were used was walking, running or bicycling. Several different test instruments were used such as Rey Auditory Verbal Learning Test, Trail Making Test A and B and Stroop Color Word Test. Exercise for two minutes to one hour at moderate to high intensity had a favorable effect on learning and memory functions in the selected studies.
Conclusions
This systematic review shows that aerobic, physical exercise before encoding improves learning and memory functions in young adults.
The neural systems that govern declarative and procedural memory processing do not always operate independently. Direct evidence of competition between these two memory systems in humans is supported by studies showing that performing a declarative learning task immediately after motor skill learning can disrupt procedural memory and abolish the off-line gains in skill performance obtained during consolidation. The aim of the present study was to extend recent investigations demonstrating that the exposure to a brief bout of cardiovascular exercise can protect procedural memory by enhancing postpractice consolidation. We used an experimental paradigm designed to assess whether exercise can also protect procedural memory consolidation from interference induced with declarative learning. The implicit acquisition of a serial reaction time task (SRTT) was tested after a 6-h waked-filled period. Participants who were exposed to a non-learning vowel counting (VC) task following the practice of the SRTT exhibited successful procedural memory consolidation and significant off-line gains in skill performance. Confirming that declarative memory processes can interfere with procedural memory consolidation, off-line gains in motor skill performance were suppressed when the performance of the VC task was replaced with a word list (WL) task requiring declarative learning. Performing a bout of cardiovascular exercise after the SRTT protected the newly formed procedural memory from the interference produced by the WL task. Protection was evidenced by a return of significant off-line gains in skill performance after the waked-filled period. Exercise optimizes the utilization of neural resources reducing interference between procedural and declarative memory systems.
Sleep spindle activity has repeatedly been found to contribute to brain plasticity and consolidation of both declarative and procedural memories. Here we propose a framework for motor memory consolidation that outlines the essential contribution of the hierarchical and multi-scale periodicity of spindle activity, as well as of the synchronization and interaction of brain oscillations during this sleep-dependent process. We posit that the clustering of sleep spindles in ‘trains', together with the temporally organized alternation between spindles and associated refractory periods, is critical for efficient reprocessing and consolidation of motor memories. We further argue that the long-term retention of procedural memories relies on the synchronized (functional connectivity) local reprocessing of new information across segregated, but inter-connected brain regions that are involved in the initial learning process. Finally, we propose that oscillatory synchrony in the spindle frequency band may reflect the cross-structural reactivation, reorganization and consolidation of motor, and potentially declarative, memory traces within broader subcortical–cortical networks during sleep.
This article is part of the Theo Murphy meeting issue ‘Memory reactivation: replaying events past, present and future'.
The aim of the present study was to investigate the effects of night-time (21:00) high-intensity, intermittent exercise on sleep architecture among well-trained athletes in a laboratory setting. In a randomized, counterbalanced order, eleven well-trained male runners completed a simulated trail-running exercise (TRAIL) on a motorized treadmill and a resting condition (REST) (no exercise during the day). After each condition, nocturnal autonomic nervous system activity and core body temperature (CBT) were measured and sleep was analyzed using polysomnography and actigraphy. Markers of muscle damage (maximal voluntary contraction [MVC], plasma creatine kinase concentration [CK] and perceived muscle soreness) were recorded before and immediately (POST), 24 h (H24) and 48 h (H48) after exercise. TRAIL induced a high level of fatigue and mild exercise-induced muscle damage, as determined by a reduction in MVC (-8.4%, p < 0.05, d = -1.23) and increases in [CK] (+179.0%, p < 0.01, d = 1.58) and perceived muscle soreness (+4.5 UA, p < 0.01, d = 2.17) compared with REST at H24. A trend for increased non-rapid eye movement (+4.2%; p = 0.07; d = 0.86) and reduced rapid eye movement (-4.8%; p = 0.07; d = -0.87) during sleep was observed for TRAIL compared with REST. Moreover, compared with REST, TRAIL significantly increased CBT and nocturnal HR during the first part of the night. In conclusion, sleep architecture was modified after night-time, high-intensity exercise among well-trained runners.
The effects of exercise on sleep have been explored from various perspectives, but little is known about how the effects of acute exercise on sleep are produced through physiological functions. We used a protocol of multiple daytime sessions of moderate-intensity aerobic exercise and examined the subsequent effects on sleep structure, core body temperature (CBT), distal-proximal skin temperature gradient (DPG), and subjective parameters. Fourteen healthy men who did not exercise regularly were evaluated under the baseline (no exercise) and exercise conditions on a within-subject crossover basis. Under the exercise condition, each participant performed a 40-min aerobic workout at 40% of maximal oxygen intake, four times between morning and early evening. We observed a 33% increase in slow-wave sleep (SWS; P = 0.005), as well as increases in slow-wave activity (SWA; P = 0.026), the fast-sigma power/SWA ratio ( P = 0.005), and subjective sleep depth and restorativeness the following morning. Moreover, both CBT and the DPG increased during sleep after exercise ( P = 0.021 and P = 0.047, respectively). Regression analysis identified an increased nocturnal DPG during sleep after exercise as a factor in the increase in SWA. The fast-sigma/SWA ratio correlated with CBT. The performance of acute exercise promotes SWS with nocturnal elevation in the DPG. Both CBT and fast-sigma power may play a role in the specific physiological status of the body after exercise.
NEW & NOTEWORTHY We used multiple daytime sessions of moderate-intensity aerobic exercise to examine the effects on the sleep structure, core body temperature (CBT), distal-proximal skin temperature gradient (DPG), and subjective parameters. Significant increases in slow-wave activity (SWA), CBT, DPG, fast-sigma power, and subjective parameters were observed during the night and the following morning. Nocturnal DPG is a factor in the increased SWA.
Background
Current recommendations advise against exercising in the evening because of potential adverse effects on sleep.
Objectives
The aim of this systematic review was to investigate the extent to which evening exercise affects sleep and whether variables such as exercise intensity or duration modify the response.
Methods
A systematic search was performed in PubMed, Cochrane, EMBASE, PsycINFO, and CINAHL databases. Studies evaluating sleep after a single session of evening physical exercise compared to a no-exercise control in healthy adults were included. All analyses are based on random effect models.
Results
The search yielded 11,717 references, of which 23 were included. Compared to control, evening exercise significantly increased rapid eye movement latency (+ 7.7 min; p = 0.032) and slow-wave sleep (+ 1.3 percentage points [pp]; p = 0.041), while it decreased stage 1 sleep (− 0.9 pp; p = 0.001). Moderator analyses revealed that a higher temperature at bedtime was associated with lower sleep efficiency (SE) (b = − 11.6 pp; p = 0.020) and more wake after sleep onset (WASO; b = + 37.6 min; p = 0.0495). A higher level of physical stress (exercise intensity relative to baseline physical activity) was associated with lower SE (− 3.2 pp; p = 0.036) and more WASO (+ 21.9 min; p = 0.044). Compared to cycling, running was associated with less WASO (− 12.7 min; p = 0.037). All significant moderating effects disappeared after removal of one study.
Conclusion
Overall, the studies reviewed here do not support the hypothesis that evening exercise negatively affects sleep, in fact rather the opposite. However, sleep-onset latency, total sleep time, and SE might be impaired after vigorous exercise ending ≤ 1 h before bedtime.
A single bout of high intensity aerobic exercise (~90% VO2peak) was previously demonstrated to amplify off-line gains in skill level during the consolidation phase of procedural memory. High intensity exercise is not always a viable option for many patient groups or in a rehabilitation setting where low to moderate intensities may be more suitable. The aim of this study was to investigate the role of intensity in mediating the effects of acute cardiovascular exercise on motor skill learning. We investigated the effects of different exercise intensities on the retention (performance score) of a visuomotor accuracy tracking task. Thirty six healthy male subjects were randomly assigned to one of three groups that performed either a single bout of aerobic exercise at 20 min post motor skill learning at 45% (EX45), 90% (EX90) maximal power output (Wmax) or rested (CON). Randomization was stratified to ensure that the groups were matched for relative peak oxygen consumption (ml O2/min/kg) and baseline score in the tracking task. Retention tests were carried out at 1 (R1) and 7 days (R7) post motor skill learning. At R1, changes in performance scores were greater for EX90 compared to CON (p<0.001) and EX45 (p = 0.011). The EX45 and EX90 groups demonstrated a greater change in performance score at R7 compared to the CON group (p = 0.003 and p<0.001, respectively). The change in performance score for EX90 at R7 was also greater than EX45 (p = 0.049). We suggest that exercise intensity plays an important role in modulating the effects that a single bout of cardiovascular exercise has on the consolidation phase following motor skill learning. There appears to be a dose-response relationship in favour of higher intensity exercise in order to augment off-line effects and strengthen procedural memory.
In animals, physical activity has been shown to induce functional and structural changes especially in the hippocampus and to improve memory, probably by upregulating the release of neurotrophic factors. In humans, results on the effect of acute exercise on memory are inconsistent so far. Therefore, the aim of the present study was to assess the effects of a single bout of physical exercise on memory consolidation and the underlying neuroendocrinological mechanisms in young adults. Participants encoded a list of German-Polish vocabulary before exercising for 30 minutes with either high intensity or low intensity or before a relaxing phase. Retention of the vocabulary was assessed 20 minutes after the intervention as well as 24 hours later. Serum BDNF and salivary cortisol were measured at baseline, after learning, and after the intervention. The high-intensity exercise group showed an increase in BDNF and cortisol after exercising compared to baseline. Exercise after learning did not enhance the absolute number of recalled words. Participants of the high-intensity exercise group, however, forgot less vocabulary than the relaxing group 24 hours after learning. There was no robust relationship between memory scores and the increase in BDNF and cortisol, respectively, suggesting that further parameters have to be taken into account to explain the effects of exercise on memory in humans.
The timing of exercise in relation to the information to be remembered is critical to maximize the effects of acute cardiovascular exercise on memory.
Endurance exercise improves cardiovascular and musculoskeletal function and may also increase the information processing capacities of the brain. Animal and human research from the past decade demonstrated widespread exercise effects on brain structure and function at the systems-, cellular-, and molecular level of brain organization. These neurobiological mechanisms may explain the well-established positive influence of exercise on performance in various behavioral domains but also its contribution to improved skill learning and neuroplasticity. With respect to the latter, only few empirical and theoretical studies are available to date. The aim of this review is (i) to summarize the existing neurobiological and behavioral evidence arguing for endurance exercise-induced improvements in motor learning and (ii) to develop hypotheses about the mechanistic link between exercise and improved learning. We identify major knowledge gaps that need to be addressed by future research projects to advance our understanding of how exercise should be organized to optimize motor learning.
The purpose of the American College of Sports Medicine's (ACSM) exercise preparticipation health screening process is to identify individuals who may be at elevated risk for exercise-related sudden cardiac death and/or acute myocardial infarction. Recent studies have suggested that using the current ACSM exercise preparticipation health screening guidelines can result in excessive physician referrals, possibly creating a barrier to exercise participation. In addition, there is considerable evidence that exercise is safe for most people and has many associated health and fitness benefits; exercise-related cardiovascular events are often preceded by warning signs/symptoms; and the cardiovascular risks associated with exercise lessen as individuals become more physically active/fit. Consequently, a scientific roundtable was convened by the ACSM in June 2014 to evaluate the current exercise preparticipation health screening recommendations. The roundtable proposed a new evidence-informed model for exercise preparticipation health screening on the basis of three factors: 1) the individual's current level of physical activity, 2) presence of signs or symptoms and/or known cardiovascular, metabolic, or renal disease, and 3) desired exercise intensity, as these variables have been identified as risk modulators of exercise-related cardiovascular events. Identifying cardiovascular disease risk factors remains an important objective of overall disease prevention and management, but risk factor profiling is no longer included in the exercise preparticipation health screening process. The new ACSM exercise preparticipation health screening recommendations reduce possible unnecessary barriers to adopting and maintaining a regular exercise program, a lifestyle of habitual physical activity, or both, and thereby emphasize the important public health message that regular physical activity is important for all individuals.
A significant body of research has investigated the effects of physical activity on sleep, yet this research has not been systematically aggregated in over a decade. As a result, the magnitude and moderators of these effects are unclear. This meta-analytical review examines the effects of acute and regular exercise on sleep, incorporating a range of outcome and moderator variables. PubMed and PsycINFO were used to identify 66 studies for inclusion in the analysis that were published through May 2013. Analyses reveal that acute exercise has small beneficial effects on total sleep time, sleep onset latency, sleep efficiency, stage 1 sleep, and slow wave sleep, a moderate beneficial effect on wake time after sleep onset, and a small effect on rapid eye movement sleep. Regular exercise has small beneficial effects on total sleep time and sleep efficiency, small-to-medium beneficial effects on sleep onset latency, and moderate beneficial effects on sleep quality. Effects were moderated by sex, age, baseline physical activity level of participants, as well as exercise type, time of day, duration, and adherence. Significant moderation was not found for exercise intensity, aerobic/anaerobic classification, or publication date. Results were discussed with regards to future avenues of research and clinical application to the treatment of insomnia.
Increased physical activity (PA) is associated with improved health and quality of life in the general population. A dose–response effect is evident between increasing levels of PA participation and a lower relative risk for cardiovascular disease and all-cause mortality. However, there is also clear evidence that PA acutely increases the risk of an adverse cardiovascular (CV) event and sudden cardiac death (SCD) significantly above levels expected at rest. Adverse CV events during PA may be triggered acutely by the physiological stress of exercise. This investigation will review the available literature describing the CV risks of exercise testing and PA participation in apparently healthy individuals. A systematic review of the literature was performed using electronic databases, including Medline, CINAHL, SPORT discus, EMBASE, Cochrane DSR, ACP Journal Club, and DARE; additional relevant articles were hand-picked and the final grouping was used for the review using the AGREE process to assess the impact and quality of the selected articles. Six hundred and sixteen relevant articles were reviewed with 51 being identified as describing adverse CV events during exercise and PA. Data suggests the risks of fatal and nonfatal events during maximal exercise testing in apparently healthy individuals rarely occur (approximately <0.8 per 10 000 tests or 1 per 10 000 h of testing). The incidence of adverse CV events is extremely low during PA of varying types and intensities, with data limited almost exclusively to fatal CV events, as nonfatal events are rarely reported. However, this risk is reduced by 25%–50% in those individuals who have prior experience with increased levels of PA, particularly vigorous PA. Throughout a wide age range, the risk of SCD and nonfatal events during PA remain extremely low (well below 0.01 per 10 000 participant hours), but both increasing age and PA intensity are associated with greater risk. In most cases of exercise-related SCD, undetected pre-existing disease is present and SCD is typically the first clinical event. The risks of an adverse CV event during exercise testing and PA are rare and are outweighed by the health benefits. Given this risk-benefit relationship, the PAR-Q is an appropriate method to identify those at higher risk across a wide age span and should be used in conjunction with appropriate clinical guidelines for guiding individuals towards graduated PA. There are not adequate data to describe the risks of PA in those individuals considered to be at higher risk but without cardiovascular disease.
Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory, depending on the specific conditions of learning and the timing of sleep. Consolidation during sleep promotes both quantitative and qualitative changes of memory representations. Through specific patterns of neuromodulatory activity and electric field potential oscillations, slow-wave sleep (SWS) and rapid eye movement (REM) sleep support system consolidation and synaptic consolidation, respectively. During SWS, slow oscillations, spindles and ripples - at minimum cholinergic activity - coordinate the re-activation and redistribution of hippocampus-dependent memories to neocortical sites, whereas during REM sleep, local increases in plasticity-related immediate-early gene activity - at high cholinergic and theta activity - might favour the subsequent synaptic consolidation of memories in the cortex.
We used meta-analytic methods to examine the influence of acute exercise on sleep. Thirty-eight studies were reviewed yielding 211 effects on 401 subjects. Mean effect sizes were calculated for sleep onset latency (SOL), stage 2, slow-wave sleep (SWS), rapid eye movement (REM) sleep, REM latency (REM-L), total sleep time (TST), and wakefulness after sleep onset (WASO). Moderating influences of subject fitness, heat load, exercise duration, time of day, associated light environment (i.e. indoor or outdoor), sleep schedule, and the scientific quality of the studies were examined.
Effect sizes for SWS, REM, REM-L, and TST were moderate [0.18–0.52 standard deviation (SD)] and their associated 95% confidence intervals did not include zero. Exercise duration and time of day were the most consistent moderator variables. In contrast with previous hypotheses, heat load had little influence on sleep.
The results of our quantitative synthesis of the literature are inconsistent with previous narrative reviews (1,2) which suggested that exercise elicits larger changes in sleep than those quantified in this meta-analysis. A major delimitation of published studies on the effects of acute exercise has been an exclusive focus on good sleepers. Hence, the effects we report herein may be underestimates of the efficacy of exercise for enhancing sleep among people with sleep disturbances.
This paper reviews the literature on the association between exercise and sleep. The epidemiological and experimental evidence for whether or not acute and chronic exercise promote sleep is discussed, as well as moderating factors and agendas for future directions of study. The expectation that exercise will benefit sleep can partly be attributed to traditional hypotheses that sleep serves energy conservation, body restoration or thermoregulatory functions, all of which have guided much of the research in this field. Exercise is a complex activity that can be beneficial to general well-being but may also stress the body. Differences in the exercise protocols studied (e.g. aerobic or anaerobic, intensity, duration) and interactions between individual characteristics (e.g. fitness, age and gender) cloud the current experimental evidence supporting a sleep-enhancing effect of exercise. In addition, the tendency to study changes in small groups of good sleepers may also underestimate the efficacy of exercise for promoting sleep. Athough only moderate effect sizes have been noted, meta-analytical techniques have shown that exercise increased total sleep time and delayed REM sleep onset (10 min), increased slow-wave sleep (SWS) and reduced REM sleep (2-5 min). The sleep-promoting efficacy of exercise in normal and clinical populations has yet to be established empirically.
Physical inactivity is a global concern, but diverse physical activity measures in use prevent international comparisons. The International Physical Activity Questionnaire (IPAQ) was developed as an instrument for cross-national monitoring of physical activity and inactivity.
Between 1997 and 1998, an International Consensus Group developed four long and four short forms of the IPAQ instruments (administered by telephone interview or self-administration, with two alternate reference periods, either the "last 7 d" or a "usual week" of recalled physical activity). During 2000, 14 centers from 12 countries collected reliability and/or validity data on at least two of the eight IPAQ instruments. Test-retest repeatability was assessed within the same week. Concurrent (inter-method) validity was assessed at the same administration, and criterion IPAQ validity was assessed against the CSA (now MTI) accelerometer. Spearman's correlation coefficients are reported, based on the total reported physical activity.
Overall, the IPAQ questionnaires produced repeatable data (Spearman's rho clustered around 0.8), with comparable data from short and long forms. Criterion validity had a median rho of about 0.30, which was comparable to most other self-report validation studies. The "usual week" and "last 7 d" reference periods performed similarly, and the reliability of telephone administration was similar to the self-administered mode.
The IPAQ instruments have acceptable measurement properties, at least as good as other established self-reports. Considering the diverse samples in this study, IPAQ has reasonable measurement properties for monitoring population levels of physical activity among 18- to 65-yr-old adults in diverse settings. The short IPAQ form "last 7 d recall" is recommended for national monitoring and the long form for research requiring more detailed assessment.
The acquisition of declarative (i.e., facts) and procedural (i.e., skills) memories may be supported by independent systems. This same organization may exist, after memory acquisition, when memories are processed off-line during consolidation. Alternatively, memory consolidation may be supported by interactive systems. This latter interactive organization predicts interference between declarative and procedural memories. Here, we show that procedural consolidation, expressed as an off-line motor skill improvement, can be blocked by declarative learning over wake, but not over a night of sleep. The extent of the blockade on procedural consolidation was correlated to participants' declarative word recall. Similarly, in another experiment, the reciprocal relationship was found: declarative consolidation was blocked by procedural learning over wake, but not over a night of sleep. The decrease in declarative recall was correlated to participants' procedural learning. These results challenge the concept of fixed independent memory systems; instead, they suggest a dynamic relationship, modulated by when consolidation takes place, allowing at times for a reciprocal interaction between memory systems.
In the present study, we evaluated the effects of a brief bout of exercise on executive function, short-term memory, and long-term memory tests. Eighteen young adults (mean age 22.2 years, s = 1.6) performed a set-switching test, a Brown-Peterson test, and a free-recall memory test before and after 40 min of moderate aerobic exercise on a cycle ergometer, and two control conditions. Exercise did not facilitate set switching or short-term memory, which suggests that exercise-induced arousal does not influence executive function processes involved in the reconfiguration of information in working memory. Exercise did alter specific aspects of delayed long-term memory. Free recall of items in the primacy and recency portions of the word list declined following the rest and non-exercise conditions, but was maintained after exercise, which suggests that exercise-induced arousal may facilitate the consolidation of information into long-term memory.
ROIG, M., J. CRISTINI, Z. PARWANTA, B. AYOTTE, L. RODRIGUES, B. DE LAS HERAS, J-F. NEPVEU, R. HUBER, J. CARRIER, S. STEIB, S.D. YOUNGSTEDT, and D.L. WRIGHT. Exercising the sleepy-ing brain: exercise, sleep, and sleep loss on memory. Exerc. Sport Sci. Rev., Vol. 50, No. 1, pp. 38–48, 2022. We examine the novel hypothesis that physical exercise and sleep have synergistic effects on memory. Exercise can trigger mechanisms that can create an optimal brain state during sleep to facilitate memory processing. The possibility that exercise could counteract the deleterious effects of sleep deprivation on memory by protecting neuroplasticity also is discussed.
Moderate-intensity exercise is generally recommended for improving sleep, whereas, high-intensity exercise (HIE) prior to bedtime is often discouraged. We conducted a systematic review and meta-analysis to determine if acute or regular (chronic) HIE performed before bedtime disrupts nighttime sleep of healthy adult, good sleepers compared with a no-exercise control. Six databases (PubMed, EMBASE, Scopus, Web of Science, CENTRAL, and PsycINFO) were searched from inception to 31st May, 2021. Studies were experimental trials published in English language, objectively (polysomnography, actigraphy) and/or subjectively assessed sleep after evening HIE in sedentary and physically fit, good sleepers (aged 18–50 y old). The revised Cochrane risk of bias tool for randomized trials was used to assess risk of bias in the included studies. The random-effects model was used for the meta-analyses. We included 15 acute evening HIE studies in the meta-analysis with a total of 194 participants. Acute evening HIE ending 0.5–4 h before bedtime decreased rapid eye movement sleep (−2.34%; p = 0.002) compared with a no-exercise control. No other significant sleep changes occurred. A regular evening HIE did not disrupt nighttime sleep. Overall, acute evening HIE performed 2–4 h before bedtime does not disrupt nighttime sleep of healthy, young and middle-aged adults.
PROSPERO, protocol registration number: CRD42020218299.
Emerging evidence indicates that acute bouts of cardiovascular exercise promote motor memory formation. In this preregistered meta-analysis (CRD42018106288) we synthesize data from 22 studies published until February 2020, including a total of 854 participants.
We calculated standardized mean differences (SMDs) with 95% confidence intervals (CIs) to assess exercise effects on motor memory encoding and consolidation, respectively. The pooled data indicate that exercise mainly benefits the consolidation of memories, with exercise prior to motor practice improving early non-sleep consolidation (SMD, 0.58; 95% CI; 0.30-0.86; p < 0.001), and post-practice exercise facilitating sleep-dependent consolidation (SMD, 0.62; 95% CI, 0.34-0.90; p < 0.001). Strongest effects exist for high exercise intensities, and motor task nature appears to be another relevant modulator.
We demonstrate that acute cardiovascular exercise particularly promotes the consolidation of acquired motor memories, and exercise timing, and intensity as well as motor task nature seem to critically modulate this relationship. These findings are discussed within currently proposed models of motor memory formation and considering molecular and systemic mechanisms of neural plasticity.
Sleep leads to the enhancement of memory, and physical exercise also improves memory along with beneficial effects on sleep quality. Potentially, sleep and exercise may operate independently upon memory; alternatively, they may operate synergistically to boost memory above and beyond exercise or sleep alone. We tested this hypothesis in 115 young healthy adults (23±3.9 years) randomly allocated to one of the four conditions in a 2 (exercise vs no exercise) x 2 (nap vs no nap) design. The exercise intervention consisted of a 40-min, moderate-intensity cycling, while the no exercise condition was an equivalent period of rest. This was followed by a learning session in which participants memorized a set of 45 neutral pictures for a later test. Subsequently, participants were exposed to either a 60-min sleep period (nap) or an equivalent time of resting wakefulness, followed by a visual recognition test. We found a significant interaction between the effects of exercise and nap (p=0.014, ηp2 = 0.053), without significant main effects of exercise or nap conditions. Participants who experienced both exercise plus nap were significantly more accurate (83.8±2.9) than those who only napped (81.1±5.4, p=0.027) and those who only exercised (78.6±10.3, p=0.012). Within the combined nap plus exercise group, higher recognition accuracies were associated with higher sleep spindle densities (r = 0.46, p=0.015). Our results demonstrate that short-term exercise and a nap improve recognition memory over a nap or exercise alone. Exercise and sleep are not independent factors operating separately upon memory but work together to enhance long-term memory.
Long-term memory formation is a major function of sleep. Based on evidence from neurophysiological and behavioral studies mainly in humans and rodents, we consider the formation of long-term memory during sleep as an active systems consolidation process that is embedded in a process of global synaptic downscaling. Repeated neuronal replay of representations originating from the hippocampus during slow-wave sleep leads to a gradual transformation and integration of representations in neocorti- cal networks. We highlight three features of this process: (i) hippocampal replay that, by capturing episodic memory aspects, drives consolidation of both hippocampus-dependent and non-hippocampus-dependent memory; (ii) brain oscillations hall- marking slow-wave and rapid-eye movement sleep that provide mechanisms for regulating both information flow across distant brain networks and local synaptic plasticity; and (iii) qualitative transformations of memories during systems consolidation resulting in abstracted, gist-like representations.
Aerobic exercise improves cognitive and motor function by inducing neural changes detected using molecular, cellular, and systems level neuroscience techniques. This review unifies the knowledge gained across various neuroscience techniques to provide a comprehensive profile of the neural mechanisms that mediate exercise-induced neuroplasticity. Using a model of exercise-induced neuroplasticity, this review emphasizes the sequence of neural events that accompany exercise, and ultimately promote changes in human performance. This is achieved by differentiating between neuroplasticity induced by acute versus chronic aerobic exercise. Furthermore, this review emphasizes experimental considerations that influence the opportunity to observe exercise-induced neuroplasticity in humans. These include modifiable factors associated with the exercise intervention and nonmodifiable factors such as biological sex, ovarian hormones, genetic variations, and fitness level. To maximize the beneficial effects of exercise in health, disease, and following injury, future research should continue to explore the mechanisms that mediate exercise-induced neuroplasticity. This review identifies some fundamental gaps in knowledge that may serve to guide future research in this area.
For the past two decades, it has generally been accepted that sleep benefits motor memory consolidation processes. This notion, however, has been challenged by recent studies and thus the sleep and motor memory story is equivocal. Currently, and in contrast to the declarative memory domain, a comprehensive overview and synthesis of the effects of post-learning sleep on the behavioral and neural correlates of motor memory consolidation is not available. We therefore provide an extensive review of the literature in order to highlight that sleep-dependent motor memory consolidation depends upon multiple boundary conditions, including particular features of the motor task, the recruitment of relevant neural substrates (and the hippocampus in particular), as well as the specific architecture of the intervening sleep period (specifically, sleep spindle and slow wave activity). For our field to continue to advance, future research must consider the multifaceted nature of sleep-related motor memory consolidation.
There is compelling evidence that sleep actively supports the formation of long-lasting memory representations. Experimental cuing of memories proved that neural replay of representations during sleep plays a causal role for this consolidation, which has also been shown to promote neocortical synaptic plasticity and spine formation. Concurrently, sleep has been proposed to facilitate forgetting through processes of synaptic renormalisation. This view received indirect support by findings in humans of sleep enhancing TMS-evoked plasticity and capabilities for encoding new information. First direct behavioural evidence of sleep inducing forgetting has only recently emerged after encoding large amounts of stimuli in adults. We propose forgetting complements sleep-dependent consolidation and facilitates gist abstraction especially at high memory loads, when reactivation-based consolidation reaches capacity limits.
A single bout of cardiovascular exercise performed immediately after practicing a motor task improves the long-term retention of the skill through an optimization of memory consolidation. However, the specific brain mechanisms underlying the effects of acute cardiovascular exercise on procedural memory are poorly understood. We sought to determine if a single bout of exercise modifies corticospinal excitability (CSE) during the early stages of memory consolidation. In addition, we investigated if changes in CSE are associated with exercise- induced off-line gains in procedural memory. Participants practiced a serial reaction time task followed by either a short bout of acute exercise or a similar rest period. To monitor changes in CSE we used transcranial magnetic stimulation applied to the primary motor cortex (M1) at baseline, 15, 35, 65 and 125 min after exercise or rest. Participants in the exercise condition showed larger (~24%) improvements in procedural memory through consolidation although differences between groups did not reach statistical significance. Exercise promoted an increase in CSE, which remained elevated 2 hours after exercise. More importantly, global increases in CSE following exercise correlated with the magnitude of off-line gains in skill level assessed in a retention test performed 8 hours after motor practice. A single bout of exercise modulates short-term neuroplasticity mechanisms subserving consolidation processes that predict off-line gains in procedural memory.
Recall of paired-associate lists (declarative memory) and mirror-tracing skills (procedural memory) was assessed after retention intervals defined over early and late nocturnal sleep. In addition, effects of sleep on recall were compared with those of early and late retention intervals filled with wakefulness. Twenty healthy men served as subjects. Saliva cortisol concentrations were determined before and after the retention intervals to determine pituitary-adrenal secretory activity. Sleep was determined somnopolygraphically. Sleep generally enhanced recall when compared with the effects of corresponding retention intervals of wakefulness. The benefit from sleep on recall depended on the phase of sleep and on the type of memory: Recall of paired-associate lists improved more during early sleep, and recall of mirror-tracing skills improved more during late sleep. The effects may reflect different influences of slow wave sleep (SWS) and rapid eye movement (REM) sleep since time in SWS was 5 times longer during the early than late sleep retention interval, and time in REM sleep was twice as long during late than early sleep (p < 0.005). Changes in cortisol concentrations, which independently of sleep and wakefulness were lower during early retention intervals than late ones, cannot account for the effects of sleep on memory. The experiments for the first time dissociate specific effects of early and late sleep on two principal types of memory, declarative and procedural, in humans.
While several models of memory consolidation have previously associated hippocampal activity with declarative memory, there is now increasing evidence that the hippocampus also plays a crucial role in procedural memory. Here, we review recent human functional neuroimaging studies demonstrating that the hippocampus is involved in the acquisition and sleep-related consolidation of procedural memories, and motor sequence-based skills in particular. More specifically, we present evidence that hippocampal activity and its functional interactions with other brain structures, particularly competition with the striatum, contribute to initial learning of sequential motor behavior. Interestingly, these early cerebral representations in the hippocampus and striatum, which may interact through the prefrontal cortex, can even predict subsequent sleep-related memory consolidation processes. We propose that sleep can reorganize the activity within, as well as the functional interactions between, these structures, ultimately favoring overnight performance enhancement. Finally, we conclude by offering insights into the respective roles of these structures in procedural memory consolidation processes. We argue that, in the context of motor sequence memory consolidation, the hippocampal system triggers subsequent sleep-dependent performance enhancement whereas the striatal system is involved in the maintenance of the motor behavior over time. © 2013 Wiley Periodicals, Inc.
Sample correlations converge to the population value with increasing sample size, but the estimates are often inaccurate in small samples. In this report we use Monte-Carlo simulations to determine the critical sample size from which on the magnitude of a correlation can be expected to be stable. The necessary sample size to achieve stable estimates for correlations depends on the effect size, the width of the corridor of stability (i.e., a corridor around the true value where deviations are tolerated), and the requested confidence that the trajectory does not leave this corridor any more. Results indicate that in typical scenarios the sample size should approach 250 for stable estimates.
A study with low statistical power has a reduced chance of detecting a true effect, but it is less well appreciated that low power also reduces the likelihood that a statistically significant result reflects a true effect. Here, we show that the average statistical power of studies in the neurosciences is very low. The consequences of this include overestimates of effect size and low reproducibility of results. There are also ethical dimensions to this problem, as unreliable research is inefficient and wasteful. Improving reproducibility in neuroscience is a key priority and requires attention to well-established but often ignored methodological principles.
Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.
To determine whether a cumulative sleep debt (in a range commonly experienced) would result in cumulative changes in measures of waking neurobehavioral alertness, 16 healthy young adults had their sleep restricted to an average 4.98 hrs per night for 7 consecutive nights. Ss slept in the laboratory, and sleep and waking were monitored. Three times each day, Ss were assessed for subjective sleepiness and mood and were evaluated on a brief performance battery that included psychomotor vigilance (PVT), probed memory (PRM), and serial-addition testing. Once each day they completed a series of visual analog scales (VASs) and reported sleepiness and somatic and cognitive/emotional problems. Sleep restriction resulted in statistically robust cumulative effects on waking functions. Subjective sleepiness ratings, subscale scores for fatigue, confusion, tension, and total mood disturbance from the mood and VAS ratings of mental exhaustion and stress were elevated across days of restricted sleep. PVT performance parameters were also significantly increased by restriction. Significant time-of-day effects were evident in subjective sleepiness and PVT data. Findings suggest that cumulative nocturnal sleep debt had a dynamic and escalating analog in cumulative daytime sleepiness and that asymptotic or steady-state sleepiness was not achieved in response to sleep restriction. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Abstract Exercise has been recommended for enhancing sleep; a claim linked to the belief that sleep need - defined by sleep duration and depth - is increased post-exercise to allow tissue recovery. Objective studies investigating exercise-sleep responses have produced mixed outcomes, and the disparity in results between studies may be due to differences in individual characteristics and/or exercise protocol, emphasising the importance of carefully controlled trials. We investigated the role of exercise on the sleep need of sedentary adults, after controlling for exercise mode, timing and duration. Twelve healthy volunteers (25.2 ± 4.0 years, 9 females, [Vdot]O(2)max 35.4 ± 8.8 ml· kg(-1) · min(-1)) were randomised to no-exercise or to a bout of treadmill exercise at 45%, 55%, 65% or 75% [Vdot]O(2)max in a crossover design. Sleep on no-exercise and exercise nights were assessed by polysomnography. Participants spent a greater proportion of sleep in light sleep (stage 1 + stage 2) after exercise at both 65% and 75% [Vdot]O(2)max (P < 0.05) than the no-exercise condition. There was a trend of a reduced proportion of rapid eye movement sleep with increased exercise intensity (P = 0.067). No other changes were observed in any other sleep variables. Two findings emerged: vigorous exercise did not increase sleep need; however, this level of exercise increased light sleep.
Sleep logs are used both in clinical and research everyday routine within sleep laboratories all over the world. Although there is a significant difference between subjective (sleep logs) and objective (polysomnography) measures of sleep, sleep logs are highly estimated tools in sleep research, because they reflect the subjective dimension of sleep wake disorders in the best way. The following study describes the development of such an instrument for the German-speaking countries in order to set a new standard for sleep laboratories with special respect to the possibility of standardized data transfer. The new developed instrument was given to a large population of normo- and insomniacs. Statistical evaluation showed good discrimination values between both populations for nearly all items. Reliability and validity were satisfactory as well. Population norms should be developed as a next step. The sleep diary discussed here is recommended for future use in German sleep laboratories. Results of different sleep laboratories could then be compared with respect to subjective sleep parameters as well.
Despite the prevalence of sleep complaints among psychiatric patients, few questionnaires have been specifically designed to measure sleep quality in clinical populations. The Pittsburgh Sleep Quality Index (PSQI) is a self-rated questionnaire which assesses sleep quality and disturbances over a 1-month time interval. Nineteen individual items generate seven "component" scores: subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime dysfunction. The sum of scores for these seven components yields one global score. Clinical and clinimetric properties of the PSQI were assessed over an 18-month period with "good" sleepers (healthy subjects, n = 52) and "poor" sleepers (depressed patients, n = 54; sleep-disorder patients, n = 62). Acceptable measures of internal homogeneity, consistency (test-retest reliability), and validity were obtained. A global PSQI score greater than 5 yielded a diagnostic sensitivity of 89.6% and specificity of 86.5% (kappa = 0.75, p less than 0.001) in distinguishing good and poor sleepers. The clinimetric and clinical properties of the PSQI suggest its utility both in psychiatric clinical practice and research activities.
Investigated whether the Stanford Sleepiness Scale (SSS), a self-rating scale used to quantify progressive steps in sleepiness, cross-validates with performance on mental tasks and whether the SSS demonstrates changes in sleepiness with sleep loss. 5 undergraduates were given a brief test of memory and the Wilkinson Addition Test in 2 test sessions and the Wilkinson Vigilance Test in 2 other sessions spaced throughout a 16-hr day for 6 days. Ss made SSS ratings every 15 min during their waking activities. On Night 4, Ss underwent all-night sleep deprivation. On all other nights, Ss were allowed only 8 hrs in bed. Mean SSS ratings correlated r = .68 with performance on the Wilkinson tests. Discrete SSS ratings correlated r = .47 with performance on the memory test. Moreover, mean baseline SSS ratings were found to be significantly lower than corresponding ratings of the deprivation period. (PsycINFO Database Record (c) 2005 APA, all rights reserved)
Improvement in motor skill performance is known to continue for at least 24 hr following training, yet the relative contributions of time spent awake and asleep are unknown. Here we provide evidence that a night of sleep results in a 20% increase in motor speed without loss of accuracy, while an equivalent period of time during wake provides no significant benefit. Furthermore, a significant correlation exists between the improved performance overnight and the amount of stage 2 NREM sleep, particularly late in the night. This finding of sleep-dependent motor skill improvement may have important implications for the efficient learning of all skilled actions in humans.
The AASM Manual for Scoring of Sleep and Associated Events: Rules Terminology and technical specifications
- R B Berry
- R Brooks
- C E Gamaldo
- S M Harding
- R M Lloyd
- C L Marcus
Berry, R. B., Brooks, R., Gamaldo, C. E., Harding, S. M., Lloyd, R. M.,
Marcus, C. L., & Vaughn, B. V. (2015). The AASM Manual for Scoring
of Sleep and Associated Events: Rules, Terminology and technical
specifications. American Academy of Sleep Medicine (Version 2.2).
- A Fothergill
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A single bout of exercise improves motor memory
- M Roig
- K Skriver
- J Lundbye-Jensen
- B Kiens
- J B Nielsen
Roig, M., Skriver, K., Lundbye-Jensen, J., Kiens, B., & Nielsen, J. B. (2012).
A single bout of exercise improves motor memory. PLoS One, 7,
e44594. https://doi.org/10.1371/journal.pone.0044594.t001