Interaction of REM Deprivation and Stage 4 Deprivation With Total Sleep Loss: Experiment 2

To determine whether prior deprivation of stage REM or stage 4 sleep would potentiate the effects of total sleep loss, 7 young adult males were denied REM sleep and 7 were denied stage 4 sleep for 3 nights before 1 night of total sleep loss. Measures of autonomic and EEG activity, mood, anxiety, Rorschach CET and on several performance tasks were obtained during baseline, following stage deprivation, total sleep loss, and during recovery. There were no marked changes in any area following 3 nights of stage REM and stage 4 deprivation. The changes following total sleep loss were similar for both groups. Prior deprivation of stage REM or stage 4 did not potentiate sleep loss effects. Ss who had no stage deprivation prior to 1 night of sleep loss had more impairment following sleep loss than did the Ss of this study.     

The Recuperative Effects of REM Sleep and Stage 4 Sleep on Human Performance After Complete Sleep Loss: Experiment 1

Twelve young (17–21 yrs) male Navy recruits volunteered for a sleep loss study. After 4 baseline days, the Ss were completely deprived of sleep for 2 days and nights. Next followed an experimental phase of 2 days and nights after which all Ss received 2 nights of uninterrupted sleep. During the experimental phase, the 4 Ss in the REM-deprived group were aroused whenever they showed signs of REM sleep. The 4 Ss of the stage 4-deprived group were aroused whenever they showed signs of entering stage 4 sleep, and the 4 Ss of the Control group had uninterrupted sleep. All tests (speed and accuracy of addition, speed and accuracy of self-paced vigilance, errors of omission in experimenter paced vigilance, immediate recall of word lists, and mood) showed significant impairment after the first night of complete sleep loss. But during the experimental (sleep-stage-deprivation) and recovery phases, all three groups showed equal rates of recovery. Depriving the S of stage REM or stage 4 during recovery sleep does not affect the recuperation rate. Frequent arousals (50–100 per night) also do not impair recovery. The amount of sleep is probably more important than the kind of sleep.     

REM Sleep Interruption: Experimental Shortening of REM Period Duration

This experiment concerns itself with the extent to which psychological factors can influence normal sleep patterns. After 4 baseline nights of uninterrupted sleep, each of 4 Ss was awakened in the course of 2 nights during every REM period about 10 min following each REM onset. Ss, however, were not REM deprived. The interruption nights were followed by a recovery night of uninterrupted sleep. All nights were consecutive. The results show that during recovery nights all Ss continued to have significantly shorter than normal REM periods by going into NREM sleep at about the time they would have been awakened during the interruption nights. These shortened REM periods occurred even during early morning hours, when REM periods normally become longer. Arguments are advanced that this finding may best be explained in terms of a conditioned avoidance response.     

Sleep deprivation and phasic activity of REM sleep: independence of middle-ear muscle activity from rapid eye movements

In the recovery nights after total and partial sleep deprivation there is a reduction of rapid eye movements during REM sleep as compared to baseline nights; recent evidence provided by a selective SWS deprivation study also shows that the highest percentage of variance of this reduction is explained by SWS rebound. The present study assesses whether the reduction of rapid eye movements (REMs) during the recovery night after total sleep deprivation is paralleled by a decrease of middle-ear muscle activity (MEMA), another phasic muscle activity of REM sleep. Standard polysomnography, MEMA and REMs of nine subjects were recorded for three nights (one adaptation, one baseline, one recovery); baseline and recovery night were separated by a period of 40 hours of continuous wake. Results show that, in the recovery night, sleep deprivation was effective in determining an increase of SWS amount and of the sleep efficiency index, and a decrease of stage 1, stage 2, intra-sleep wake, and NREM latencies, without affecting REM duration and latency. However, MEMA frequency during REM sleep did not diminish during these nights as compared to baseline ones, while there was a clear effect of REM frequency reduction. Results indicate an independence of phasic events of REM sleep, suggesting that the inverse relation between recovery sleep after sleep deprivation and REM frequency is not paralleled by a concomitant variation in MEMA frequency.     

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.     

Biperiden administration during REM sleep deprivation diminished the frequency of REM sleep attempts.

Sixteen subjects were assigned to a group using either placebo or biperiden, with eight subjects in each group. Both groups were studied for one acclimatization night, one baseline night, four nights of rapid eye movement (REM) sleep deprivation and two recovery nights. All the subjects received either placebo or 4 mg biperiden 1 hour before sleep during the four nights of REM sleep deprivation. During the baseline and the recovery nights both groups received placebo capsules. The results showed that REM sleep time during the REM sleep deprivation was reduced by 70-75% below the baseline night in both groups. The number of attempts to enter REM sleep was significantly reduced by biperiden as compared to placebo for each of the four REM sleep deprivation nights. Because the total sleep time in the biperiden group was reduced, the number of REM sleep attempts was corrected by the total sleep time. The adjusted number of REM sleep attempts was also significantly reduced in the biperiden group. REM sleep latency showed a reduction in the placebo group, whereas in the biperiden group REM sleep latency was unchanged throughout the deprivation nights. In the recovery night REM sleep time was increased in both groups, with no differences between the groups. The REM sleep latency showed a reduction in the first recovery night in both groups that persisted through the second recovery night. The above findings support the role of biperiden as a REM sleep suppressive drug.     

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.     

Neurobehavioral Dynamics Following Chronic Sleep Restriction: Dose-Response Effects of One Night for Recovery

Objective:

Establish the dose-response relationship between increasing sleep durations in a single night and recovery of neurobehavioral functions following chronic sleep restriction.

Design:

Intent-to-treat design in which subjects were randomized to 1 of 6 recovery sleep doses (0, 2, 4, 6, 8, or 10 h TIB) for 1 night following 5 nights of sleep restriction to 4 h TIB.

Setting:

Twelve consecutive days in a controlled laboratory environment.

Participants:

N = 159 healthy adults (aged 22-45 y), median = 29 y).

Interventions:

Following a week of home monitoring with actigraphy and 2 baseline nights of 10 h TIB, subjects were randomized to either sleep restriction to 4 h TIB per night for 5 nights followed by randomization to 1 of 6 nocturnal acute recovery sleep conditions (N = 142), or to a control condition involving 10 h TIB on all nights (N = 17).

Measurements and Results:

Primary neurobehavioral outcomes included lapses on the Psychomotor Vigilance Test (PVT), subjective sleepiness from the Karolinska Sleepiness Scale (KSS), and physiological sleepiness from a modified Maintenance of Wakefulness Test (MWT). Secondary outcomes included psychomotor and cognitive speed as measured by PVT fastest RTs and number correct on the Digit Symbol Substitution Task (DSST), respectively, and subjective fatigue from the Profile of Mood States (POMS). The dynamics of neurobehavioral outcomes following acute recovery sleep were statistically modeled across the 0 h-10 h recovery sleep doses. While TST, stage 2, REM sleep and NREM slow wave energy (SWE) increased linearly across recovery sleep doses, best-fitting neurobehavioral recovery functions were exponential across recovery sleep doses for PVT and KSS outcomes, and linear for the MWT. Analyses based on return to baseline and on estimated intersection with control condition means revealed recovery was incomplete at the 10 h TIB (8.96 h TST) for PVT performance, KSS sleepiness, and POMS fatigue. Both TST and SWE were elevated above baseline at the maximum recovery dose of 10 h TIB.

Conclusions:

Neurobehavioral deficits induced by 5 nights of sleep restricted to 4 h improved monotonically as acute recovery sleep dose increased, but some deficits remained after 10 h TIB for recovery. Complete recovery from such sleep restriction may require a longer sleep period during 1 night, and/or multiple nights of recovery sleep. It appears that acute recovery from chronic sleep restriction occurs as a result of elevated sleep pressure evident in both increased SWE and TST.

Citation:

Banks S; Van Dongen HPA; Maislin G; Dinges DF. Neurobehavioral dynamics following chronic sleep restriction: dose-response effects of one night for recovery. SLEEP 2010;33(8):1013–1026.     

The Effects of Continuous, High Intensity, White Noise on the Human Sleep Cycle

Eight male college students slept for 8 consecutive nights under conditions of 93 ± 2 dB white noise (N) and under normal quiet conditions (Q). On N nights the percentage of total sleep time spent in stage REM was decreased (p < .001), the percentages of stages 1 and 2 were increased (p < .05, p < .001, respectively) and REM latency was increased (p < .02) compared to Q nights prior to N nights. On Q nights following N nights the percentages of stage REM increased above baseline levels indicating compensatory recovery effects from REM sleep deprivation on the prior N nights. Stages 3 and 4 remained unchanged throughout the study. The reduction in stage REM on N nights was directly attributed to the effects of noise on the CNS and not a secondary result of an increased number of awakenings on N nights.     

Reliability of Sleep Measures

The reliability of sleep measures was calculated over two nights (and within the nights) for 20 young adult males. Percent time in stages 1, 2, 3, and 4, percent movement time, number of movements, and number of stage changes were significantly correlated between Ss over nights. The percent REM time and REM cycle duration were not significantly correlated over nights. Within Ss, the length of the REM period had a significant negative correlation with the length of the preceding NREM period but not with the following NREM period. These data raise questions as to the use of the standard sleep measures as reliable human traits in young male adults.     

Effects of Sleep Deprivation on Memory and Sleep Latencies in Connection with Repeated Awakenings From Sleep

Twelve subjects were kept awake 64 hrs. During baseline and recovery sleep, subjects were given a simple memory task. The subjects were awakened 3 times each night during slow-wave sleep and shown 4 playing cards. Approximately 90 min later the subjects were again awakened and tested for retention of the previous cards and given 4 new cards to learn. This procedure was repeated 3 times each night and upon awakening the following morning. On the recovery night recall was reduced, slow-wave sleep was lengthened, sleep latency was shortened, and body motility was reduced. It was suggested that the reason for the poorer recall was deeper sleep induced by the sleep deprivation.     

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.     

Sleep restriction increases blood neutrophils, total cholesterol and low density lipoprotein cholesterol in postmenopausal women: A preliminary study

OBJECTIVES: This study examines the effects of sleep restricted to 4h for three consecutive nights on blood parameters known to be associated with cardiovascular risk in healthy postmenopausal women. MATERIAL AND METHODS: Ten healthy postmenopausal women aged 55-65 years treated with hormonal replacement therapy (HT) were included in the study. After one baseline night, three nights of sleep restricted to 4h were performed and were followed by one recovery night of 8h. Blood samplings were performed after the baseline night and after the third night of sleep restriction. RESULTS: A significant increase in white blood cells (WBC), monocytes, neutrophils, total cholesterol, and low density lipoprotein cholesterol (LDL-c) was observed after the third night of sleep restriction. CONCLUSION: Sleep restriction to 4h of sleep for three consecutive nights affected two factors associated with cardiovascular risk in healthy postmenopausal women treated with HT.     

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.     

Body Movements in Sleep During 30-Day Exposure to Tone Pulse

Body movements during sleep stages 2 and REM were measured using an artifact method to determine the effects of a tone pulse given every 22 sec, 24 hrs a day, over a period of 30 consecutive days in 10 Navy recruits, aged 19 to 23. The tone pulse produced no significant increase in the number of body movements during stage 2, but it increased body movements in REM sleep to a significant but small (3 movement increase per night) extent. The percentages of body movements observed in the first 7 sec after the tone pulse in sleep stages 2 and REM were significantly higher than those observed during the epochs 8–14 and 15–21 sec, and those observed to the pseudostimulus. The tone pulse used in this study redistributed or regulated the appearance of the body movements to the proximity of the noise, but did not increase the total number of body movements which appeared to be under endogenous control.     

Cumulative Effects of Sleep Restriction on Daytime Sleepiness

Sleep and daytime sleepiness were evaluated in 10 young adult subjects to determine whether restricting nocturnal step by a constant amount produces cumulative impairment. Subjects were studied for 12 consecutive days, including 3 baseline days with a 10-hr time in bed, 7 days with sleep restricted to 5 hrs, and 2 recovery days. In 5 subjects, recovery included a 10-hr time in bed; in the remaining subject, recovery induced a 5-hr time in bed with a 1-hr daytime nap. Sleepiness was measured using two self-rating scales and the multiple sleep latency test. During sleep restriction, nocturnal stage 2 and REM sleep were reduced and slow wave sleep was unaffected. Stanford Sleepiness Scales showed an immediate increase in daytime sleepiness that reached a plateau after 4 days. An analog sleepiness rating scale showed increased sleepiness after 2 restricted nights and leveled off after the fourth restricted night. The multiple sleep latency tests showed no effect of sleep restriction until the second day, followed by a progressive increase in sleepiness that persisted through the seventh sleep restriction day. During the recovery period, daytime sleepiness returned to basal values on all three measures following one full night of sleep; with a daytime nap, no further cumulative effects of sleep restriction were seen.     

Sleep loss in elderly volunteers

Sleep, performance, and sleepiness were assessed in 10 elderly volunteers (8 women, 2 men; aged 61-77 years) before, during, and after 38 h of sleep loss. Recovery night 1 sleep showed increased total sleep and stages 3 and 4 sleep and decreased stage 1 sleep, wakefulness, brief arousals, and latency to stages 3 and 4 sleep. An increase in stage 4 sleep persisted to the second recovery night. Increased arousal threshold was suggested by a lengthening of respiratory events and a reduction in arousals associated with leg movements. Performance was impaired during sleep loss, associated with an increased tendency to fall asleep. Reported sleepiness increased, except in three subjects who denied sleepiness. Latency to sleep onset declined. All measures returned to basal values after a night of sleep. Sleep in one volunteer failed to respond to sleep loss. With this exception, the response was similar to that reported in younger volunteers, although shorter-lived.     

Effect of 64 hours of sleep deprivation upon sleep in geriatric normals and insomniacs

Fifty-eight geriatric normal and chronic insomniac sleepers were screened with sleep recordings to define groups of 12 Normal (Sleep Efficiency greater than 85%) and Insomniac (Sleep Efficiency less than 80%) sleepers. All subjects then had 4 baseline sleep nights, 64 hours of total sleep loss, and 4 recovery nights. Insomniacs, had lower sleep efficiencies and less REM than Normals during baseline. Sleep efficiency was high (97%) in both groups on the first recovery night but decreased toward baseline values in both groups between the second (Normal) and fourth (Insomniac) recovery night. The groups had relatively little slow wave sleep, but had a significant increase on the first recovery night. Five Normals and one Insomniac had REM latency of less than 15 min on their first recovery night. This REM latency was found to be significantly correlated with the amount of slow wave sleep on baseline. Decreased REM latency in initial recovery sleep was interpreted as evidence of decreased pressure for slow wave sleep in aging.     

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.     

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.