An average adult needs around 7-9 hours of sleep per night meaning that with the average UK life expectancy being 79.1 for boys born between 2012-2014 and 82.8 being the life expectancy for girls born during the same period, we will spend on average over 26 years of our life asleep.
Sleep is a huge part of being a living organism with every single known creature displaying some kind of sleep-like behaviour but despite the obvious importance, perhaps one of the oddest facts about sleep is that there is no solid consensus as to what the purpose is. Surely it would make far more sense from an evolutionary perspective to be able to eat, explore and procreate 24 hours per day, and a sleeping individual is one which is obviously in more danger than one which is fully alert. To this latter point, you could state that being still and hidden away during the hours of darkness may be protective but you only have to look to nocturnal animals to see that hiding in the dark is at best an incomplete picture.
There are three main theories as to why we sleep referred to as the restorative, adaptive and energy conservational theories of sleeping. We’ll explain each here in turn:
This is the theory that an organism needs to rest, repair and replenish its energy stores after a period of energy consumption and tissue breakdown (being awake). During sleep a large number of genes in the brain alter their expression patterns, a process which is the same across a number of species including fruit flies, rodents and birds and a number of different brain regions. These genes seem to encode proteins important for protein synthesis, intracellular transport, cholesterol synthesis and other basic cellular functions in the neurons for which expression was altered, indicating a replenishment of important macromolecules there. In contrast, being awake is associated with the expression of different genes including those responsible for RNA processing and the production of molecular chaperones which aid in the folding of proteins (both of which mean that protein synthesis is being performed in the brain during the waking period).
This all suggests that the brain uses sleep as period of recovery, leading up to a subsequent period of wakefulness. What it does not suggest, however, is that sleep is a generalised recovery period because whole body and muscle protein synthesis is typically suppressed during this time owing to the extended period of overnight fasting. There is, of course, the case that protein consumption in the middle of the night will re-stimulate muscle protein synthesis during sleeping hours (in much the same way as consuming sufficient leucine would stimulate MPS at any other time of day, as discussed in module 2) but it’s extremely unlikely that this is something evolutionarily relevant.
Wakefulness across all animals peaks at times of performance and food availability and sleep peaks at the opposite times. Animals which see by daylight and/or eat animals which are present at daytime are awake during this time and sleep when their comparative food availability is lower, while the opposite is true of nocturnal animals. This has played a large role in the evolution of the theory that animals sleep to conserve energy when they are not capable of consuming as much as they may need. This is supported by the fact that your metabolic rate is suppressed during non-REM sleep and the fact that your brain (a major energy user) reduces activity.
This theory has some key flaws, however. Firstly, the metabolic reduction during sleep only happens during non-REM sleep – during REM sleep your metabolic rate increases which would have no adaptive benefit if energy conservation was the goal. Furthermore, the actual reduction in metabolic rate, while being significant and reliable enough to measure and use as a diagnostic tool, is unlikely to actually impact on energy needs as much as you might think. Your metabolic rate drops by around 15% at most during sleeping hours (unless you are in late pregnancy where the difference is smaller) which in real terms means you might use around 100-150kcals less during the night. A very small difference.
This is the theory that sleep is vital for memory, learning and processing information, evidenced by the fact that sleep deprivation rapidly decreases these factors but also by a number of physiological events which occur during sleeping hours.
When individuals are given a memory task and then allowed to sleep before being tested, they reliably perform better at the task than groups who have undergone the same procedure without sleep (simply with rest in between learning and testing). Neuroimaging studies (a more in-depth analysis than EEG which can map out active brain areas) shows that at least some of the brain activity seen during REM sleep correlates with the brain areas involved with a task learned during prior wakefulness (so if you learn something then sleep, the brain area you used during learning is active during REM sleep) which hints at memory consolidation. How does this work?
When you learn something, synapses between neurons are created which reinforce your new knowledge, movement pattern or skill – a process called neural plasticity which is the process of physically altering brain connections to consciously learn. During waking hours, a large number of synapses are created in accordance to a task, some of which are relatively weak, in a process called Long-Term Potentiation (LTP). LTP is not sustainable, however, because an excess of connections leads to a ‘noisy signal’ and takes up vital space that may be needed for other new insights. During sleep, there is a synaptic downscaling which consolidates these memories to leave only the most robust connections. You may experience this when you read something which only half makes sense, go to sleep and then re-read it with perfect clarity.
Evidence for this process lies in the following – Brain Derived Neurotrophic Factor which is a Growth Factor (growth factors are chemicals which bind to specific cellular receptors to cause growth), activity regulated cytoskeleton-associated protein (a plasticity protein), Nerve Growth Factor and P-CREB (Phospho-cAMP response element binding protein) which is important for spatial memory, are all increased proportionally with sleep debt, indicating that an increased amount of time awake leads to an increased amount of non-consolidated neural plasticity. Furthermore, the higher these markers become, the longer you spend in stage 3 sleep which is the stage most associated with net consolidation.
This is a very strong theory, though it still raises some questions. For example, the above theory focuses only on the parts of the brain which form from the telencephalon (the telencephalon in humans develops during the pre-natal period into the cerebral cortex and the basal ganglia – two of the most important brain areas). Some animals do not have a telencephalon such as fruit flies, but these animals still display sleep or sleep-like behaviour.
Because no one theory is wholly correct, and because all three have good evidence to justify them to at least some degree, it’s very likely that the truth is all three played a small role during the evolution of sleep. Whatever the reason why we sleep, it’s evidently important and your body agrees. Sleep is one of the strongest urges we have, and maintaining sleeplessness for more than a few days is extremely difficult. There are two primary drivers to sleep, the circadian pathway and the adenosine pathway which are both fascinating and intricate. Let’s look at those now.