A study using electroencephalography found that the extent of memory retention after sleep is associated with time spent in slow wave sleep. The location where the brain shows neural activity associated with successful memory recall shifted from the parietal areas to the anterior temporal lobe after sleep. The paper was published in Neuropsychologia.

Slow wave sleep is the deepest stage of non-REM sleep, characterized by large, slow brain waves and a highly reduced level of consciousness. During this stage, the brain significantly alters its activity, allowing neurons to rest and recover from daytime demands. It plays a central role in consolidating memories, especially facts and skills learned throughout the day.

Slow wave sleep also supports physical restoration by promoting the release of growth hormone and facilitating tissue repair. The immune system becomes more active during this phase, helping the body fight infections and maintain long-term health. Because the brain is less responsive to external stimuli, slow wave sleep provides the most uninterrupted and restorative rest.

This stage helps clear metabolic waste from the brain, contributing to long-term cognitive health. People who get too little slow wave sleep experience reduced attention, poorer memory, and diminished emotional regulation the following day. Slow wave sleep also helps stabilize neural circuits, making future learning easier.

Study author Simon Faghel-Soubeyrand and his colleagues wanted to assess how sleep may support the reorganization of memory recall networks in the brain. They note that our memories are not static, but that they change in both strength and quality over time. Previous studies indicate that, as these changes happen, the location of brain activity during recall changes. The optimal time for this consolidation to occur is during sleep, when the brain is sheltered from external stimulation. They conducted a study to examine this using high-density electroencephalography (EEG).

Study participants were 24 university students. Their average age was roughly 23 years. Five of them were male.

The participants completed two separate sessions of word-image memory tasks. Word-image memory tasks require people to learn and later recall or recognize associations between written words and corresponding pictures. The two sessions were 7–8 days apart. One set of sessions was “object sessions,” where the images participants learned to associate with words were either a car or a guitar. The other set of sessions was “scene sessions,” where participants associated words with either a house or a corridor. Within a session, images were paired with 100 unique verbs.

Each of these sessions was followed by two recall sessions. One recall session happened before sleep, while the second happened after sleep. In general, the first recall session happened in the evening. The participants then slept through the night. The experimenter would wake them at 7:30 the next morning, and after a few minutes to fully awaken, they would again try to recall what they learned. During these activities, study authors took EEG recordings of the participants’ brain activity.

Results showed that the location in the brain where the strongest signs of recall activity occurred shifted from before to after sleep. While the primary activity during memory recall was in the parietal area of the brain before sleep, it moved towards the anterior temporal lobe after sleep. Individuals who spent more time in slow wave sleep tended to recall more of what they learned after sleep, and the shift in the location of brain activity during recall tended to be greater in these individuals.

Overall, results indicated that the profiles of brain activity during successful recall of memories changed overnight and that the extent of these changes was higher in individuals who spent more time in slow wave sleep.

“Together, these findings suggest a link between SWS [slow wave sleep] and the consolidation and functional reorganisation of episodic memory networks,” study authors concluded.

The study contributes to the scientific understanding of the way memory retention and recall function. However, the study was conducted on a small sample of students. Results on other demographic groups and older individuals might differ.

The paper, “Slow wave sleep is associated with a reorganisation of episodic memory networks,” was authored by Simon Faghel-Soubeyrand, Polina Perzich, and Bernhard P. Staresina.

The brain has its own waste disposal system – known as the glymphatic system – that’s thought to be more active when we sleep.

But disrupted sleep might hinder this waste disposal system and slow the clearance of waste products or toxins from the brain. And researchers are proposing a build-up of these toxins due to lost sleep could increase someone’s risk of dementia.

There is still some debate about how this glymphatic system works in humans, with most research so far in mice.

But it raises the possibility that better sleep might boost clearance of these toxins from the human brain and so reduce the risk of dementia.

Here’s what we know so far about this emerging area of research.

Why waste matters

All cells in the body create waste. Outside the brain, the lymphatic system carries this waste from the spaces between cells to the blood via a network of lymphatic vessels.

But the brain has no lymphatic vessels. And until about 12 years ago, how the brain clears its waste was a mystery. That’s when scientists discovered the “glymphatic system” and described how it “flushes out” brain toxins.

Let’s start with cerebrospinal fluid, the fluid that surrounds the brain and spinal cord. This fluid flows in the areas surrounding the brain’s blood vessels. It then enters the spaces between the brain cells, collecting waste, then carries it out of the brain via large draining veins.

Scientists then showed in mice that this glymphatic system was most active – with increased flushing of waste products – during sleep.

One such waste product is amyloid beta (Aβ) protein. Aβ that accumulates in the brain can form clumps called plaques. These, along with tangles of tau protein found in neurons (brain cells), are a hallmark of Alzheimer’s disease, the most common type of dementia.

In humans and mice, studies have shown that levels of Aβ detected in the cerebrospinal fluid increase when awake and then rapidly fall during sleep.

But more recently, another study (in mice) showed pretty much the opposite – suggesting the glymphatic system is more active in the daytime. Researchers are debating what might explain the findings.

So we still have some way to go before we can say exactly how the glymphatic system works – in mice or humans – to clear the brain of toxins that might otherwise increase the risk of dementia.

Does this happen in humans too?

We know sleeping well is good for us, particularly our brain health. We are all aware of the short-term effects of sleep deprivation on our brain’s ability to function, and we know sleep helps improve memory.

In one experiment, a single night of complete sleep deprivation in healthy adults increased the amount of Aβ in the hippocampus, an area of the brain implicated in Alzheimer’s disease. This suggests sleep can influence the clearance of Aβ from the human brain, supporting the idea that the human glymphatic system is more active while we sleep.

This also raises the question of whether good sleep might lead to better clearance of toxins such as Aβ from the brain, and so be a potential target to prevent dementia.

How about sleep apnoea or insomnia?

What is less clear is what long-term disrupted sleep, for instance if someone has a sleep disorder, means for the body’s ability to clear Aβ from the brain.

Sleep apnoea is a common sleep disorder when someone’s breathing stops multiple times as they sleep. This can lead to chronic (long-term) sleep deprivation, and reduced oxygen in the blood. Both may be implicated in the accumulation of toxins in the brain.

Sleep apnoea has also been linked with an increased risk of dementia. And we now know that after people are treated for sleep apnoea more Aβ is cleared from the brain.

Insomnia is when someone has difficulty falling asleep and/or staying asleep. When this happens in the long term, there’s also an increased risk of dementia. However, we don’t know the effect of treating insomnia on toxins associated with dementia.

So again, it’s still too early to say for sure that treating a sleep disorder reduces your risk of dementia because of reduced levels of toxins in the brain.

So where does this leave us?

Collectively, these studies suggest enough good quality sleep is important for a healthy brain, and in particular for clearing toxins associated with dementia from the brain.

But we still don’t know if treating a sleep disorder or improving sleep more broadly affects the brain’s ability to remove toxins, and whether this reduces the risk of dementia. It’s an area researchers, including us, are actively working on.

For instance, we’re investigating the concentration of Aβ and tau measured in blood across the 24-hour sleep-wake cycle in people with sleep apnoea, on and off treatment, to better understand how sleep apnoea affects brain cleaning.

Researchers are also looking into the potential for treating insomnia with a class of drugs known as orexin receptor antagonists to see if this affects the clearance of Aβ from the brain.

If you’re concerned

This is an emerging field and we don’t yet have all the answers about the link between disrupted sleep and dementia, or whether better sleep can boost the glymphatic system and so prevent cognitive decline.

So if you are concerned about your sleep or cognition, please see your doctor.

 

This article is republished from The Conversation under a Creative Commons license. Read the original article.

 

Adolescents and young adults who consume pre-workout dietary supplements may be sacrificing essential rest for their fitness goals. A recent analysis indicates that individuals in this age group who use these performance-enhancing products are more likely to report sleeping fewer than five hours per night. These findings were published recently in the journal Sleep Epidemiology.

The pressure to achieve an ideal physique or enhance athletic performance drives many young people toward dietary aids. Pre-workout supplements, often sold as powders or drinks, are designed to deliver an acute boost in energy and endurance. These products have gained popularity in fitness communities and on social media platforms.

Despite their widespread use, the potential side effects of these multi-ingredient formulations are not always clear to consumers. The primary active ingredient in most pre-workout blends is caffeine, often in concentrations far exceeding that of a standard cup of coffee or soda. While caffeine is a known performance enhancer, its stimulant properties can linger in the body for many hours.

Kyle T. Ganson, an assistant professor at the Factor-Inwentash Faculty of Social Work at the University of Toronto, led the investigation into how these products affect sleep. Ganson and his colleagues sought to address a gap in current public health knowledge regarding the specific relationship between these supplements and sleep duration in younger populations.

The researchers drew data from the Canadian Study of Adolescent Health Behaviors. This large-scale survey collects information on the physical, mental, and social well-being of young people across Canada. The team focused on a specific wave of data collected in late 2022.

The analysis included 912 participants ranging in age from 16 to 30 years old. The researchers recruited these individuals through advertisements on popular social media platforms, specifically Instagram and Snapchat. This recruitment method allowed the team to reach a broad demographic of digital natives who are often the target audience for fitness supplement marketing.

Participants answered questions regarding their use of appearance- and performance-enhancing substances over the previous twelve months. They specifically indicated whether they had used pre-workout drinks or powders. Additionally, the survey asked participants to report their average nightly sleep duration over the preceding two weeks.

To ensure the results were robust, the researchers accounted for various factors that might influence sleep independently of supplement use. They adjusted their statistical models for variables such as age, gender, and exercise habits. They also controlled for symptoms of depression and anxiety, as mental health struggles frequently disrupt sleep patterns.

The results showed a clear distinction between users and non-users of these supplements. Approximately 22 percent of the participants reported using pre-workout products in the past year. Those who did were substantially more likely to report very short sleep durations.

Specifically, the study found that pre-workout users were more than 2.5 times as likely to sleep five hours or less per night compared to those who did not use the supplements. This comparison used eight hours of sleep as the healthy baseline. The association remained strong even after the researchers adjusted for the sociodemographic and mental health variables.

The researchers did not find a statistically significant link between pre-workout use and sleeping six or seven hours compared to eight. The strongest signal in the data was specifically for the most severe category of sleep deprivation. This suggests that the supplements may be contributing to extreme sleep deficits rather than minor reductions in rest.

Biology offers a clear explanation for this phenomenon. Caffeine functions by blocking adenosine receptors in the brain. Adenosine is a chemical that accumulates throughout the day and promotes sleepiness; by blocking it, caffeine induces a state of alertness.

This mechanism helps during a workout but becomes a liability when trying to rest. Ganson highlights the dosage as a primary concern.

“These products commonly contain large doses of caffeine, anywhere between 90 to over 350 mg of caffeine, more than a can of Coke, which has roughly 35 mg, and a cup of coffee with about 100 mg,” said Ganson. “Our results suggest that pre-workout use may contribute to inadequate sleep, which is critical for healthy development, mental well-being, and academic functioning.”

Beyond simple wakefulness, caffeine also delays the body’s internal release of melatonin. This hormone signals to the body that it is time to sleep. Disrupting this rhythm can make it difficult to fall asleep at a reasonable hour.

Additionally, high doses of stimulants activate the sympathetic nervous system. This biological response increases heart rate and blood pressure. A body in this heightened state of physiological arousal is ill-equipped for the relaxation necessary for deep sleep.

The timing of consumption plays a major role in these effects. Young adults often exercise in the afternoon or evening after school or work. Consuming a high-stimulant beverage at this time means the caffeine is likely still active in their system when they attempt to go to bed.

This sleep disruption is particularly concerning for the age group studied. Adolescents generally require between 8 and 10 hours of sleep for optimal development. Young adults typically need between 7 and 9 hours.

Chronic sleep deprivation in this developmental window is linked to a host of negative outcomes. These include impaired cognitive function, emotional instability, and compromised physical health. The authors note that the very products used to improve health and fitness might be undermining recovery and overall well-being.

“Pre-workout supplements, which often contain high levels of caffeine and stimulant-like ingredients, have become increasingly popular among teenagers and young adults seeking to improve exercise performance and boost energy,” said Ganson. “However, the study’s findings point to potential risks to the well-being of young people who use these supplements.”

The study does have limitations that readers should consider. The data is cross-sectional, meaning it captures a snapshot in time rather than tracking individuals over years. As a result, the researchers cannot definitively prove that the supplements caused the sleep loss.

It is possible that the relationship works in the opposite direction. Individuals who are chronically tired due to poor sleep habits may turn to pre-workout supplements to power through their exercise routines. This could create a cycle of dependency and fatigue.

Furthermore, the study relied on self-reported data. Participants had to recall their sleep habits and supplement use, which introduces the possibility of memory errors. The survey also did not ask about the specific dosage or timing of the supplement intake.

Despite these limitations, the authors argue the association is strong enough to warrant attention from healthcare providers. They suggest that pediatricians and social workers should ask young patients about their supplement use. Open conversations could help identify potential causes of insomnia or fatigue.

Harm reduction strategies could allow young people to exercise safely without compromising their rest. The most effective approach involves timing. Experts generally recommend avoiding high doses of caffeine 12 to 14 hours before bedtime to ensure the substance is fully metabolized.

“Young people often view pre-workout supplements as harmless fitness products,” Ganson noted. “But these findings underscore the importance of educating them and their families about how these supplements can disrupt sleep and potentially affect overall health.”

Future research will need to examine the nuances of this relationship. Longitudinal studies could track users over time to establish a clearer causal link. Researchers also hope to investigate how specific ingredients beyond caffeine might interact to affect sleep quality.

The study, “Use of pre-workout dietary supplements is associated with lower sleep duration among adolescents and young adults,” was authored by Kyle T. Ganson, Alexander Testa, and Jason M. Nagata.