A significant proportion (one third) of our lives is spent asleep, suggesting that it is, indeed, a very important process. The importance of sleep is reiterated by the rebound of sleep after total sleep deprivation and the fact that chronic sleep deprivation can be lethal, e.g., rats die following 2–3 weeks of chronic sleep deprivation.1 Furthermore, the brain is very active during sleep. At some point during sleep, brain neurones are at or near their maximal level of activity as seen in the awake state. This high activity makes it unlikely that there is one function of sleep, but more probable that sleep may have multiple roles.2-4
Researchers are still debating the function of NREM and REM sleep and the reasons why both phases are required. However, since the NREM sleep (Stages 3 and 4) contains the slow waves thought to be associated with the deepest state of sleep it has been proposed that NREM sleep functions to bring about a feeling of refreshment following a night of sleep.
To date, the purpose of sleep has not been fully elucidated. However, various theories have been put forward in an attempt to explain the possible function of sleep. These theories are:
It is well know that smaller animals have higher metabolic rates than animals of a larger body size. Given that metabolic processes are responsible for the generation of free radicals that can damage and even kill cells, smaller animals are at a higher risk of injury to the nucleic acids, proteins, and fats found within the cells.2 Cellular repair is especially crucial for the brain as, unlike other organs and tissues, the cells of the brain are not continually being replaced.5
Just as smaller animals have a higher metabolic rate, they also need more sleep than larger animals, suggesting a possible relationship between metabolic rate and the amount of sleep required. One theory that has been proposed is that the lower energy consumption (and, therefore, lower metabolic rate) occurring in NREM sleep may be one mechanism serving to counteract cellular damage caused by free radicals.2 For example, enzymes may repair cells more efficiently during periods of inactivity, or old enzymes – which themselves have been damaged by free radicals – may be replaced by those that are newly synthesised.2
Reimund (1994) proposed that sleep functions essentially as an antioxidant for the brain.6 According to the proposal, free radicals that accumulate during wakefulness are eliminated during sleep through the increased efficiency of endogenous antioxidant mechanisms and a decreased rate of free radical formation, consistent with a lower metabolic rate as seen in NREM sleep.2 However, this theory only provides a function for NREM sleep. Cellular repair cannot be achieved during REM sleep as most of the neurones are maximally active and may even be as active as during the awake state.2
Where the theory of cellular repair offers a function for NREM sleep, the receptor recovery theory may involve REM sleep. One further characteristic of REM sleep is the cessation of the release of monoamine neurotransmitters responsible for activating motoneurones, e.g., noradrenaline, serotonin, and histamine. The resultant effect is a disabling of body movement and a reduced environmental awareness during REM.
During the awake state, the brain cells responsible for synthesising monoamine neurotransmitters are maximally and continuously active.2 This constant release of monoamines may desensitise the receptors, impacting negatively on their function.
In 1988, Siegel and Rogawski theorised that the cessation of neurotransmitter release is vital for the proper function of onoaminergic neurones and their receptors.2 The interruption of monoamine release during REM sleep may provide time for the monoamine neurotransmitter receptors to recover and regain full sensitivity, and this may be crucial during wake periods and in mood regulation.2
It has been hypothesised that sleep functions to conserve energy by constituting a state of reduced metabolism compared to the resting state.2,7 Support for this theory comes from the fact that infants require a large amount of sleep, possibly to conserve energy for growth. Furthermore, the amount of sleep required decreases with age, representing reduced energy demands reflected by parallel declines in basal metabolic rate and physical activity.7 However, only 5–15% of energy is saved during sleep,8,9 casting doubt on the theory that sleep is a means of energy conservation. Furthermore, research has shown that it is not the need for sleep, but rather the ability to sleep, that decreases with age,10 suggesting that energy conservation is not the main function of sleep.
A more recent hypothesis postulates that both NREM and REM sleep are involved in processing and storing complex sensory information – memory consolidation.11,12 The slow waves of NREM sleep are thought to reinforce individual neural components of complex memory and the links between these components, whereas the fast waves of REM sleep are thought to reinforce both sensory and neural circuitry. Evidence supporting the memory consolidation theory for sleep comes from both humans and rats where the ability to learn new tasks is impaired following REM sleep deprivation.13 However, arguments against the role of sleep in memory consolidation include demonstrations of people with brain damage that prevents REM sleep, or who have a drug-induced blockade of REM sleep, showing normal – or even improved – memory.2
References:
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2. Siegel JM. Why we sleep. The reasons that we sleep are gradually becoming less enigmatic. Scientific American November 2003; 92–97.
3. Giuditta A, Ambrosini MV, Montagnese P, et al. The sequential hypothesis of the function of sleep. Behav Br Res 1995; 69: 157–166.
4. Sejnowski TJ, Destexhe A. Why do we sleep? Br Res 2000; 886: 208–223.
5. Savage VW, West GB. A quantitative, theoretical framework for understanding mammalian sleep. Proc Natl Acad Sci USA 2007; 104 (3): 1051–1056.
6. Reimund E. The free radical flux theory of sleep. Med Hypotheses 1994; 43 (4): 231–233.
7. Berger RJ. Bioenergetic functions of sleep and activity rhythms and their possible relevance to aging. Fed Proc 1975; 34 (1): 97–102.
8. Ravussin E, Lillioja S, Anderson TE, et al. Determinants of 24-hour energy expenditure in man. Methods and results using a respiratory chamber. J Clin Invest 1986; 78: 1568–1578.
9. Shapiro C, Goll CC, Cohen GR, et al. Heat production during sleep. J Appl Physiol 1984; 56: 671–677.
10. Ancoli-Israel S. Sleep problems in older adults: putting myths to bed. Geriatrics 1997; 52 (1): 20–30. 11. Cartwright RD. The role of sleep in changing our minds: a psychologist’s discussion of papers on memory reactivation and consolidation in sleep. Learning & Memory 2004; 11: 660–663.
12. Norman WM, Hayward LF. The neurobiology of sleep. In: Carney PR, Berry RB, Geyer JD, eds. Clinical Sleep Disorders.© Lippincott Williams & Wilkins, Philadelphia, USA, 2005: 38–55.
13. Bear MF, Connors BW, Paradiso MA, eds. Neuroscience. Exploring the brain.© Lippincott Williams & Wilkins, 2001: p620.