Performance during frequent sleep disruption

Performance on a simple addition task was measured during three schedules of frequent sleep disruption for 2 nights. Five young adults had their sleep briefly disturbed for 2 nights in 3 separate weeks either every 1 min, every 10 min, or at sleep onset after an undisrupted 2.5-h sleep period. Subjects were required to perform a two-number, two-digit addition problem as rapidly as possible on awakening. Main effects were found for sleep disruption condition and time of night, and a significant interaction between the two was also observed. Latency to response was longest for the 10-min condition on night 1, on night 2, however, response latencies were longest in the 1-min condition. Response latencies were fastest in the 2.5-h condition for both nights of disruption. Arousal thresholds were also gathered across both nights. Arousal thresholds were consistently the highest in the 1- and 10-min conditions for both nights of disruption, reaching maximum threshold levels at the end of night 1. Arousal threshold was significantly positively correlated with response latency. Sleep stages (slow-wave sleep (SWS), SWS + REM (SWSR), and total sleep time minus stage 1 sleep) were poor predictors of performance changes across the 2 disruption nights. The data were best explained by sleep continuity theory, which posits that a period of at least 10 min of uninterrupted sleep is required for restoration to take place.     

Effects of different sleep duration on delta sleep in recovery nights

The study assessed the effects of different amounts of sleep restriction on slow wave sleep (SWS) in the ensuing recovery nights. After one adaptation night and an 8-hr baseline night, six healthy men were individually studied during and following five nights in which sleep was reduced to 5, 4, 3, 2, and 1 hr with a 1-week interval between conditions. Bach sleep reduction was followed by an 8-hr recovery night. Finally, a second 8-hr baseline night was recorded. A trend analysis revealed that SWS amount in recovery nights increases with decreasing previous sleep duration. Regression analyses showed that, within each participant, the rebound of SWS after a sleep reduction is predicted better by the total duration of sleep than by the specific amount of SWS lost.     

The effects of slow-wave sleep (SWS) deprivation and time of night on behavioral performance upon awakening

The aim of the present study is to evaluate the effects of selective SWS deprivation on the motor and sensory motor performance impairment immediately after awakening from nocturnal sleep at different times of the night. Ten normal males slept for 6 consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation, and one recovery night. During the last 4 nights performance was assessed four times: (a) before sleep, as a baseline measure; (b) within 30 s from the first nighttime awakening, after 2 h of sleep; (c) within 30 s from the second nighttime awakening, after 5 h of sleep; (d) within 30 s from the final morning awakening. After each awakening, following a 3-min cognitive test, a simple Auditory Reaction Time task (ART, about 5 min) and a Finger Tapping Task (FTT, 3 min) were administered. Median of Reaction Times (RT) and of Intertapping Intervals (ITI), 10% fastest RT, 10% slowest RT, and number of misses were considered as dependent variables. The selective SWS deprivation was very effective: SWS percentage during both the deprivation nights was close to zero. This strong manipulation of SWS amount interacted with time-of-night factors in influencing sleep inertia. The SWS deprivation procedure caused a worsening of behavioral performance during the deprivation nights. as well as upon the final awakening of the recovery night. Behavioral performance slowing upon awakening is accounted for by: (1) a general decrement in overall response speed (median of RT); (2) an "optimum response shift", i.e., a decrease in speed of the fastest responses; (3) an increase of lapsing, with more marked response delays resulting in a further decrease in response speed in the "lapse domain". Finally, our results do not support the existence of a circadian rhythm of sleep inertia linked to body temperature rhythm.     

Sleep During and After Gradual Sleep Reduction

To determine: 1) the minimum amounts of sleep subjects would tolerate, 2) the changes in EEG sleep measures, and 3) whether subjects would revert to baseline sleep after study termination, 4 couples gradually reduced their sleep. Three couples reduced their TST in 30-min steps from a baseline of 8 hrs and one couple from a baseline of 6.5 hrs. Subjective estimates of sleep time, sleep quality, and mood were collected daily. Home EEG sleep recordings were obtained 3 nights a week. Two of the 8-hr sleepers reduced their sleep to 5.5 hrs, 2 to 5.0 hrs, and 2 reached 4.5 hrs. These 6 subjects continued sleeping 1 to 2.5 hrs below baseline amounts a year after reduction terminated. The 6.5-hr baseline couple reached 5.0 hrs and returned to 6.5 hrs TST during follow-up. Stages W, 2, and REM decreased significantly in absolute amounts. Percentage of stages W and 2 also decreased significantly. REM percent remained constant. Stage 3 was constant while stage 4 increased in both absolute and relative amounts. REM cycle length remained constant. Stage 4 rebound on 7-hr nights was not observed during times of greatest sleep reduction. Occurrences of stage REM within 10 min of stage 1 onset were observed in 2 subjects when their TST was below 6.5 hrs. Our results are consistent with other studies of shortened sleep, indicating that TST is the major determinant of sleep-stage characteristics.     

Relationship between sleep inertia and sleepiness: cumulative effects of four nights of sleep disruption/restriction on performance following abrupt nocturnal awakenings

Performance deficits are usually evident following both extended wakefulness (sleep deprivation effects) and immediately upon awakening from sleep (sleep inertia effects). In order to determine whether sleep inertia effects are qualitatively different from sleep deprivation effects, performance on addition tests, Stanford Sleepiness Scale (SSS) ratings, and return-to-sleep latencies (RSLs) were assessed during four nights of sleep disruption/restriction. Eight subjects were polygraphically monitored in the sleep laboratory for five consecutive nights, from 2400 to 0700. On the last four nights (after an adaptation night) subjects were awakened at 0040, 0140, 0240, 0340, 0440, and 0540 for a 20-min test session. Sleepiness ratings and performance on 5-min addition tests were measured at 1.5, 7.5, and 13.5 min post-awakening, and RSL was measured at the end of each test session. Analysis of addition test performance across nights revealed that both speed and accuracy of calculations were adversely affected by the sleep disruption/restriction procedure, indicating that increasing sleepiness exacerbates sleep performance deficits upon awakening. Although divergence of SSS ratings and addition test performance across nights was suggestive, there was no conclusive evidence that sleep inertia is qualitatively different from "typical" sleepiness.     

Sleep restoration as a function of periodic awakening, movement, or electroencephalographic change

Eleven young adults had their sleep briefly disturbed following each 2 min of accumulated sleep for 2 consecutive nights in 3 different weeks. During 1 week the disturbance was a brief awakening followed by a subjective response. During another week subjects were required to make a quarter-body turn response. During the final week, the disturbance was an ongoing electroencephalographic (EEG) change. As expected, the three disturbance conditions differentially impacted sleep, with the most sleep disturbance seen in the awakening condition and the least disturbance seen in the EEG change condition. Morning vigilance performance and nap latency were decreased and fatigue was increased as compared with baseline following all three disturbance conditions. However, no significant condition interaction was found for any performance variable or for morning nap latency. For the mood scales, significant condition interactions indicated that subjects reported being sleepier only after the awakening condition. The data were interpreted as providing evidence that the restorative function of sleep is equally impaired by any periodic change in ongoing EEG and that impairment does not require a return to waking consciousness. However, mood, as a subjective rating, is dependent upon conscious events that occur during the sleep period.     

Selective slow-wave sleep deprivation and time-of-night effects on cognitive performance upon awakening

We evaluated the effects of selective slow-wave sleep (SWS) deprivation and time-of-night factors on cognitive performance upon awakening. Ten normal men slept for 6 consecutive nights in the laboratory: 1 adaptation, 2 baseline, 2 selective SWS deprivation, and 1 recovery night. Cognitive performance was assessed by means of a Descending Subtraction Task after 2, 5, and 7.5 h of sleep. There was an almost complete selective SWS suppression during both deprivation nights, and a significant SWS rebound during the recovery sleep. Regarding cognitive performance, a progressive linear decrease of sleep inertia upon successive awakenings was found during all experimental nights except for the recovery night. In addition, a significant decrease of sleep inertia was observed upon the morning awakening of the second deprivation night for the measure of performance speed, and a significant increase of sleep inertia upon the morning awakening of the recovery night for the measure of performance accuracy. The results show that cognitive performance upon awakening is adversely affected by sleep depth and that, during the sleep-wake transition, cognitive performance accuracy is more impaired than performance speed.     

Effect of sleep disruption on sleep, performance, and mood

Eleven young adult subjects were briefly awakened after each minute of electroencephalographic-defined sleep for 2 consecutive nights after undisturbed laboratory adaptation and baseline nights. Two undisturbed recovery nights followed disruption nights. On disruption nights, subjects were awakened with an audiometer and signaled the awakening by subjective rating of sleep state or button push response. The disruption procedure resulted in severely fragmented sleep with only very small amounts of slow-wave and REM sleep. Total sleep time was reduced by approximately 1 h on each night. Arousal threshold increased 56 dB across the disruption nights. Following disruption, subjects performed more poorly and rated themselves sleepier than on baseline. The level of decline was similar to that seen after periods of total sleep loss of 40-64 h. Recovery sleep was also similar to that seen after total sleep loss. It was concluded that periodic disruption of sleep, perhaps by destroying sleep continuity, quickly results in impaired function. These data may help explain function loss in severe sleep apneics.     

Long-term extension to sleep -Are we really chronically sleep deprived?

During 26 consecutive nights, electroencephalographic recordings and/or actigraphs were used to monitor the nighttime sleep of 10 asymptomatic healthy sleepers (mean age = 23.6 years). The schedule comprised: 7 nights of base line sleep, 14 nights of extended sleep (up to 10 hr/night), and 5 nights of recovery sleep. During extended sleep, subject1, slept significantly longer (approximately 1 hr), but sleep latency and interim wakefulness deteriorated. Extended sleep produced no improvements to sell-rated mood or subjective sleepiness. Vigilance tests showed a small but significant reduction in reaction time following extended compared with both baseline and recovery nights. Ability to detect target tones did not change significantly. Multiple Sleep Latency Test scores during extended sleep showed small (about 1 min) reductions. These findings give little support to the view of chronic sleep deprivation in the average 7.5-hr sleeper.     

Temporal characteristics of the augmentation of paradoxal sleep following learning in the rat

In a previous work, we have shown that an avoidance conditioning is followed by an increased number of Paradoxical Sleep (PS) phases during the first hour after learning. In Experiment 1, sleep is experimentally delayed after each conditioning session. When sleep is delayed for 180 min, learning is severely impaired and PS doesn't increase; but the 90-min sleep delay after the conditioning session is followed by the same PS increase as that when sleep is free immediately after learning. In Experiment 2, we show that a 90-min free sleep period, between learning and a 180-min sleep deprivation allowed a learning as good as that without any sleep deprivation. In our experimental conditions, PS increase after avoidance conditioning is brief and immediate when sleep is possible and if it begins less than 180 min after learning.     

Altered sleep duration and sleep period time displacements: Effects on performance in habitual long sleepers

Performance was studied in 10 healthy young adult males who characteristically sleep 9 $\text{1}\text{2}$ – 10 $\text{1}\text{2}$ hr following an electroencephalographically (EEG) recorded habitual sleep night and 4 nights on which their customary sleep was altered by 3 hr as follows: extended (E), deprived (D), delayed shift (DS), and advanced shift (AS). In the E condition sleep was extended by advancing sleep onset 3 hr corresponding to the AS condition which had the same retiring time, but differing from it with awakening occurring 3 hr earlier. In the D and DS conditions time of sleep onset was delayed 3 hr and the subjects were awakened at their customary time in the D condition, but 3 hr later than usual in the DS condition. Subjects performed an auditory vigilance task 35 min after awakening, at midday and in the early evening. Throughout the day after both shifted sleep and altered sleep duration performance was significantly impaired to an equivalent degree as reflected by longer reaction time, increased misses and a decline of intrinsic perceptual capacity. Changes in the vigilance measures did not correlate with sleep duration or any other specific alterations in the EEG patterns of sleep. The behavioral deficits which resulted from altered sleep schedules are discussed viewing sleep as a biological adaptive process with respect to the feature of its occurrence under natural conditions in a temporally rhythmic sequence.     

Effects of ad lib extended-delayed sleep on sensorimotor performance,memory and sleepiness in the young adult

Behavioral functions were studied in 16 healthy young adult males who slept regularly for 7–8 hr following two electrographically recorded conditions of continuous sleep. The conditions consisted of a rigidly scheduled 12–8:00 a.m. control night and an ad lib session when the times for sleep were at the subjects' own inclination. Thirty minutes after awakening from each condition measurements were obtained from (1) short-term memory, (2) visual choice reaction time and (3) auditory vigilance tasks, and (4) the Stanford Sleepiness Scale. A statistically significant augmentation of total sleep occurred on the ad lib nights (mean=9.6 hr) compared with the control condition (mean=7.5 hr) which was mainly due to an average 2.7 hr delay in awakening times. Following ad lib extended-delayed sleep there was a significant decline in performance on all tasks and significant elevation of sleepiness scale ratings 90 min after awakening. This effect of ad lib sleep, like behavioral deficits characteristically arising from disturbances in the diurnal rhythm, was mainly apparent early during testing and increased little with time. The results of the present study support the assumption that phase-delays in accustomed awakening times were largely the cause for the specific performance decrements observed rather than extended sleep per se.     

Infrequent periodic sleep disruption: effects on sleep, performance and mood

In the first of two experiments, 12 normal young adults had their sleep periodically disturbed for two nights in the laboratory at three different rates: 10 min of sleep followed by 20 min of disturbance, 20 min of sleep followed by 40 min of disturbance and 40 min of sleep followed by 80 min of disturbance. Sleep and disturbance alternated throughout the night. While all disturbance conditions resulted in decreased daytime performance and increased sleepiness, the disturbance conditions did not differ from each other. In the second experiment, sleep was periodically disturbed for two nights at three new rates to act as control conditions for Experiment 1. The three conditions were: 2 min of sleep followed by 4 min of disturbance, 20 min of sleep followed by a single awakening, and 40 min of sleep followed by a single awakening. Sleep and disturbance again alternated throughout the night. As expected, sleep was less disturbed and daytime decrements were smaller in the conditions allowing 20 and 40 min of sleep followed by a single awakening. The data from both experiments were interpreted as support for sleep continuity theory; i.e., as the length of periods of consolidated sleep decrease, residual decrements increase.     

Recovery of Performance During Sleep Following Sleep Deprivation

Very few studies have systematically examined recovery of performance after sleep deprivation. In the present study, 12 young adult males were sleep deprived for periods of 40 and 64 hrs. Each period was preceded by baseline nights of sleep and followed by two recovery nights of sleep. Immediate recall and reaction time were tested at 2300, 0145, 0400, 0615, and 0830 during baseline, deprivation, and recovery nights. Performance efficiency showed a progressive decline after 2 hrs of recovery sleep following both periods of deprivation. Return to baseline was apparent after 4 hrs of steep following 40 hrs awake and after 8 hrs of sleep following 64 hrs awake. These results suggested that, in terms of behavioral efficiency, an equal amount of sleep is not required to compensate for sleep lost.     

Dopamine Transporter Regulation during Four Nights of REM Sleep Deprivation Followed by Recovery – An in vivo Molecular Imaging Study in Humans

Objectives:

To assess the influence of total or selective REM sleep deprivation on the dopamine transporter (DAT) densities and sleep patterns of healthy volunteers.

Design:

Prospective study.

Setting:

Evaluation of polysomnography recordings and DAT density after 4 nights of selective REM sleep deprivation followed by 3 nights of sleep recovery compared to a control group and a group that was subjected to 2 nights of total sleep deprivation. Single positron emission computed tomography and [^99mTc]TRODAT-1 were used to assess the cerebral DAT density in the striatum at baseline, after REM sleep deprivation and total sleep deprivation as well as after sleep recovery. Blood was collected daily to examine prolactin and estradiol levels, which were correlated with dopaminergic activity.

Patients or Participants:

Thirty healthy male volunteers ranging from 19 to 29 years of age were randomly assigned to one of three experimental groups after giving written informed consent (10 non-sleep deprived, 10 total sleep deprived, and 10 REM sleep deprived).

Measurements and Results:

Four nights of REM sleep deprivation and 2 nights of total sleep deprivation induced distinct and heterogeneous patterns of sleep recovery. No significant modulation of DAT availability was observed within groups. In the recovery nights, changes in cortisol, prolactin and estradiol concentrations were significantly correlated with specific sleep stages in the total and REM sleep deprived groups. In addition, DAT density was positively correlated with estradiol concentration and inversely associated with SWS latency only after total sleep deprivation.

Conclusion:

Our study demonstrates that although sleep deprivation did not promote significant alterations in DAT density within the striatum, there were significant correlations among transporter availability, hormonal concentrations and sleep parameters.

Citation:

Martins, RCS; Andersen ML; Garbuio SA; Bittencourt LR: Guindalini C; Shih MC; Hoexter MQ; Bressan RA; Castiglioni MLV; Tufik S. Dopamine transporter regulation during four nights of REM sleep deprivation followed by recovery – an in vivo molecular imaging study in humans. SLEEP 2010;33(2):243-251.     

Behavioral Control of Respiration in Sleep and Sleepiness Due to Signal-Induced Sleep Fragmentation

The effects of sleep fragmentation on behavioral control of sleeping respiration and on daytime sleepiness were investigated in 20 college students. All were polygraphically monitored both during nighttime sleep and during daytime naps. Ten experimental subjects were informed while awake that tones would be presented to them during nighttime sleep. Their task was to terminate the tones by taking a deep breath. Half of the subjects first received tones every 4 min; the other half received them every 8 min. After 4 consecutive nights subjects received 3 days off and conditions were reversed for 4 more consecutive nights. Tones started at 45dB and, in the absence of a response, increased 10dB every 10 seconds up to 95dB. Control subjects (N = 10) did not receive tones. The absolute number of arousals to tones was greater but the percentage of arousals was lower under the 4-min condition. Full awakenings occurred infrequently. Probability of making a breathing response remained high across days for both fragmentation conditions, but latency to respond was shorter and probability higher under the 8-min condition. Sleep fragmentation, whether “frequent” (4-min) or “infrequent” (8-min), did not induce greater daytime sleepiness than did the nonfragmentation control condition, and sleepiness did not differ between the two experimental conditions. Implications for developing behavioral techniques for treating sleep-related breathing disorders are discussed.     

Sleep, Performance and Mood After the Energy-Expenditure Equivalent of 40 Hours of Sleep Deprivation

Twelve Marine subjects marched approximately 20 miles to expend as much energy in one 16-hr day as is expended during 40 hrs of relatively inactive sleep deprivation. At the end of the march, performance on addition, vigilance, choice reaction time, tapping, short-term memory, symbol substitution, and three mood scales was decremented significantly. Those decrements closely approximated decrements reported in the literature following 40 hrs of sleep deprivation. However, recovery sleep stages and arousal thresholds were essentially unchanged as compared to baseline and were significantly different from those predicted after 40 hrs of sleep loss. It was concluded that while changes in performance were probably linked to total energy consumption, the commonly measured sleep variables were not.     

Effects of Long Term Exposure to Tone Pulse Noise on Human Sleep

Electrophysiological and self-report data were obtained from 10 and 20 Ss, respectively, during 15 days of baseline, 30 days of 24-hr per day exposure to a 660 msec, 3.5K Hz tone pulse with a 22 sec interstimulus interval (10 days each at 80, 85, and 90 dB), and during a 10-day post-exposure period. A self-reported increase in difficulty falling asleep was not substantiated by objective sleep latency measures. Changes in total hours of sleep, number of awakenings, and percent time for sleep stages were of small magnitude and not consistently related to stimulus intensity. All 10 monitored Ss gave clear EEG and autonomic responses to the stimulus, with no evidence of response extinction over the 30-day exposure period. There was no change in average all-night heart rate. Total number of body movements during the night did not change. However, the movements that did occur, tended to be triggered by the stimulus, with most movements closely following the tone pulse. The youth and good health of the Ss, and the 24-hr per day exposure, favoring rapid adaptation to the stimulus, are suggested to account for the lack of disruption of sleep.     

Thirty-Six Hour Correspondence Between Performance and Sleepiness Cycles

The present work investigates the correspondence between rhythmicity in performance efficiency and sleepiness. Eight subjects kept a repeating schedule of 7 Min in bed, 13 min awake out of bed, for two 36-hr periods. Each 36-hr period followed 28 hrs of sleep deprivation. Periods were separated by a one-week interval. Time in bed was subject to two experimental conditions, either attempting or resisting sleep. During each 13-min period outside the bedroom, subjects were tested on a choice reaction time task with three levels of movement difficult). In both the attempting sleep and resisting sleep conditions, reaction time and movement lime showed marked circadian modulation, generally matching the sleepiness cycle. There was no interaction between movement difficulty and (he effects of sleep loss. There were no significant differences in total sleep between the conditions of attempting and resisting sleep; however, subjects instructed to resist sleep had slower reaction times and less stable movement times. The significance of these findings is discussed in terms of differences between attentional mechanisms and multiple processing resources. Results support a theory that the performance and sleep wake cycles are not causally related but rather, may be regulated independently.     

Sleep Stage Deprivation and Total Sleep Loss: Effects On Sleep Behavior

The combined effects of total sleep loss and the deprivation of stage 4 or stage REM were studied in I two separate experiments. Two full nights or sleep loss preceded stage 4 deprivation or stage REM deprivation in Experiment 1 (N=12); 1 full night of sleep loss followed 3 nights or stage 4 deprivation or stage REM deprivation in Experiment 2 (N=I4). Total sleep loss before sleep stage deprivation significantly increased the number of attempts to enter stage 4, but had little influence on stage REM. A significant REM rebound was found in only one of the REM-deprived groups, but there was a significant stage 4 rebound in all groups on the first full recovery night, supporting the hypothesis from other studies that stage 4 has priority over REM in terms of recovery from sleep loss. The results suggested that stages 2, 3, and 4 partially overlap in their recuperative functions.