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Postgraduate Education Corner: CONTEMPORARY REVIEWS IN SLEEP MEDICINE |

Sleep Loss and Sleepiness: Current Issues FREE TO VIEW

Thomas J. Balkin, PhD; Tracy Rupp, PhD; Dante Picchioni, PhD; Nancy J. Wesensten, PhD
Author and Funding Information

*From the Department of Behavioral Biology, Walter Reed Army Institute of Research, Silver Spring, MD.

Correspondence to: Thomas J. Balkin, PhD, Department of Behavioral Biology, Walter Reed Army Institute of Research, 503 Robert Grant Ave, Room 2A26, Silver Spring, MD 20910; e-mail: thomas.balkin@us.army.mil


This material has been reviewed by the Walter Reed Army Institute of Research, and there is no objection to its presentation and/or publication. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the position of the Department of the Army or the Department of Defense.

The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(3):653-660. doi:10.1378/chest.08-1064
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Awareness of the consequences of sleep loss and its implications for public health and safety is increasing. Sleep loss has been shown to generally impair the entire spectrum of mental abilities, ranging from simple psychomotor performance to executive mental functions. Sleep loss may also impact metabolism in a manner that contributes to obesity and its attendant health consequences. Although objective measures of alertness and performance remain degraded, individuals subjectively habituate to chronic partial sleep loss (eg, sleep restriction), and recovery from this type of sleep loss is slow, factors that may help to explain the observation that many individuals in the general population are chronically sleep restricted. Individual differences in habitual sleep duration appear to be a trait-like characteristic that is determined by several factors, including genetic polymorphisms.

Although sleep loss has been studied scientifically for the past 112 years, it is only within the past 2 decades that the magnitude of the effects of insufficient sleep (eg, on health, personal and public safety, mood, productivity, and general quality of life) has begun to be widely appreciated. This burgeoning awareness has likely been due to a confluence of factors and events, including the following: (1) increased general knowledge about the pervasiveness and consequences of sleep disorders, in particular, sleep apnea; (2) a complementary profusion of sleep disorders centers; (3) well-publicized catastrophes in which sleepiness has been implicated as a possible causal factor (eg, the Chernobyl meltdown, the Exxon-Valdez oil spill, and the release of poison gas in Bhopal, India); and (4) public awareness campaigns by the National Sleep Foundation and the National Center on Sleep Disorders Research at the National Institutes of Health. In addition, increased awareness of fall-asleep crashes and experimental evidence of impairment from “drowsy driving” comparable to the impairment from alcohol consumption1 have facilitated legislation that is aimed at prosecuting drowsy drivers who cause crashes.2

Ultimately, the efficacy with which sleep loss is gainfully managed at the individual patient and societal levels will be a function of the extent to which its effects on alertness, cognitive performance capacity, and physical and psychological health are specified and understood. Accordingly, for the first 80 to 90 years of the scientific study of sleep loss, a primary focus was on the discovery and cataloguing of the consequences of sleep loss.

In many early studies,35 relatively simple cognitive/psychomotor measures were employed, such as mental addition/subtraction tasks, simple-reaction and choice-reaction time tasks, and measures involving short-term memory. From these studies, general characteristics of sleep loss-mediated performance decrements have been gleaned. These include findings that, for example, sleep loss tends to result in the following: (1) slowed response times; (2) a narrowing of attention, and, not surprisingly; (3) an increased propensity to initiate sleep.

More recently, and spurred in part by findings from functional brain-imaging studies showing that sleep loss results in brain deactivation, especially in the prefrontal cortex, inferior parietal/superior temporal cortex, thalamus, and anterior cingulate,6 contemporary studies of sleep loss have focused more on the potential effects of sleep loss on the higher-order, so-called “executive” cognitive functions like problem solving7 and moral reasoning.8Table 1715 lists a number of relatively recent studies in which the effects of sleep loss on tasks reflecting performance in a variety of cognitive domains have been reported.

Table Graphic Jump Location
Table 1 Example Studies of the Effects of Sleep Deprivation on Different Cognitive Domains

The implication from the plethora of studies conducted over the years, and especially from the more recent studies, is that sleep loss impacts a wide array of cognitive abilities. In fact, the array is so extensive that it is reasonable to posit that sleep loss exerts a nonspecific effect on cognitive performance; that is, that it impairs some essential capacity that is basic to cognitive performance in general (and therefore common to each of the hypothetical constructs such as “decision-making ability” that are ostensibly reflected by such cognitive performance tests). As implied above, this “essential capacity” likely relates to sleep loss-induced brain deactivation (however, the exact neurophysiologic mechanisms driving this deactivation, and thus the function of sleep itself, remain unknown). Thus, at best, cognitive tests administered during sleep loss can currently be considered to be “probes” of the general brain state (as previously suggested5,16), rather than absolute scales that reflect the extent to which sleep loss impacts specific cognitive abilities.

Despite problems in quantifying and comparing the effects of sleep loss on particular cognitive abilities, it has proven possible and useful to develop valid, objective, quantifiable measures of sleepiness itself. The multiple sleep latency test (MSLT) currently serves as the “gold standard” measure of sleepiness in both clinical and research settings.17 In this test, the patient reclines comfortably in bed in a quiet, dark room and is instructed to try to fall asleep when the lights are turned off. Sleep latency (time from lights off to sleep onset) is monitored polysomnographically, and, when used in a research protocol, the patient is awakened shortly after sleep onset so as to prevent a significant accumulation of sleep.18 This test thus serves as a measure of sleep propensity. The nap tests are administered four to six times across the day, and the average sleep latency is calculated to reflect the general level of sleepiness.

The maintenance of wakefulness test (MWT) is similar to the MSLT except that the instructions to the patient are to try to remain awake.19 Therefore, rather than sleep propensity, this test reflects one's ability to resist sleep onset under conditions that are conducive to sleep, an ability that has clear relevance to a number of occupational settings. Accordingly, the Federal Aviation Administration has approved the use of the MWT to determine fitness for duty in pilots who have been treated for sleep apnea.20

The psychomotor vigilance task (PVT) is a 10-min simple reaction time task with a visual vigilance component.21 Decrements in PVT performance such as lapses (ie, reaction times of > 0.5 s) are thought to reflect underlying sleepiness. Although the PVT is a performance task, and thus is susceptible to many non-sleep/sleepiness-related influences (ie, degraded performance on the PVT is not specific to sleep loss), it has been shown to be sensitive to sleep loss effects.22 This, along with logistical considerations such as its portability and ease of administration,23 have likely contributed to its increasing use in sleep research settings.

Several subjective sleepiness scales are also available and widely used, including the following: the Stanford Sleepiness Scale (SSS), in which the patient selects the one statement (of seven) that best describes his/her extant level of sleepiness24; the Karolinska Sleepiness Scale,25 in which sleepiness is rated on a 9-point scale; and the Epworth Sleepiness Scale,26 in which patients rate their likelihood of dozing in various common situations (eg, while riding as a passenger in a car). The validity of such scales have generally been established in studies in which subjective ratings of healthy subjects were found to be correlated with objective sleepiness and/or performance measures across a period of acute sleep deprivation.27

However, the relationship between subjective sleepiness and objective indexes of sleepiness is more tenuous in individuals with chronic sleep disorders such as sleep apnea. Such individuals may report normal subjective alertness despite objective evidence of pathologic sleepiness, suggesting that gradual habituation to the feelings associated with increased sleep pressure has occurred, without a corresponding diminution of the actual pressure to sleep.28

One possibility is that the sleep apnea patient's continued objective performance deficits in the face of a reduced ability to self-assess sleepiness is the result of sleep apnea-mediated damage to the CNS (eg, the result of multiple years of exposure to intermittent hypoxemia during sleep).29 Indeed, the fact that many sleep apnea patients also continue to exhibit objective performance and alertness deficits even after treatment for sleep apnea (eg, with continuous positive airway pressure) has been initiated30 is consistent with the possibility of long-term, and possibly permanent, hypoxia-induced changes in brain physiology and/or structure. However, data that strongly support this hypothesis are currently lacking; it has proven difficult to specify the extent to which neurocognitive deficits are a function of repeated, intermittent hypoxemia vs chronic sleep disturbance.31

Recent evidence has suggested that a similar dissociation between subjective and objective measures of sleepiness also occurs in healthy (ie, non-sleep-apneic) individuals who are subjected to as little as 7 days of sleep restriction. After 1 week of sleep restricted to 3, 5, or 7 h of sleep per night, volunteers' levels of subjective sleepiness returned to baseline levels for all groups after 1 night of 8 h of recovery sleep, while performance (PVT lapses) did not recover to baseline even after 3 nights of recovery sleep.9 This implies that changes in the subjective experience of sleepiness occur as a function of exposure to reduced sleep over time per se, rather than being secondary to apnea-related factors like intermittent hypoxia (although this does not rule out other hypoxia-mediated effects).

Historically, acute (1 to 3 nights) total sleep deprivation and chronic sleep restriction were considered to be quantitatively, but not qualitatively, different. For this reason (and perhaps because of its relative efficiency), acute total sleep deprivation has generally been employed in the preponderance of prior sleep loss studies.

However, results from previous studies suggest that the effects of acute total sleep deprivation may differ from those of extended, chronic sleep restriction in an important way. Although cognitive performance deficits resulting from partial sleep restriction (eg, slow reaction time, impaired decision making, lapses in attention, and memory impairment) appear to be comparable to those occurring as a result of total sleep deprivation, the rate at which these deficits are reversed during subsequent recovery sleep varies considerably. Evidence from the literature on “total sleep deprivation” generally indicates that obtaining 1 or 2 nights of (often extended) recovery sleep restores alertness and performance to previous rested (baseline) levels. However, evidence from the sleep restriction literature indicates that an accommodative/adaptive response to longer term sleep restriction can result in a slower rate of recovery. Table 29,11,3237 presents a summary of chronic sleep restriction and recovery studies, including the effects of sleep restriction on sleepiness and cognitive performance, and recovery rate.

Table Graphic Jump Location
Table 2 Summary of Prior Sleep Restriction and Recovery Studies on Sleepiness and Cognitive Performance*

*POMS = profile of mood states scale (subjective mood); SAST = serial addition/subtraction task (higher order cognitive processing); DSST = digit symbol substitution task (higher order cognitive processing); ANAM = automated neuropsychological assessment metric (computerized battery with serial addition/subtraction task and serial reaction time subtests); SRT = serial reaction time; KSS = Karolinska sleepiness scale (subjective sleepiness).

As shown in Table 2, variability exists in reported recovery rates from partial sleep loss, ranging from as a little as 2 nights consisting of 8 to 10 h of time in bed (TIB) for full recovery to 3 to 5 nights of 8 h TIB being insufficient for full recovery (in some cases varying by task). Although discrepancies exist concerning the number of nights of sleep needed to effect full recovery (ie, to pre-sleep loss, baseline levels), recovery from chronic partial sleep loss is apparently a slow process relative to that of total sleep deprivation.

The physiologic basis underlying the relative extension of the recovery process following partial sleep loss (ie, sleep restriction) is unknown, but one compelling possibility has been suggested by a 2006 animal study conducted by researchers at Harvard University.38 This group showed that extracellular adenosine (AD) accumulates in the brains (especially the cholinergic basal forebrain [BF]) of animals during extended wakefulness, and it declines during subsequent sleep (an effect that promotes subsequent wakefulness via disinhibition of cholinergic BF neurons).39 With an extended (ie, 5-day) exposure to sleep fragmentation procedures, AD levels in the BF of rats gradually wane to baseline levels.40 It has been found that waning AD levels (perhaps reflecting a fatigued capacity for the production and/or release of extracellular AD over an extended period of sleep loss) are offset by a concomitant up-regulation of AD-A1 receptors,41 a process that might effectively keep the drive for sleep high despite reduced extracellular AD levels. However, with subsequent recovery sleep, the baseline capacity to produce/release AD in the BF might be restored quickly, creating a relative “imbalance” in the amount of extracellular AD in the BF relative to the (up-regulated) number of AD-A1 receptors. Down-regulation to a normal density of AD-A1 receptors might take several days, during which time extra sleep (and a continuing depression of alertness/performance) would be manifested. In contrast, recovery following acute total sleep deprivation might occur more quickly because a relatively short time course of the sleep loss (1) would not allow as much “fatiguing” of the AD production/release in the BF; and/or (2) would not be long enough to produce as much up-regulation of AD-A1 receptors.

Epidemiologic evidence42,43 has suggested that both positive and negative deviations from sleep duration norms are associated with increased mortality. The mechanisms underlying this correlational relationship are not clear,44 but results from laboratory studies have suggested that sleep loss impacts metabolic hormones in a manner that may, at least in part, help to account for the relationship between short sleep and mortality. According to a review by Knutson and colleagues,45 the relationships among sleep loss, weight gain, and diabetes risk involves the following multiple pathways: (1) alterations in glucose levels; (2) up-regulation of appetite; and (3) decreased energy expenditure. In one study46,47 in which subjects underwent 6 nights of sleep restricted to 4 h TIB, glucose response/insulin sensitivity was impacted in a manner that was consistent with a diagnosis of “impaired glucose tolerance.” In addition, a dose-response relationship between leptin (a hormone that suppresses appetite) and sleep has been demonstrated. Leptin levels decrease (exacerbating hunger) with less sleep.48 Changes in leptin and ghrelin levels may lead to increased food intake based on an internal perception of an insufficient amount of energy available and the misperception of caloric need.45

To date, only the short-term effects of sleep loss on metabolism have been elucidated. However, there have been some more recent findings49,50 suggesting that chronic sleep restriction may produce similar long-term effects on metabolism. For example, it has recently been found49 that persons sleeping for a short time (ie, 5 to 6 h per night) were 35% more likely to experience a 5-kg weight gain over a period of 6 years than were sleepers of normal duration (ie, 7 to 8 h per night). Also, epidemiologic data from the Nurses Health Study50 revealed an increased risk of diabetes over 10 years in women reporting a sleep duration of ≤ 6 h. Considered together, the short-term laboratory findings and the epidemiologic findings suggest that chronic sleep restriction may be a causative factor in the development of obesity and its attendant health consequences.

There are clearly individual differences in the amount of nightly sleep needed to maintain normal levels of daytime alertness, and there are individual differences in the sensitivity/resilience to sleep loss.51 Based on their finding that the same individual responds similarly to bouts of sleep loss separated by up to 8 weeks, Van Dongen and colleagues52 have suggested that “vulnerability” to the effects of total sleep loss is a stable, trait-like characteristic. In fact, there is evidence53 suggesting that specific polymorphisms in the PER3 gene may mediate the vulnerability to sleep loss.

The extent to which such results might generalize from total sleep deprivation to chronic sleep restriction is not clear. However, there is evidence that persons who habitually sleep for shorter periods generally tend to carry a higher sleep debt (and are therefore potentially more sensitive to the effects of sleep loss) than those who habitually sleep for longer periods. Klerman and Dijk54 found that persons who habitually sleep for shorter periods fell asleep faster on the MSLT, and slept longer during an opportunity for extended sleep, than did those who habitually sleep for longer periods. This suggests that the amount of sleep that is habitually obtained at night is not necessarily an accurate reflection of the amount of nightly sleep that is actually needed.

Similarly, Rupp and colleagues32,33 found that increasing the amount of time spent in bed for 1 week (and thus ostensibly reducing the chronic sleep debt) improved resilience across a subsequent week of sleep restriction (3 h TIB per night) and also improved the rate of subsequent recovery. Based on such results, it is clear that further research is needed to determine the extent to which trait-like characteristics like resilience to the effects of sleep loss are modifiable by long-term changes in sleep habits/duration and whether the identified genetic polymorphisms that serve as markers of resilience/sensitivity to sleep loss actually reflect individual differences in “sleep need” or mediate behaviors that determine individual differences in the amount of sleep typically obtained at night (eg, the amount of chronic sleep debt that one tolerates or carries).

It is beyond the scope of the present article to review the literature on the pharmacologic reversal of sleep loss-related alertness and performance deficits, but some general trends warrant discussion. The extent to which stimulants reverse various sleep loss-induced effects has received much attention, particularly for simple psychomotor tasks and sleep propensity. In short, the currently available stimulants (or “wakefulness-promoting agents” in the case of modafinil), including caffeine, modafinil, dextroamphetamine, and methylphenidate, improve response speed and the ability to maintain wakefulness in a dose-dependent fashion and along a time course that is consistent with the half-lives of various compounds (eg, longer duration effects with dextroamphetamine and modafinil relative to caffeine). Stimulant effects on executive functions have been less well studied. The results of several studies10,55 have suggested that some functions are restored by some compounds but that no one compound restores all functions. The results from these studies are limited by a lack of dose-response information, the inclusion of only a subset of executive function tasks, and a lack of baseline (ie, non-sleep deprived) performance measures on tasks for which multiple versions do not exist (which is the case for many tasks of executive function). Also largely unstudied is the extent to which stimulants maintain efficacy when used long term to reverse chronic sleep restriction effects (whether due to chronic insufficient nighttime sleep or daytime sleep associated with night shift work) in otherwise healthy adults. The effects of stimulants on subsequent sleep generally vary as a function of their half-lives and the timing of sleep periods. Sleep is not overtly disrupted when initiated 20 h after the administration of a stimulant (eg, caffeine, modafinil, or d-amphetamine),55 but is disrupted if attempted within 3 h of caffeine administration56 or within 6.5 h after the administration of dextroamphetamine or modafinil.57 The roles of various neurotransmitter systems in sleep/wake periods continue to be explored and elucidated, and it is likely that better pharmacologic methods of managing sleep and wakefulness will be developed in the coming decades.

Historically, the focus of sleep loss studies has been the effects of total sleep deprivation on generally simple tasks (eg, reaction time). More recent evidence has suggested that executive functions (eg, risk taking and moral reasoning) are also negatively impacted by sleep loss and that chronic sleep restriction leads to physiologic changes that may be linked to obesity and diabetes. A disparity between subjective feelings of sleepiness and objectively measured alertness and performance suggests subjective habituation to chronic sleep loss, a phenomenon that could help to explain why some patients with chronic sleep disruption (eg, those with sleep apnea) deny excessive daytime sleepiness. Whereas total and partial sleep loss each produce similar effects on objectively measured alertness and performance, the time course for recovery from chronic partial sleep loss is relatively extended. It is anticipated that future studies will elucidate the neurophysiologic mechanisms underlying changes in waking functions with sleep loss, the physiologic basis of individual differences in nightly sleep duration (eg, PER3 gene polymorphisms), and lead to more effective sleepiness countermeasures.

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Figures

Tables

Table Graphic Jump Location
Table 1 Example Studies of the Effects of Sleep Deprivation on Different Cognitive Domains
Table Graphic Jump Location
Table 2 Summary of Prior Sleep Restriction and Recovery Studies on Sleepiness and Cognitive Performance*

*POMS = profile of mood states scale (subjective mood); SAST = serial addition/subtraction task (higher order cognitive processing); DSST = digit symbol substitution task (higher order cognitive processing); ANAM = automated neuropsychological assessment metric (computerized battery with serial addition/subtraction task and serial reaction time subtests); SRT = serial reaction time; KSS = Karolinska sleepiness scale (subjective sleepiness).

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