Gambling when sleep deprived: don't bet on stimulants

Recent evidence suggests that sleep deprivation leads to suboptimal decision-making on the Iowa Gambling Task (IGT), a pattern that appears to be unaffected by moderate doses of caffeine. It is not known whether impaired decision-making could be reversed by higher doses of caffeine or by other stimulant countermeasures, such as dextroamphetamine or modafinil. Fifty-four diurnally active healthy subjects completed alternate versions of the IGT at rested baseline, at 23 and 46?h awake, and following a night of recovery sleep. After 44?h awake, participants received a double-blind dose of caffeine (600?mg), dextroamphetamine (20?mg), modafinil (400?mg), or placebo. At baseline, participants showed a normal pattern of advantageous performance, whereas both sleep-deprived sessions were associated with suboptimal decision-making on the IGT. Following stimulant administration on the second night of sleep deprivation, groups receiving caffeine, dextroamphetamine, or modafinil showed significant reduction in subjective sleepiness and improvement in psychomotor vigilance, but decision-making on the IGT remained impaired for all stimulants and did not differ from placebo. Decision-making returned to normal following recovery sleep. These findings are consistent with prior research showing that sleep deprivation leads to suboptimal decision-making on some types of tasks, particularly those that rely heavily on emotion processing regions of the brain, such as the ventromedial prefrontal cortex. Moreover, the deficits in decision-making were not reversed by commonly used stimulant countermeasures, despite restoration of psychomotor vigilance and alertness. These three stimulants may restore some, but not all, aspects of cognitive functioning during sleep deprivation.     

Mood, alertness, and performance in response to sleep deprivation and recovery sleep in experienced shiftworkers versus non-shiftworkers

Previous studies have shown increased sleepiness and mood changes in shiftworkers, which may be due to sleep deprivation or circadian disruption. Few studies, however, have compared responses of experienced shiftworkers and non-shiftworkers to sleep deprivation in an identical laboratory setting. The aim of this laboratory study, therefore, was to compare long-term shiftworkers and non-shiftworkers and to investigate the effects of one night of total sleep deprivation (30.5 h of continuous wakefulness) and recovery sleep on psychomotor vigilance, self-rated alertness, and mood. Eleven experienced male shiftworkers (shiftwork ≥5 yrs) were matched with 14 non-shiftworkers for age (mean ± SD: 35.7 ± 7.2 and 32.5 ± 6.2 yrs, respectively) and body mass index (BMI) (28.7 ± 3.8 and 26.6 ± 3.4 kg/m(2), respectively). After keeping a 7-d self-selected sleep/wake cycle (7.5/8 h nocturnal sleep), both groups entered a laboratory session consisting of a night of adaptation sleep and a baseline sleep (each 7.5/8 h), a sleep deprivation night, and recovery sleep (4-h nap plus 7.5/8 h nighttime sleep). Subjective alertness and mood were assessed with the Karolinska Sleepiness Scale (KSS) and 9-digit rating scales, and vigilance was measured by the visual psychomotor vigilance test (PVT). A mixed-model regression analysis was carried out on data collected every hour during the sleep deprivation night and on all days (except for the adaptation day), at .25, 4.25, 5.25, 11.5, 12.5, and 13.5 h after habitual wake-up time. Despite similar circadian phase (melatonin onset), demographics, food intake, body posture, and environmental light, shiftworkers felt significantly more alert, more cheerful, more elated, and calmer than non-shiftworkers throughout the laboratory study. In addition, shiftworkers showed a faster median reaction time (RT) compared to non-shiftworkers, although four other PVT parameters did not differ between the groups. As expected, both groups showed a decrease in subjective alertness and PVT performance during and following the sleep deprivation night. Subjective sleepiness and most aspects of PVT performance returned to baseline levels after a nap and recovery sleep. The mechanisms underlying the observed differences between shiftworkers and non-shiftworkers require further study, but may be related to the absence of shiftwork the week prior to and during the laboratory study as well as selection into and out of shiftwork.     

Sleep-related hippocampo-cortical interplay during emotional memory recollection

Emotional events are usually better remembered than neutral ones. This effect is mediated in part by a modulation of the hippocampus by the amygdala. Sleep plays a role in the consolidation of declarative memory. We examined the impact of sleep and lack of sleep on the consolidation of emotional (negative and positive) memories at the macroscopic systems level. Using functional MRI (fMRI), we compared the neural correlates of successful recollection by humans of emotional and neutral stimuli, 72 h after encoding, with or without total sleep deprivation during the first post-encoding night. In contrast to recollection of neutral and positive stimuli, which was deteriorated by sleep deprivation, similar recollection levels were achieved for negative stimuli in both groups. Successful recollection of emotional stimuli elicited larger responses in the hippocampus and various cortical areas, including the medial prefrontal cortex, in the sleep group than in the sleep deprived group. This effect was consistent across subjects for negative items but depended linearly on individual memory performance for positive items. In addition, the hippocampus and medial prefrontal cortex were functionally more connected during recollection of either negative or positive than neutral items, and more so in sleeping than in sleep-deprived subjects. In the sleep-deprived group, recollection of negative items elicited larger responses in the amygdala and an occipital area than in the sleep group. In contrast, no such difference in brain responses between groups was associated with recollection of positive stimuli. The results suggest that the emotional significance of memories influences their sleep-dependent systems-level consolidation. The recruitment of hippocampo-neocortical networks during recollection is enhanced after sleep and is hindered by sleep deprivation. After sleep deprivation, recollection of negative, potentially dangerous, memories recruits an alternate amygdalo-cortical network, which would keep track of emotional information despite sleep deprivation.     

Facilitation of task performance and removal of the effects of sleep deprivation by an ampakine (CX717) in nonhuman primates

The deleterious effects of prolonged sleep deprivation on behavior and cognition are a concern in modern society. Persons at risk for impaired performance and health-related issues resulting from prolonged sleep loss would benefit from agents capable of reducing these detrimental effects at the time they are sleep deprived. Agents capable of improving cognition by enhancing brain activity under normal circumstances may also have the potential to reduce the harmful or unwanted effects of sleep deprivation. The significant prevalence of excitatory alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamatergic receptors in the brain provides a basis for implementing a class of drugs that could act to alter or remove the effects of sleep deprivation. The ampakine CX717 (Cortex Pharmaceuticals), a positive allosteric modulator of AMPA receptors, was tested for its ability to enhance performance of a cognitive, delayed match-to-sample task under normal circumstances in well-trained monkeys, as well as alleviate the detrimental effects of 30-36 h of sleep deprivation. CX717 produced a dose-dependent enhancement of task performance under normal alert testing conditions. Concomitant measures of regional cerebral metabolic rates for glucose (CMRglc) during the task, utilizing positron emission tomography, revealed increased activity in prefrontal cortex, dorsal striatum, and medial temporal lobe (including hippocampus) that was significantly enhanced over normal alert conditions following administration of CX717. A single night of sleep deprivation produced severe impairments in performance in the same monkeys, accompanied by significant alterations in task-related CMRglc in these same brain regions. However, CX717 administered to sleep-deprived monkeys produced a striking removal of the behavioral impairment and returned performance to above-normal levels even though animals were sleep deprived. Consistent with this recovery, CMRglc in all but one brain region affected by sleep deprivation was also returned to the normal alert pattern by the drug. The ampakine CX717, in addition to enhancing cognitive performance under normal alert conditions, also proved effective in alleviating impairment of performance due to sleep deprivation. Therefore, the ability to activate specific brain regions under normal alert conditions and alter the deleterious effects of sleep deprivation on activity in those same regions indicate a potential role for ampakines in sustaining performance under these types of adverse conditions.     

Mood,Alertness, and Performance in Response to Sleep Deprivation and Recovery Sleep in Experienced Shiftworkers Versus Non-Shiftworkers

Previous studies have shown increased sleepiness and mood changes in shiftworkers, which may be due to sleep deprivation or circadian disruption. Few studies, however, have compared responses of experienced shiftworkers and non-shiftworkers to sleep deprivation in an identical laboratory setting. The aim of this laboratory study, therefore, was to compare long-term shiftworkers and non-shiftworkers and to investigate the effects of one night of total sleep deprivation (30.5?h of continuous wakefulness) and recovery sleep on psychomotor vigilance, self-rated alertness, and mood. Eleven experienced male shiftworkers (shiftwork ≥5 yrs) were matched with 14 non-shiftworkers for age (mean?±?SD: 35.7?±?7.2 and 32.5?±?6.2 yrs, respectively) and body mass index (BMI) (28.7?±?3.8 and 26.6?±?3.4?kg/m², respectively). After keeping a 7-d self-selected sleep/wake cycle (7.5/8?h nocturnal sleep), both groups entered a laboratory session consisting of a night of adaptation sleep and a baseline sleep (each 7.5/8?h), a sleep deprivation night, and recovery sleep (4-h nap plus 7.5/8?h nighttime sleep). Subjective alertness and mood were assessed with the Karolinska Sleepiness Scale (KSS) and 9-digit rating scales, and vigilance was measured by the visual psychomotor vigilance test (PVT). A mixed-model regression analysis was carried out on data collected every hour during the sleep deprivation night and on all days (except for the adaptation day), at .25, 4.25, 5.25, 11.5, 12.5, and 13.5?h after habitual wake-up time. Despite similar circadian phase (melatonin onset), demographics, food intake, body posture, and environmental light, shiftworkers felt significantly more alert, more cheerful, more elated, and calmer than non-shiftworkers throughout the laboratory study. In addition, shiftworkers showed a faster median reaction time (RT) compared to non-shiftworkers, although four other PVT parameters did not differ between the groups. As expected, both groups showed a decrease in subjective alertness and PVT performance during and following the sleep deprivation night. Subjective sleepiness and most aspects of PVT performance returned to baseline levels after a nap and recovery sleep. The mechanisms underlying the observed differences between shiftworkers and non-shiftworkers require further study, but may be related to the absence of shiftwork the week prior to and during the laboratory study as well as selection into and out of shiftwork. (Author correspondence: sophie.wehrens@surrey.ac.uk)     

Sleep deprivation and cognitive testing in internal medicine house staff.

There is increased concern about the effects of sleep deprivation on physician performance. We administered four standard tests of cognitive function to 23 university hospital house staff. Each physician served as his or her own control, and the tests were administered at rest, after a night on call, and after a night of sleep for recovery. The study was designed so that normal learning would minimize any deterioration in the post-on-call test performance. Statistically significant deterioration occurred in 3 of the 4 tests after a night on call. Even physicians acclimated to sleep deprivation on a regular, every-third-or-fourth-night basis showed functional impairment. The results have implications for patient care under conditions where house staff are stressed by sleep deprivation and prolonged fatigue.     

Daytime napping after a night of sleep loss decreases sleepiness, improves performance, and causes beneficial changes in cortisol and interleukin-6 secretion

Sleep loss has been associated with increased sleepiness, decreased performance, elevations in inflammatory cytokines, and insulin resistance. Daytime napping has been promoted as a countermeasure to sleep loss. To assess the effects of a 2-h midafternoon nap following a night of sleep loss on postnap sleepiness, performance, cortisol, and IL-6, 41 young healthy individuals (20 men, 21 women) participated in a 7-day sleep deprivation experiment (4 consecutive nights followed by a night of sleep loss and 2 recovery nights). One-half of the subjects were randomly assigned to take a midafternoon nap (1400-1600) the day following the night of total sleep loss. Serial 24-h blood sampling, multiple sleep latency test (MSLT), subjective levels of sleepiness, and psychomotor vigilance task (PVT) were completed on the fourth (predeprivation) and sixth days (postdeprivation). During the nap, subjects had a significant drop in cortisol and IL-6 levels (P < 0.05). After the nap they experienced significantly less sleepiness (MSLT and subjective, P < 0.05) and a smaller improvement on the PVT (P < 0.1). At that time, they had a significant transient increase in their cortisol levels (P < 0.05). In contrast, the levels of IL-6 tended to remain decreased for approximately 8 h (P = 0.1). We conclude that a 2-h midafternoon nap improves alertness, and to a lesser degree performance, and reverses the effects of one night of sleep loss on cortisol and IL-6. The redistribution of cortisol secretion and the prolonged suppression of IL-6 secretion are beneficial, as they improve alertness and performance.     

Sleep Deprivation Influences Diurnal Variation of Human Time Perception with Prefrontal Activity Change: A Functional Near-Infrared Spectroscopy Study

Human short-time perception shows diurnal variation. In general, short-time perception fluctuates in parallel with circadian clock parameters, while diurnal variation seems to be modulated by sleep deprivation per se. Functional imaging studies have reported that short-time perception recruits a neural network that includes subcortical structures, as well as cortical areas involving the prefrontal cortex (PFC). It has also been reported that the PFC is vulnerable to sleep deprivation, which has an influence on various cognitive functions. The present study is aimed at elucidating the influence of PFC vulnerability to sleep deprivation on short-time perception, using the optical imaging technique of functional near-infrared spectroscopy. Eighteen participants performed 10-s time production tasks before (at 21:00) and after (at 09:00) experimental nights both in sleep-controlled and sleep-deprived conditions in a 4-day laboratory-based crossover study. Compared to the sleep-controlled condition, one-night sleep deprivation induced a significant reduction in the produced time simultaneous with an increased hemodynamic response in the left PFC at 09:00. These results suggest that activation of the left PFC, which possibly reflects functional compensation under a sleep-deprived condition, is associated with alteration of short-time perception.     

The effects of extended nap periods on cognitive,physiological and subjective responses under simulated night shift conditions

Extended nap opportunities have been effective in maintaining alertness in the context of extended night shifts (+12?h). However, there is limited evidence of their efficacy during 8-h shifts. Thus, this study explored the effects of extended naps on cognitive, physiological and perceptual responses during four simulated, 8-h night shifts. In a laboratory setting, 32 participants were allocated to one of three conditions. All participants completed four consecutive, 8-h night shifts, with the arrangements differing by condition. The fixed night condition worked from 22h00 to 06h00, while the nap early group worked from 20h00 to 08h00 and napped between 00h00 and 03h20. The nap late group worked from 00h00 to 12h00 and napped between 04h00 and 07h20. Nap length was limited to 3 hours and 20 minutes. Participants performed a simple beading task during each shift, while also completing six to eight test batteries roughly every 2?h. During each shift, six test batteries were completed, in which the following measures were taken. Performance indicators included beading output, eye accommodation time, choice reaction time, visual vigilance, simple reaction time, processing speed and object recognition, working memory, motor response time and tracking performance. Physiological measures included heart rate and tympanic temperature, whereas subjective sleepiness and reported sleep length and quality while outside the laboratory constituted the self reported measures. Both naps reduced subjective sleepiness but did not alter the circadian and homeostatic-related changes in cognitive and physiological measures, relative to the fixed night condition. Additionally, there was evidence of sleep inertia following each nap, which resulted in transient reductions in certain perceptual cognitive performance measures. The present study suggested that there were some benefits associated with including an extended nap during 8-h night shifts. However, the effects of sleep inertia need to be effectively managed to ensure that post-nap alertness and performance is maintained.     

Partial sleep deprivation reduces phase advances to light in humans

Partial sleep deprivation is increasingly common in modern society. This study examined for the first time if partial sleep deprivation alters circadian phase shifts to bright light in humans. Thirteen young healthy subjects participated in a repeated-measures counterbalanced design with 2 conditions. Each condition had baseline sleep, a dim-light circadian phase assessment, a 3-day phase-advancing protocol with morning bright light, then another phase assessment. In one condition (no sleep deprivation), subjects had an 8-h sleep opportunity per night during the advancing protocol. In the other condition (partial sleep deprivation), subjects were kept awake for 4 h in near darkness (<0.25 lux), immediately followed by a 4-h sleep opportunity per night during the advancing protocol. The morning bright light stimulus was four 30-min pulses of bright light (~5000 lux), separated by 30-min intervals of room light. The light always began at the same circadian phase, 8 h after the baseline dim-light melatonin onset (DLMO). The average phase advance without sleep deprivation was 1.8 ± 0.6 (SD) h, which reduced to 1.4 ± 0.6 h with partial sleep deprivation (p < 0.05). Ten of the 13 subjects showed reductions in phase advances with partial sleep deprivation, ranging from 0.2 to 1.2 h. These results indicate that short-term partial sleep deprivation can moderately reduce circadian phase shifts to bright light in humans. This may have significant implications for the sleep-deprived general population and for the bright light treatment of circadian rhythm sleep disorders such as delayed sleep phase disorder.     

Sleep deprivation reduces total plasma homocysteine levels in rats

Hyperhomocysteinemia has been associated with pathological and stressful conditions and is a risk factor for cardiovascular disease. Since sleep deprivation is a stressful condition that is associated with disruption of various physiological processes, we investigated whether it would also be associated with increases in plasma homocysteine levels. Further, since hyperhomocysteinemia may promote oxidative stress, and we had previously found evidence of oxidative stress in brain following sleep deprivation, we also searched for evidence of systemic oxidative stress by measuring glutathione and thiobarbituric acid reactive substance levels. Rats were sleep deprived for 96 h using the platform technique. A group was killed after sleep deprivation and another two groups were allowed to undergo sleep recovery for 24 or 48 h. Contrary to expectation, plasma homocysteine was reduced in sleep-deprived rats as compared with the control group and did not revert to normal levels after 24 or 48 h of sleep recovery. A trend was observed towards decreased glutathione and increased thiobarbituric acid reactive substance levels in sleep-deprived rats. It is possible that the observed decreases in homocysteine levels may represent a self-correcting response to depleted glutathione in sleep-deprived animals, which would contribute to the attenuation of the deleterious effects of sleep deprivation.     

A world record in marathon tennis: sleep deprivation and performance

We studied the effects of marked sleep deprivation on the EEG patterns and performance of a physically fit man (age 26) on the occasion of the world record continuous marathon tennis play (147 hours, 20 minutes). Before and immediately after the marathon, the sleep patterns of the player were recorded in our laboratory. After playing for 40 and 80 hours and within 24 hours, the performance changes were evaluated each hour. Amounts of the different sleep stages during the first recovery night compared with those of the baseline indicate an increase of 56% for total sleep time, 54% for stages 1 and 2, 154% for stages 3 and 4 and 20% for REM sleep. During the second recovery night, only REM sleep showed an increase. Activity index showed a marked decrease after 80 hours of sleep deprivation compared with that after 40 hours and was dramatically worsened during nighttime. The number of faults and pauses was also increased after 80 hours, suggesting a clear performance deterioration. Our results confirmed the effects of sleep deprivation on the recovery and performance deterioration.     

Sleep modulates the neural substrates of both spatial and contextual memory consolidation

It is known that sleep reshapes the neural representations that subtend the memories acquired while navigating in a virtual environment. However, navigation is not process-pure, as manifold learning components contribute to performance, notably the spatial and contextual memory constituents. In this context, it remains unclear whether post-training sleep globally promotes consolidation of all of the memory components embedded in virtual navigation, or rather favors the development of specific representations. Here, we investigated the effect of post-training sleep on the neural substrates of the consolidation of spatial and contextual memories acquired while navigating in a complex 3D, naturalistic virtual town. Using fMRI, we mapped regional cerebral activity during various tasks designed to tap either the spatial or the contextual memory component, or both, 72 h after encoding with or without sleep deprivation during the first post-training night. Behavioral performance was not dependent upon post-training sleep deprivation, neither in a natural setting that engages both spatial and contextual memory processes nor when looking more specifically at each of these memory representations. At the neuronal level however, analyses that focused on contextual memory revealed distinct correlations between performance and neuronal activity in frontal areas associated with recollection processes after post-training sleep, and in the parahippocampal gyrus associated with familiarity processes in sleep-deprived participants. Likewise, efficient spatial memory was associated with posterior cortical activity after sleep whereas it correlated with parahippocampal/medial temporal activity after sleep deprivation. Finally, variations in place-finding efficiency in a natural setting encompassing spatial and contextual elements were associated with caudate activity after post-training sleep, suggesting the automation of navigation. These data indicate that post-training sleep modulates the neural substrates of the consolidation of both the spatial and contextual memories acquired during virtual navigation.     

Sustained attention performance during sleep deprivation: evidence of state instability

Nathaniel Kleitman was the first to observe that sleep deprivation in humans did not eliminate the ability to perform neurobehavioral functions, but it did make it difficult to maintain stable performance for more than a few minutes. To investigate variability in performance as a function of sleep deprivation, n = 13 subjects were tested every 2 hours on a 10-minute, sustained-attention, psychomotor vigilance task (PVT) throughout 88 hours of total sleep deprivation (TSD condition), and compared to a control group of n = 15 subjects who were permitted a 2-hour nap every 12 hours (NAP condition) throughout the 88-hour period. PVT reaction time means and standard deviations increased markedly among subjects and within each individual subject in the TSD condition relative to the NAP condition. TSD subjects also had increasingly greater performance variability as a function of time on task after 18 hours of wakefulness. During sleep deprivation, variability in PVT performance reflected a combination of normal timely responses, errors of omission (i.e., lapses), and errors of commission (i.e., responding when no stimulus was present). Errors of omission and errors of commission were highly intercorrelated across deprivation in the TSD condition (r = 0.85, p = 0.0001), suggesting that performance instability is more likely to include compensatory effort than a lack of motivation. The marked increases in PVT performance variability as sleep loss continued supports the "state instability" hypothesis, which posits that performance during sleep deprivation is increasingly variable due to the influence of sleep initiating mechanisms on the endogenous capacity to maintain attention and alertness, thereby creating an unstable state that fluctuates within seconds and that cannot be characterized as either fully awake or asleep.     

Recovery of cognitive performance from sleep debt: do a short rest pause and a single recovery night help?

We studied the recovery of multitask performance and sleepiness from acute partial sleep deprivation through rest pauses embedded in performance sessions and an 8 h recovery sleep opportunity the following night. Sixteen healthy men, aged 19-22 yrs, participated in normal sleep (two successive nights with 8 h sleep) and sleep debt (one 2 h night sleep followed by an 8 h sleep the following night) conditions. In both conditions, the participants performed four 70 min multitask sessions, with every other one containing a 10 min rest pause with light neck-shoulder exercise. The multitask consisted of four simultaneously active subtasks, with the level of difficulty set in relation to each participant's ability. Physiological sleepiness was assessed with continuous electroencephalography/electro-oculography recordings during themultitask sessions, and subjective sleepiness was self-rated with the Karolinska Sleepiness Scale. Results showed that multitask performance and physiological and subjective sleepiness were impaired by the sleep debt ( p > .001). The rest pause improved performance and subjective sleepiness for about 15 min, regardless of the amount of prior sleep ( p > .01-.05). Following recovery sleep, all outcome measures showed marked improvement ( p < .001), but they failed to reach the levels observed in the control condition ( p < .001-.05). A correlation analysis showed the participants whose multitask performance deteriorated the most following the night of sleep loss tended to be the same persons whose performance was most impaired following the night of the recovery sleep ( p < .001). Taken together, our results suggest that a short rest pause with light exercise is not an effective countermeasure in itself for sleep debt-induced impairments when long-term effects are sought. In addition, it seems that shift arrangements that lead to at least a moderate sleep debt should be followed by more than one recovery night to ensure full recovery. Persons whose cognitive performance is most affected by sleep debt are likely to require the most sleep to recover.     

Interaction between Hippocampal and Striatal Systems Predicts Subsequent Consolidation of Motor Sequence Memory

The development of fast and reproducible motor behavior is a crucial human capacity. The aim of the present study was to address the relationship between the implementation of consistent behavior during initial training on a sequential motor task (the Finger Tapping Task) and subsequent sleep-dependent motor sequence memory consolidation, using functional magnetic resonance imaging (fMRI) and total sleep deprivation protocol. Our behavioral results indicated significant offline gains in performance speed after sleep whereas performance was only stabilized, but not enhanced, after sleep deprivation. At the cerebral level, we previously showed that responses in the caudate nucleus increase, in parallel to a decrease in its functional connectivity with frontal areas, as performance became more consistent. Here, the strength of the competitive interaction, assessed through functional connectivity analyses, between the caudate nucleus and hippocampo-frontal areas during initial training, predicted delayed gains in performance at retest in sleepers but not in sleep-deprived subjects. Moreover, during retest, responses increased in the hippocampus and medial prefrontal cortex in sleepers whereas in sleep-deprived subjects, responses increased in the putamen and cingulate cortex. Our results suggest that the strength of the competitive interplay between the striatum and the hippocampus, participating in the implementation of consistent motor behavior during initial training, conditions subsequent motor sequence memory consolidation. The latter process appears to be supported by a reorganisation of cerebral activity in hippocampo-neocortical networks after sleep.     

Sleep stages,memory and learning.

Learning and memory can be impaired by sleep loss during specific vulnerable "windows" for several days after new tasks have been learned. Different types of tasks are differentially vulnerable to the loss of different stages of sleep. Memory required to perform cognitive procedural tasks is affected by the loss of rapid-eye-movement (REM) sleep on the first night after learning occurs and again on the third night after learning. REM-sleep deprivation on the second night after learning does not produce memory deficits. Declarative memory, which is used for the recall of specific facts, is not similarly affected by REM-sleep loss. The learning of procedural motor tasks, including those required in many sports, is impaired by the loss of stage 2 sleep, which occurs primarily in the early hours of the morning. These findings have implications for the academic and athletic performance of students and for anyone whose work involves ongoing learning and demands high standards of performance.     

Recovery of Cognitive Performance from Sleep Debt: Do a Short Rest Pause and a Single Recovery Night Help?

We studied the recovery of multitask performance and sleepiness from acute partial sleep deprivation through rest pauses embedded in performance sessions and an 8 h recovery sleep opportunity the following night. Sixteen healthy men, aged 19–22 yrs, participated in normal sleep (two successive nights with 8 h sleep) and sleep debt (one 2 h night sleep followed by an 8 h sleep the following night) conditions. In both conditions, the participants performed four 70 min multitask sessions, with every other one containing a 10 min rest pause with light neck‐shoulder exercise. The multitask consisted of four simultaneously active subtasks, with the level of difficulty set in relation to each participant's ability. Physiological sleepiness was assessed with continuous electroencephalography/electro‐oculography recordings during the multitask sessions, and subjective sleepiness was self‐rated with the Karolinska Sleepiness Scale. Results showed that multitask performance and physiological and subjective sleepiness were impaired by the sleep debt (p>.001). The rest pause improved performance and subjective sleepiness for about 15 min, regardless of the amount of prior sleep (p>.01–.05). Following recovery sleep, all outcome measures showed marked improvement (p<.001), but they failed to reach the levels observed in the control condition (p<.001–.05). A correlation analysis showed the participants whose multitask performance deteriorated the most following the night of sleep loss tended to be the same persons whose performance was most impaired following the night of the recovery sleep (p<.001). Taken together, our results suggest that a short rest pause with light exercise is not an effective countermeasure in itself for sleep debt‐induced impairments when long‐term effects are sought. In addition, it seems that shift arrangements that lead to at least a moderate sleep debt should be followed by more than one recovery night to ensure full recovery. Persons whose cognitive performance is most affected by sleep debt are likely to require the most sleep to recover.