Recent studies using mathematical modelling have demonstrated that the neurotransmitter orexin may allow us to resist the actions of the VPLO. Nerve cells in the VLPO can die off as we age – this is thought to be part of the reason our sleep quality declines later in life. Our sleepiness needs to be almost completely dissipated before the VPLO will switch off and allow us to wake up. This is why (at least in good sleepers) we don’t wake up soon after falling asleep. This action can be described as a switch that gets stuck on either one of two states – wakefulness or wake inhibition. It does so by blocking the action of the wake-promoting brain regions, which induces sleepiness and promotes the state of sleep. There are thought to be “wake-promoting” centres in the brain that use chemical messengers (“neurotransmitters”, such as serotonin) to stimulate the arousal centres of the brain.Ī small cluster of cells in the brain (called the ventrolateral preoptic nucleus – VLPO) is thought to monitor the sleepiness levels of the brain, triggering sleep when these levels become excessive. What’s happening in our brain during the sleep-wake process is largely unknown. Sleep disorders such as obstructive sleep apnoea, hypersomnia (excessive sleepiness) and narcolepsy can cause significant daytime sleepiness, increase the risk of accidents and reduce productivity. While these different factors occur in healthy people, daytime sleepiness may also be a sign of an underlying sleep disorder. This could be due to environmental noise or light, stress, a newborn baby, or difficulty sleeping on hot summer nights. These factors are made worse if we didn’t get enough sleep at night. With enough stimulation, variety and motivation, we can usually overcome a certain level of sleepiness. He recommends lecturers introduce variation every ten minutes, such as engaging the students by asking a question, or changing the delivery style. In John Medina’s book “ Brain Rules”, he says students’ attention levels start to decline around ten minutes into a lecture. This may explain why if we are in a lecture or meeting that is not particularly stimulating, we may drift off. Boredom can make the time-on-task effect worse. The same can be true over longer periods of time, for example, during a long work shift or lecture. from There can also be a time-on-task effect: the longer a person is engaged in a repetitive task the more mental fatigue accumulates. While there may be climatic and cultural reasons for this midday nap, there are also biological processes in play that make it easier to fall asleep at this time of day.įalling asleep in lectures – it’s not just boredom. This is a common time for a midday siesta (derived from the Latin hora sexta “sixth hour”) to take place. Most of us have experienced that dozy feeling we get in the mid-afternoon, aptly referred to as the “post-lunch dip”. Our lowest alertness level (the nadir) is around 4am, with a second drop in the early afternoon. Our alertness also waxes and wanes across the day and night, reflecting a circadian rhythm. Once sleep is initiated, the propensity for sleep reduces the longer we are asleep. The longer we stay awake, the higher our drive or propensity for sleep (making it easier to fall asleep) and the sleepier we feel. We might feel drowsy during the day for a number of reasons, including prescription medication, eating a big meal, dehydration and medical conditions.įrom a sleep science perspective, our alertness levels can be influenced by three factors: time awake, time of day, and time on task.
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