According to research even while resting these huge amphibians were awake enough to respond to painful stimuli and show respiratory changes. Alpine swifts take their travel very seriously. So seriously in fact that when they travel from Switzerland to West Africa they are in flight continuously for days, six months straight. Research shows that there are periods of slowdowns when the birds do not flap as much. But it is still unclear what kind of sleep they get up in air inflight.
Walruses are talented sleepers who can break into snoozes just about anywhere and in any position—they can sleep floating in water, at the bottom of the sea, standing, leaning or lying down on land. They fill themselves with air in parts of their bodies called pharyngeal pouches and stay bobbing in water sleeping without drowning. But these blubbery sleep-loving mammals also have the ability to stay up for a very long time without complete sleep.
Scientists say that walruses can swim and stay awake continuously for 84 hours. They probably rest as much to have energy for these intense periods of non-stop activity.
While most infants of many species sleep a lot more and more deeply than adults, killer whale calves and baby dolphins are exceptions. They will spend the first few months of their lives wide awake with absolutely no sleep.
We interpret these findings to mean that light is a powerful arousing stimulus in zebrafish, not that sleep in this animal is dispensable. Moreover, it is unknown whether in zebrafish prolonged light exposure affects sleep intensity or causes long-term detrimental effects. In the dolphin, not only the existence of sleep itself, but sleep homeostasis has been questioned also. The single published study on this issue, however, clearly shows that unihemispheric sleep is homeostatically regulated Figure 2.
By reviewing the data used to support the claim that sleep is not universal [ 7 ], we instead reach the opposite conclusion: sleep is present and strictly regulated in all animal species that have been carefully studied so far. Harmful consequences of sleep deprivation have been described in many studies. Most dramatically, prolonged sleep deprivation leads to death.
Rats kept awake using the disk-over-water method develop a peripheral syndrome characterized by increased metabolic rate and decreased body weight, which culminates in death after 2—4 wk [ 36 ]. Prolonged sleep deprivation is also fatal in flies [ 37 ], cockroaches [ 38 ], and humans with fatal familial insomnia, who die after developing a syndrome not unlike that seen in sleep-deprived rats [ 39 ].
Pigeons, however, appear capable of surviving prolonged sleep deprivation [ 40 ]. Prolonged sleep deprivation has not been studied in other species. Thus, it is unclear whether death, when it occurs, is due to loss of sleep per se or to other factors, such as forced arousals and the associated stress. Whether or not sleep loss is lethal, sleep deprivation has two consequences that never fail to occur but see Figure 2.
The first one is intrusion of sleep into wakefulness. When wakefulness is enforced, sleep pressure increases and sleep cannot be avoided, irrespective of stimulation. It is easier to keep humans awake. Especially motivated subjects can be kept awake for up to several days for 11 d in the famous case of Randy Gardner [ 47 ] by keeping busy with pleasurable activities. Although seriously sleep deprived humans have been reported to fall asleep even in the most dangerous situations [ 48 ].
People may seem superficially awake moving and with eyes open even though the EEG slows down or exhibits microsleeps [ 49 , 50 ]. Few studies so far have investigated the leakage of slower brain activity in the EEG of sleep deprived humans, though several studies show an increase in power in the theta frequency bands with prolonged wakefulness and sleep deprivation [ 50 , 51 ].
Whatever the underlying cellular events, it seems impossible to completely deprive an animal of sleep for more than 24 h [ 54 ]. The second documented consequence of sleep deprivation is performance deterioration, especially cognitive impairment. Intriguingly, there is great inter-individual variability in the susceptibility of humans to the effects of sleep deprivation, and subjects whose performance is little impaired by one task may show great impairment in another task [ 55 , 56 ].
Partial sleep restriction also impairs cognitive performance, although subjects may not realize that they are impaired [ 57 , 58 ]. Cognitive impairment is easier to study in humans than in animals, but there is now evidence that both acute sleep loss and sleep restriction affect cognitive function in flies [ 59 ], birds [ 60 ], and rodents e. For instance, when we are jet-lagged, the circadian system may at times dampen the activity of arousal systems and boost that of sleep-promoting systems in brainstem, hypothalamus, and basal forebrain [ 62 ], even though we may not have been awake for long and presumably do not need extra sleep.
Conversely, it may be that brain cells actually do get tired as a function of waking activities, whether or not the arousal systems are pushing the organism to stay awake. This may be the case, for instance, when we try to prolong wakefulness using amphetamines or other arousal-promoting drugs: though we are alert, certain aspects of performance seem to deteriorate [ 63 ].
Pure tiredness can be conceptualized as the inability of brain cells to continue functioning in their normal waking mode, despite the central wake-promoting mechanisms telling the brain it should be fully alert. PET studies show that glucose metabolism decreases more in prefrontal and parietal association areas involved in attention, judgment, and associative functions than in primary sensory and motor areas [ 64—67 ]. Altogether, then, while we still do not understand whether sleep deprivation is followed by sleep intrusions and cognitive impairment because we become sleepy, tired, or both, the evidence so far indicates that, contrary to the predictions of the null hypothesis, lack of sleep has serious consequences, especially for the brain.
The three corollaries of the null hypothesis do not seem to square well with the available evidence: there is no convincing case of a species that does not sleep, no clear instance of an animal that forgoes sleep without some compensatory mechanism, and no indication that one can truly go without sleep without paying a high price. What many concluded long ago still seems to hold: the case is strong for sleep serving one or more essential functions [ 9 , 10 ].
But which ones? The points below represent judgment calls that may be helpful in provoking discussions, guiding hypotheses and, above all, inspiring experimental tests. It may still be wise to search for a function or functions that apply to all animals. It is unknown whether a proto-sleep state emerged early in evolution, perhaps out of the rest—activity cycle, or whether sleep emerged multiple times in the course of evolution.
In either case, the simplest hypothesis after the null hypothesis is that sleep evolved to serve the same function in all species. There is no doubt that sleep, by changing so many aspects of physiology and behavior, affects the vast majority of body functions, from immunity to hormonal regulation to metabolism to thermoregulation.
However, the simplest hypothesis after the null hypothesis is that there may be a single core function that requires sleep, and adventitious functions that take advantage of sleep. Sleep comes in many forms. It is therefore assumed that these two phases of sleep perform quite different functions. It is highly unlikely that fly brains can produce slow waves or spindles [ 18 ], and they do not seem to have the equivalent of REM sleep. The mechanisms of sleep can also vary considerably: the hypocretin—orexin system has an arousing action in mammals but may have a hypnogenic effect in zebrafish [ 21 ].
It may be, of course, that each variation in sleep phenotype or mechanism implies a different function and to some extent functional differences must exist , but it is perhaps more parsimonious to assume that there may be many ways to achieve the same goal. After all, in NREM as in REM stages, in fruit flies as in zebrafish as in humans, the organism or parts of it is quiescent and unresponsive—that is, asleep.
Although the entire body benefits from sleep [ 71 ], the most immediate, unavoidable effect of sleep deprivation is cognitive impairment. The brain suffers most from sleep deprivation. It is less clear that the rest of the body suffers as rapidly, significantly, or inevitably from lack of sleep. Although we talk about a muscle that is active or at rest, muscle rest can be achieved during quiet wakefulness, and does not seem to require sleep. However, few studies have compared directly the restorative value of quiet wakefulness and sleep for either the brain or any other organ [ 48 , 72 ].
This is a research approach that clearly deserves more emphasis in the future. If sleep has a core function involving the brain, such a function might be identifiable at the cellular level and there would be a price for brain cells to remain indefinitely awake.
Indeed, the search for the function of sleep has often focused on identifying neuronal resources depleted during wakefulness and restored during sleep or, alternatively, neurotoxic substances that accumulate during wakefulness and dissipate during sleep.
In mice, sleep may favor the replenishment of glycogen in glial stores [ 73 ], but this may be the case in only a few brain regions, and not in all mouse strains [ 74 , 75 ]. It has also been proposed that sleep may allow the removal of toxic free radicals accumulated in the brain during wakefulness [ 76 , 77 ]. However, studies in long-term sleep deprived rats found evidence for oxidative stress, but not oxidative damage e. This result suggests that the cellular stress response induced during wakefulness may be sufficient to avoid long-term negative effects [ 80 , 81 ].
Other possibilities that are worth exploring are inspired by the recent systematic data on changes in brain gene expression that occur between sleep and wakefulness or after sleep deprivation [ 16 , 17 , 80 , 82—89 ]. In all species studied flies, mice, rats, hamsters, and sparrows , wakefulness leads to the up-regulation of three categories of transcripts—those involved in energy metabolism, in the response to cellular stress, and in activity-dependent processes of synaptic potentiation.
One way to make sense of these apparently disparate findings is in terms of plastic processes. For example, we have suggested that during wakefulness, when animals interact with the environment and need to learn, there is a net increase in synaptic strength in many brain areas, in which case sleep would be needed to renormalize such changes [ 90 , 91 ].
A net increase of synaptic strength at the end of a waking day would result in higher energy consumption [ 92 , 93 ], larger synapses that take up precious space [ 94 ], and saturation of the capacity to learn. Also, a net strengthening of synapses likely represents a major source of cellular stress [ 80—82 ], due to the need to synthesize and deliver cellular constituents ranging from mitochondria to synaptic vesicles to various proteins and lipids.
In this view, then, sleep would be necessary to renormalize synapses to a baseline level that is sustainable and ensures cellular homeostasis.
If wakefulness were as good as sleep in fulfilling a fundamental biological function or even nearly as good , is it likely that sleep would be so ubiquitous? Why would an animal choose to spend long periods of time not just immobile, but above all disconnected from the environment?
It would seem that, if sleep has a core function, and if this function is for the brain, it should be one the brain cannot fulfill during wakefulness, and one that benefits from being performed off-line. Among several options, those related to plasticity and memory are especially intriguing, not least since during sleep, despite the functional disconnection from the environment, most neurons remain spontaneously active at levels similar to wakefulness [ 95 ].
Off-line activity may be necessary to stimulate synapses that remain underused during the waking day [ 96—98 ], so they can be ready when their turn comes. A related idea is that an offline activation of neural circuits may be especially important during development [ ], perhaps to rehearse innate behavioral patterns [ ]. And perhaps sleep may even favor the formation of new synaptic contacts to refresh the repertoire of circuits available for the selection and acquisition of new memories [ ].
Alternatively, sleep may be a good time for consolidating and integrating new memories without interference from ongoing activities, and indeed human studies have provided evidence for sleep-dependent memory consolidation, at least in some tasks [ , ].
Consolidation may happen, for instance, by further strengthening synapses already potentiated during wakefulness [ , , ]. This scenario would prevent runaway synaptic potentiation and the saturation of the ability to learn.
Moreover, it would dovetail nicely with the cellular need for synaptic homeostasis: renormalizing synapses during sleep would counteract the cellular stress brought about by synaptic potentiation during wakefulness.
While there is still no consensus on why animals need to sleep, it would seem that searching for a core function of sleep, particularly at the cellular level, remains a worthwhile exercise. Especially if, as argued here, sleep is universal, tightly regulated, and cannot be eliminated without deleterious consequences.
In the end, the burden of proof rests with those who are attempting not only to reject the null hypothesis, but to gather positive evidence for the elusive phoenix of sleep. We thank Drs. Irene Tobler and Emmanuel Mignot for providing some of the pictures shown in Figure 1.
National Center for Biotechnology Information , U. PLoS Biol. Published online Aug Author information Copyright and License information Disclaimer. E-mail: ude. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
This article has been cited by other articles in PMC. Sleep Function: The Null Hypothesis So far the null hypothesis has survived better than alternatives positing some core function for sleep [ 8—10 ]. Open in a separate window. Figure 1. Figure 2. Sleep in Dolphins: A Difficult Case? Sleep intrusion. Cognitive impairment. Sleepy or tired? Sleep Function: Beyond the Null Hypothesis The three corollaries of the null hypothesis do not seem to square well with the available evidence: there is no convincing case of a species that does not sleep, no clear instance of an animal that forgoes sleep without some compensatory mechanism, and no indication that one can truly go without sleep without paying a high price.
A universal function. A core function. A function transcending specific phenotypes and mechanisms. A neural function. A cellular function. A function that cannot be provided by quiet wakefulness and that benefits from environmental disconnection.
Conclusion While there is still no consensus on why animals need to sleep, it would seem that searching for a core function of sleep, particularly at the cellular level, remains a worthwhile exercise.
Acknowledgments We thank Drs. References Zepelin H, Rechtschaffen A. Mammalian sleep, longevity, and energy metabolism. Brain Behav Evol. Animal sleep: a review of sleep duration across phylogeny.
Neurosci Biobehav Rev. Phylogenetics and the correlates of mammalian sleep: A reappraisal. Sleep Med Rev. Asked 8 years, 11 months ago. Active 6 years ago. Viewed 15k times. Today I came across this picture: So I searched a bit about it. In this wiki answer it is stated that: Bullfrogs do sleep. They sleep underground from 2- 4 weeks.
Sounded ok, but in this website, frogmatters , it 1 says the opposite, thus confirming the picture: [ Improve this question. Community Bot 1. Alenanno Alenanno 1, 2 2 gold badges 10 10 silver badges 23 23 bronze badges. Add a comment. Active Oldest Votes.
Trends Neurosci — 23 Hobson JA Electrographic correlates of behavior in the frog with special reference to sleep. Improve this answer. Thanks for the answer. Alenanno - Yes, but there were some problems with the testing, so the results should be taken with a grain of salt. Featured on Meta.
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