Obstructive sleep apnoea may be a risk factor for developing abdominal aortic aneurysms, according to researchers from the University of Missouri School of Medicine and NextGen Precision Health.
Abdominal aortic aneurysms occur when the aorta swells and potentially ruptures, causing life-threatening internal bleeding. Obstructive sleep apnoea is characterised by episodes of a complete or partial airway collapse with an associated drop in oxygen saturation or arousal from sleep. It can increase the risk of developing cardiovascular problems. Citing studies that indicate a higher prevalence of abdominal aortic aneurysms in patients with obstructive sleep apnoea, MU researchers examined the link between the two using mouse models.
The research team found that intermittent hypoxia caused by obstructive sleep apnoea increased the susceptibility of mice to develop abdominal aortic aneurysms.
“Chronic intermittent hypoxia by itself is not enough to cause abdominal aortic aneurysms, but for a patient with obstructive sleep apnoea who also has additional metabolic problems like obesity, our findings suggest it may help degrade aortic structures and promote aneurysm development,” said Luis Martinez-Lemus, study author and a professor of medical pharmacology and physiology.
Intermittent hypoxia happens during obstructive sleep apnoea when throat muscles relax and block the flow of air into the lungs. According to the research, the loss of oxygen triggers certain enzymes called MMPs. The increased enzyme activity can degrade the extracellular matrix, which acts like a cell scaffolding network, weakening the aorta.
“Patients with abdominal aortic aneurysms usually don’t notice any symptoms, except for some back and belly pain, until the aneurysm bursts. Once that happens, it’s crucial to get the patient to surgery quickly so doctors can repair the aorta,” said Neekun Sharma, the lead author of the study. “Learning how these aneurysms develop can help us find ways to monitor or slow down their progression, especially for patients who have obstructive sleep apnoea.”
In the US, nearly 40 million adults have sleep apnoea, and more than 30 million of them use a continuous positive airway pressure (CPAP) machine while sleeping. But the machines tend to be expensive, clunky and uncomfortable – resulting in many users giving up on using them.
Hypertension is often linked with sleep apnoea because the brain works harder to regulate blood flow and breathing during sleep. A recent study at the University of Missouri (Mizzou) offers new insight into the underlying mechanisms within the brain contributing to hypertension for those with sleep apnoea.
The findings, which are published in the Journal of Physiology, can help pave the way for new drugs that target the brainstem to bring blood pressure back down to normal levels for those with sleep apnoea.
The study took place in the lab of David Kline, a professor in Mizzou’s College of Veterinary Medicine and researcher at the Dalton Cardiovascular Research Center.
“When oxygen levels in the blood drop during sleep apnoea, the forebrain sends warning signals to the brainstem area that controls heart and lung functions,” Kline said. “By studying these signals, we found that two neurochemicals, oxytocin and corticotropin-releasing hormone (CRH), cause the brainstem to become overactive. Over time, this leads to hypertension.”
Hypertension leads to an increased risk of stroke, complications in the metabolism and a variety of other health issues.
“Not only do those with sleep apnoea often have high blood pressure, but they also lose a lot of sleep, they have more cognitive and memory issues, and they are more prone to injury at work due to sleepiness,” Kline said.
By being the first to identify the role that oxytocin and CRH play in strengthening and overexciting the pathways and mechanisms involved in sleep apnoea, Kline and his fellow researchers hope to pave the way for the design of better therapeutic approaches for humans and animals.
“Our ultimate goal is to eventually help clinicians develop specific drugs to target either these neurochemicals or the proteins they bind to in a way that reduces high blood pressure,” Kline said. “This discovery opens the door for future research to block the pathways these neurochemicals use, ultimately helping to bring blood pressure back to normal levels.”
In an international phase III study, researchers have demonstrated the potential of tirzepatide, known to manage type 2 diabetes, as the first effective drug therapy for obstructive sleep apnoea (OSA), a sleep-related disorder characterised by repeated episodes of irregular breathing due to complete or partial blockage of the upper airway.
The results, published in the New England Journal of Medicine, highlight the treatment’s potential to improve the quality of life for millions around the world affected by OSA.
“This study marks a significant milestone in the treatment of OSA, offering a promising new therapeutic option that addresses both respiratory and metabolic complications,” said Atul Malhotra, MD, lead author of the study, professor of medicine at University of California San Diego School of Medicine and director of sleep medicine at UC San Diego Health.
OSA can result in reduced blood oxygen levels and can also be associated with an increased risk of cardiovascular complications, such as hypertension and heart disease. Recent studies, also led by Malhotra, suggest that the number of OSA patients worldwide is close to 936 million.
Conducted in two Phase III, double-blinded, randomised, controlled trials, the new study cohort recruited 469 participants from 9 countries with clinical obesity and living with moderate-to-severe OSA. Participants either used or did not use continuous positive airway pressure (CPAP) therapy, the most common sleep apnoea treatment which uses a machine to maintain an open airway during sleep, preventing interruptions in breathing. Patients were administered either 10 or 15mg of the drug by injection or a placebo and followed for 52 weeks.
Researchers found that tirzepatide led to a significant decrease in the number of breathing interruptions during sleep, a key indicator used to measure the severity of OSA. This improvement was much greater than what was seen in participants that were given a placebo. Importantly, some participants that took the drug reached a point where CPAP therapy might not be necessary. Considerable data suggest that a drug therapy that targets both sleep apnoea and obesity is beneficial rather than treating either condition alone.
Additionally, the drug therapy improved other aspects related to OSA, such as reducing the risk factors of cardiovascular diseases and improved body weight. The most common side effect reported was mild stomach issues.
“Historically, treating OSA meant using devices during sleep, like a CPAP machine, to alleviate breathing difficulties and symptoms,” Malhotra said. “However, its effectiveness relies on consistent use. This new drug treatment offers a more accessible alternative for individuals who cannot tolerate or adhere to existing therapies. We believe that the combination of CPAP therapy with weight loss will be optimal for improving cardiometabolic risk and symptoms. Tirzepatide can also target specific underlying mechanisms of sleep apnoea, potentially leading to more personalised and effective treatment.”
Malhotra adds that having a drug therapy for OSA represents a significant advancement in the field.
“It means we can offer an innovative solution, signifying hope and a new standard of care to provide relief to countless individuals and their families who have struggled with the limitations of existing treatments,” said Malhotra. “This breakthrough opens the door to a new era of OSA management for people diagnosed with obesity, potentially transforming how we approach and treat this pervasive condition on a global scale.”
Next steps include conducting clinical trials to examine longer term effects of tirzepatide.
A new review of research evidence has explored the key differences in how women and men sleep, variations in their body clocks, and how this affects their metabolism. Published in Sleep Medicine Reviews, the paper highlights the crucial role sex plays in understanding these factors and suggests a person’s biological sex should be considered when treating sleep, circadian rhythm and metabolic disorders.
Differences in sleep
The review found women rate their sleep quality lower than men’s and report more fluctuations in their quality of sleep, corresponding to changes throughout the menstrual cycle.
“Lower sleep quality is associated with anxiety and depressive disorders, which are twice as common in women as in men,” says senior author Dr Sarah L. Chellappa from the University of Southampton. “Women are also more likely than men to be diagnosed with insomnia, although the reasons are not entirely clear. Recognising and comprehending sex differences in sleep and circadian rhythms is essential for tailoring approaches and treatment strategies for sleep disorders and associated mental health conditions.”
The paper’s authors also found women have a 25 to 50% higher likelihood of developing restless legs syndrome and are up to four times as likely to develop sleep-related eating disorder, where people eat repeatedly during the night.
Meanwhile, men are three times more likely to be diagnosed with obstructive sleep apnoea (OSA). OSA manifests differently in women and men, which might explain this disparity. OSA is associated with a heightened risk of heart failure in women, but not men.
Sleep lab studies found women sleep more than men, spending around 8 minutes longer in non-REM (Rapid Eye Movement) sleep, where brain activity slows down. While the time we spend in NREM declines with age, this decline is more substantial in older men. Women also entered REM sleep, characterised by high levels of brain activity and vivid dreaming, earlier than men.
Variations in body clocks
The all-woman research ream from the University of Southampton in the UK, and Stanford University and Harvard University in the United States, found differences between the sexes are also present in our circadian rhythms.
They found melatonin, a hormone that helps with the timing of circadian rhythms and sleep, is secreted earlier in women than men. Core body temperature, which is at its highest before sleep and its lowest a few hours before waking, follows a similar pattern, reaching its peak earlier in women than in men.
Corresponding to these findings, other studies suggest women’s intrinsic circadian periods are shorter than men’s by around six minutes.
Dr Renske Lok from Stanford University, who led the review, says: “While this difference may be small, it is significant. The misalignment between the central body clock and the sleep/wake cycle is approximately five times larger in women than in men. Imagine if someone’s watch was consistently running six minutes faster or slower. Over the course of days, weeks, and months, this difference can lead to a noticeable misalignment between the internal clock and external cues, such as light and darkness.
“Disruptions in circadian rhythms have been linked to various health problems, including sleep disorders, mood disorders and impaired cognitive function. Even minor differences in circadian periods can have significant implications for overall health and well-being.”
Men tend to be later chronotypes, preferring to go to bed and wake up later than women. This may lead to social jet lag, where their circadian rhythm doesn’t align with social demands, like work. They also have less consistent rest-activity schedules than women on a day-to-day basis.
Impact on metabolism
The research team also investigated if the global increase in obesity might be partially related to people not getting enough sleep – with 30% of 30- to 64-year-olds sleeping less than six hours a night in the United States, with similar numbers in Europe.
There were big differences between how women’s and men’s brains responded to pictures of food after sleep deprivation. Brain networks associated with cognitive (decision making) and affective (emotional) processes were twice as active in women than in men. Another study found women had a 1.5 times higher activation in the limbic region (involved in emotion processing, memory formation, and behavioural regulation) in response to images of sweet food compared to men.
Despite this difference in brain activity, men tend to overeat more than women in response to sleep loss. Another study found more fragmented sleep, taking longer to get to sleep, and spending more time in bed trying to get to sleep were only associated with more hunger in men.
Both women and men nightshift workers are more likely to develop type 2 diabetes, but this risk is higher in men. Sixty-six per cent of women nightshift workers experienced emotional eating and another study suggests they are around 1.5 times more likely to be overweight or obese compared to women working day shifts.
The researchers also found emerging evidence on how women and men respond differently to treatments for sleep and circadian disorders. For example, weight loss was more successful in treating women with OSA than men, while women prescribed zolpidem may require a lower dosage than men to avoid lingering sleepiness the next morning.
Dr Chellappa added: “Most of sleep and circadian interventions are a newly emerging field with limited research on sex differences. As we understand more about how women and men sleep, differences in their circadian rhythms and how these affect their metabolism, we can move towards more precise and personalised healthcare which enhances the likelihood of positive outcomes.”
Research into the link between disordered sleep and disease show an outsized burden on the most vulnerable. It’s sounding alarms for sleep equity to have a place on the public health agenda, reports Ufrieda Ho.
Scientists are increasingly connecting the dots on how a lack of sleep places a disproportionate health burden on at-risk population groups, including people living with HIV, women, informal workers, the elderly and the poor.
This year’s World Sleep Day on 15 March focuses on sleep equity. Researchers say that tackling sleep inequity and raising awareness for the importance of sleep as a pillar of good health could help stave off several looming public health pressures.
The lack of healthy sleep is linked to cardiovascular disease, obesity, hypertension, diabetes, mental health conditions and dementia. In South Africa, understanding the connection between sleep and HIV is also key to managing the health of the large ageing population of people living with the disease.
Karine Scheuermaier is associate professor at the Wits University Brain Function Research Group. The country’s oldest sleep laboratory founded in 1982 is based at the university’s medical school in Parktown, Johannesburg.
“Society understands the role of exercise and diet in good health but somehow sleep has not had the same kind of awareness or priority, even if sleep is linked to how well your body functions and your chances of developing disease,” she says. “We do everything else at the expense of sleep. Sleep is somehow a symbol of laziness in a work-driven society and we need to change this thinking.”
Sleep inequity in SA
Sleep inequity is linked to socio-economic realities, she says. Sleep inequity might affect the person who lives in an environment where safety and security is neglected or where there is a high threat of gender-based violence. It could also be having to navigate apartheid city planning that forced black people to live far from job hubs. This legacy means today many workers still wake up early to face long work commutes daily. There could also be inequity in division of labour in households, when one person wakes up to take care of children or elderly family members in the home.
Living in overcrowded informal settlements also presents disturbances for good sleep, including high levels of noise and bright floodlights as street lighting. Those who work in unregulated or informal sectors, including shift work or digital platform workers, like e-hailing drivers, are prone to lose out on quality sleep.
clinic that does clinical work, research, and training. Chandiwana says homing in on the intersection of HIV and sleep is critical in a South African context.
“The average person living with HIV who has started antiretroviral treatment on time should live as long as a person who doesn’t have HIV. But what we know is that the person with HIV is on average, living 16 years less of good health. They are more likely to develop type II diabetes, mental health issues, obesity, and heart disease – and we know poor sleep is linked to this,” she says.
Chandiwana says sleep science is still a relatively new field of medicine and the nascent research is still looking to better understand how sleep deprivation triggers immune pathways and chronic inflammation in people living with HIV, even those who are healthy and respond positively on treatment.
A current study at the clinic is looking into the intersection of obesity, sleep apnoea, and women living with HIV. Chandiwana says because so much is unknown, the issue of sleep equity extends to support and funding for more locally appropriate sleep research. Medical school curricula needs to change and more avenues to train people in sleep research needs to be established, she says.
“We have very little African data on sleep disorders and disordered sleep,” she says. She argues we need better data on things like how many people are affected by poor sleep, a better understanding of what is causing it and what it means, and then we need to present these findings to public health authorities to look at it as a public health issue.
“We do have specific challenges in our country. If you are trying to explain to someone, who isn’t South African, how the impact of load-shedding affects sleep or how living in a shack affects sleep, it’s not always easy to do,” she says.
Chandiwana says countries in the global North are already counting insufficient quality sleep as an economic cost measured in loss of productivity, efficiency, safety and society’s well-being. They are also changing public health policies accordingly. South Africa and the rest of the continent stand to be left behind, she says.
How to get better sleep in SA
Chandiwana says: “There is no lab in South Africa that does sleep studies for people in the public sector and no place in the public sector for people to even be diagnosed for a sleep disorder – so services are extremely limited. With something like sleep apnoea, we can’t offer patients in the public sector the gold standard intervention of CPAP [continuous positive airway pressure, which is a device of a face mask, a nose piece, and a hose that delivers a steady flow of air pressure to keep airways open while someone sleeps] because this is financially out of reach. Instead, we have to work with patients to help them lose weight and do positional therapy like training them to sleep on their backs.”
Other ways to get better sleep without costly intervention or sleeping tablets, the two scientists say, include getting exercise, not having food, stimulants or alcohol two to three hours before bedtime, limiting screen time of all kinds in the hour around bedtime, getting exposure to the early morning sunlight each day, keeping sleeping areas dark, quiet and at a comfortable temperature, and developing fixed sleep routines and sleep time rituals – like brushing your teeth, putting on pyjamas, reading for a short period and then going to sleep.
Ultimately, Chandiwana suggests it all comes back to building awareness that healthy sleep is part of health rights.
“We have to fight for sleep equity and we need people to know that sleep is not elitist – it’s not just reserved for some,” she says, “and we should not be accepting poor sleep as the norm”.
New research in the Annals of Internal Medicine reports that the drug solriamfetol is the most effective treatment for excessive daytime sleepiness (EDS) for people with obstructive sleep apnoea (OSA).
The standard treatment for OSA is a positive airway pressure (PAP) mask that uses compressed air to support lung airways during sleep. However, some people with OSA still experience EDS and may benefit from anti-fatigue medication.
“The most important thing that people with OSA should do is use their PAP machine, but if they are still sleepy there are options in the form of medications that can reduce their tiredness,” said first author Tyler Pitre, a resident physician in internal medicine at McMaster University and incoming respirology fellow at the University of Toronto.
“Fifteen to 30 per cent of people in North America have a diagnosis of OSA and the prevalence could be much higher as many others are undiagnosed. Many people have symptoms as the condition is highly associated with obesity, which affects a large and increasing number of people in Canada, the United States and other high-income countries,” he said.
“Among those patients, many will have EDS, which affects their quality of life, making them less productive and also puts them at risk of other psychological issues. Improving this situation is of paramount importance to physicians.”
Pitre said that OSA affects nearly one billion people globally, leaving many of them at risk of EDS.
Zeraatkar and Pitre made their findings by conducting a systematic review of 14 clinical trials of anti-fatigue medications involving 3085 people, as well as analysing data from MEDLINE, CENTRAL, EMBASE and ClinicalTrials.gov in a specific network meta-analysis. They conducted their research from October 2022 to January 2023.
Senior author Zeraatkar said that while solriamfetol is likely the best medication for EDS, the drugs armodafinil-modafinil and pitolisant are also effective in combatting fatigue.
Solriamfetol can also raise blood pressure, especially risky for people with OSA, as many of them also have cardiovascular issues.
“It would be interesting to see how effective these anti-fatigue medications will be for treating related illnesses such as chronic fatigue syndrome and long COVID, now that we know they work for a similar condition,” said Zeraatkar, an assistant professor of the Department of Anesthesia.
A new study published in the American Journal of Respiratory and Critical Care Medicine has tested a sleep apnoea treatment using a drug that inhibits carbonic anhydrase – an enzyme that balances carbonic acid and carbon dioxide in the body. The treatment reduced breathing pauses by more than 20 per hour for patients given the drug.
Several drugs with carbonic anhydrase (CA) inhibitory properties are already available on the market, and used for treatment of glaucoma, epilepsy and other disorders.
Previous research has not systematically tested whether CA inhibitors also might be used to treat obstructive sleep apnoea. A total of 59 patients with moderate or severe sleep apnoea completed the four-week trial, and were randomised to two groups receiving either 400 or 200 mg of the CA inhibitor, and a control group that received placebo.
The results show that, overall, the treatment reduced the number of breathing pauses and promoted oxygenation during the night. A few patients experienced side effects, such as headache and breathlessness, which were more common in those receiving the highest dose.
The study results together with established safety data of the drug sulthiame provide support for continued research on CA inhibition as a new potential treatment for obstructive sleep apnoea.
“Among the patients who received the higher dosage of the drug, the number of breathing pauses decreased by approximately 20 per hour. For just over a third of patients in the study, only half of their breathing pauses were left, and in one in five the number fell by at least 60 percent,” said first authpr Professor Jan Hedner.
The fact that several approved drugs in the CA inhibitor category are available on the market makes fast-tracking development of an approved drug for sleep apnoea practicable. The drug used in this clinical trial was sulthiame, which is sometimes used to treat epilepsy in children.
Current treatment for a patient with sleep apnoea is either an oral appliance therapy or a CPAP (Continuous Positive Airway Pressure) mask. Both help to maintain airway patency during sleep.
“These therapy options take time to get used to and, since they frequently are perceived as intrusive or bulky. Insufficient user time is therefore common. If we develop an effective drug, it will therefore make life easier for many patients and, in the long run, potentially also save more lives,” said senior author Ludger Grote.
Hearing names repeated during deep sleep may help bolster recall of names and faces, according to new research from Northwestern University.
The researchers found that people’s name recall improved significantly when memories of newly learned face-name associations were reactivated while they were napping. Uninterrupted deep sleep was key in this improvement.
“It’s a new and exciting finding about sleep, because it tells us that the way information is reactivated during sleep to improve memory storage is linked with high-quality sleep,” said lead author Nathan Whitmore, a PhD candidate in the Interdepartmental Neuroscience Program at Northwestern University.
The three main stages of the experiment of Whitmore et al. (2022). First, participants learned 80 face-name associations. Next, they slept while EEG was monitored to determine sleep stage, and 20 of the spoken names were presented softly over background music during slow-wave sleep. Finally, memory testing showed superior memory due to memory reactivation during sleep, but only when sleep was undisturbed by sound presentations. Credit: Nathan Whitmore, a Ph.D. candidate in the Interdepartmental Neuroscience Program at Northwestern University.
The results also highlighted the importance of adequate sleep: for study participants with EEG measurements that indicated disrupted sleep, the memory reactivation had no effect and may even be detrimental. But in those with uninterrupted sleep during the specific times of sound presentations, the reactivation helped participants recall just over 1.5 more names.
The study recruited 24 participants, aged 18-31 years old, who were asked to memorise the faces and names of 40 pupils from a hypothetical Latin American history class and another 40 from a Japanese history class. When each face was presented again, they were asked to recall the associated name. After the learning exercise, participants took a nap while the researchers carefully monitored brain activity using EEG measurements. When participants reached the N3 “deep sleep” state, some of the names were softly played on a speaker with music that was associated with one of the classes.
When participants awoke, they were again tested on recognising faces and recalling their names.
According to the researchers, the finding on the relationship between sleep disruption and memory accuracy is noteworthy for several reasons.
“We already know that some sleep disorders like apnoeacan impair memory,” said Whitmore. “Our research suggests a potential explanation for this—frequent sleep interruptions at night might be degrading memory.”
The lab is currently exploring the reactivation of memories and deliberately disrupting sleep in order to learn more about the relevant brain mechanisms.
In a first-of-its-kind, scientists from the Heart Research Institute (HRI) have made the link between amounts of nicotine in the blood and their sleep apnoea risk.
Sleep apnoea occurs when a person’s throat and upper airway become partly or totally blocked during sleep, causing short periods where breathing ceases.
In a new paper published in ESC Heart Failure, Heart Research Institute (HRI) scientists found increases in nicotine levels were associated with a 2.3 minute increase in the time spent with oxygen saturations below 90%.
One of the markers of severity of sleep apnoea is time spent with an oxygen saturation less than 90%.
Lead researcher Dr John O’Sullivan, said this meant that for every cigarette a person smoked, the more they increased the risk of “dangerously low” oxygen levels.
“People who spend more time with an oxygen saturation less than 90 percent end up with more cardiovascular death than people who don’t,” Dr O’Sullivan said.
“We know smoking is bad for the heart – it’s one of the major risks for heart attacks – and although smoking is known to reduce oxygen concentration in the blood, the interaction of smoking with sleep apnoea has not been quantified. Using blood concentrations of the major nicotine metabolite, we were able for the first time to quantify the effect of smoking on oxygen concentrations at night in people with sleep apnoea.
“A standardised increase in levels of this metabolite was associated with 2.3 more minutes with an oxygen concentration less than 90 percent in people with sleep apnea. Time with an oxygen concentration less than 90% is a proven indicator of bad cardiovascular outcome.”
Sleep apnoea and congestive heart failure comorbidities are common, but their interaction is unclear. To find out more, Dr O’Sullivan’s team used hundreds metabolites to understand this interaction.
“Believe it or not, stiff heart failure – when the heart muscle can still pump blood but is stiff and cannot relax properly – is the most common form of heart failure today and we have almost no treatment options,” Dr O’Sullivan said.
“We measured molecules in the blood called metabolites and looked at the changes in these metabolites and related these to the severity of sleep apnoea.”
Metabolomics is a relatively new field of study that investigates metabolites, which are the components of your metabolism and play key roles in disease. They can provide insight into how one disease is linked to another, like in this case the consequences of sleep apnea and heart failure. Several metabolites are also key fuels for the working heart, and others form the units of energy by which the heart works.
The team studied metabolites and lipids in 3443 people from two US studies, including the landmark Framingham study.
Dr O’Sullivan said Framingham was known as the “town that changed America” because of the multi-generational study started in 1948 that subsequently identified the cardiovascular risk factors we still use today. Much research using this study is openly available internationally, enabling researchers around the world.
“Accurate measurement of disease combined with blood metabolite levels is far more accurate than self-reported questionnaires – that’s one of the strengths of this study,” he said.
While sleep apnoea is very common (up to one in four adults), its consequences and interactions with other diseases remain poorly understood. Almost no studies have sleep study data, heart failure data, and metabolomic data in the same individuals, which is a major new feature of this study.
In a small study, researchers found that exercise could help reduce sleep apnoea symptoms and improve brain function.
Sleep apnoea is characterised by loud snoring and disrupted breathing and is a risk factor for cardiovascular disease and cognitive decline. It is typically treated with continuous positive airway pressure, or CPAP, which is uncomfortable for patients and often not adhered to.
“Exercise training appears to be an attractive and adjunctive (add-on) non-pharmacological treatment,” said lead investigator Linda Massako Ueno-Pardi, an associate professor at the School of Arts, Science and Humanities at the University of São Paulo in Brazil. She also is a research collaborator at the university’s Heart Institute and Institute of Psychiatry, Faculty of Medicine.
Sleep apnoea is more common in men than women and becomes more prevalent as people age. According to a scientific statement by the American Heart Association, between 40% and 80% of people with cardiovascular disease have sleep apnoea. Cigarette smoking and type 2 diabetes are among the risk factors for sleep apnoea, as well as obesity, which narrows the airway when sleeping.
People with sleep apnoea have been shown to experience a decrease in brain glucose metabolism, which can impair cognitive function. The researchers sought to find out whether exercise could help correct that, building on a small 2019 study where aerobic activity improved brain glucose metabolism and executive functioning in Alzheimer’s patients.
The new study recruited 47 adults with moderate to severe obstructive sleep apnoea. Half did 60 minutes of supervised exercise three times a week for six months, and the other half were a control group.
Participants in both groups were given a series of tests to measure exercise capacity, brain glucose metabolism and cognitive function, including attention and executive function. Obstructive sleep apnoea symptom severity was measured, such as hypoxia.
At the end of six months, those in the exercise group showed an increased capacity for exercise; improvements in brain glucose metabolism; sleep apnoea symptom reduction; and a boost in cognitive function, including a 32% improvement in attention and executive function. The control group experienced no changes except a decline in brain glucose metabolism.
A “significant reduction” seen in the exercise group’s body fat may have improved sleep apnoea severity by decreasing body fat, especially around the airways.
