Sleep hygiene is the set of behavioural recommendations that sleep specialists have promoted for decades, and it is the area of sleep improvement with the most robust scientific evidence. That said, there is a meaningful difference between the individual recommendations, some of which are backed by high-quality evidence with clinically meaningful effect sizes, and others which are better supported in principle than they are in rigorous clinical trials.
I want to go through each recommendation honestly, explain the mechanism, describe what the evidence actually shows, and where possible give you a sense of how large the effect is likely to be. I should also say at the outset that sleep hygiene, even perfectly implemented, does not fix structural problems. If your airway obstructs during sleep, no bedtime routine will unobstruct it. The hygiene recommendations below are appropriate for people whose sleep problems are primarily behavioural, environmental, or driven by lifestyle. They are necessary but not sufficient for people with untreated sleep disorders.
Consistent Sleep and Wake Times
Of all the sleep hygiene recommendations, this one has the strongest and most consistent evidence base. Maintaining the same bedtime and wake time every day, including weekends, anchors the circadian rhythm and regulates what sleep scientists call the homeostatic sleep drive, the pressure to sleep that builds throughout wakefulness.
The circadian rhythm is a roughly 24-hour biological clock that governs not just sleep but a remarkable range of physiological processes: hormone secretion, metabolism, immune function, and mood regulation. This clock is primarily set by light exposure, but it is also strongly influenced by the consistency of the sleep-wake schedule. When that schedule varies substantially from one day to the next, particularly between weekdays and weekends, the circadian system is placed under a form of stress analogous to repeatedly crossing multiple time zones. Sleep researchers call this social jetlag.
Social jetlag — the mismatch between your biological clock and the social clock you are forced to follow — has measurable effects on cardiometabolic health, mood, and cognitive function. It is not a trivial concept, and the evidence for it is substantial.
A 2020 systematic review by Chaput and colleagues examined 41 studies involving 92,340 participants from 14 countries, looking at the associations between sleep timing, sleep consistency, and health outcomes [1]. Later sleep timing and greater variability in sleep patterns were consistently associated with adverse health outcomes, including cardiometabolic risk, mental health difficulties, and poorer cognitive performance. Importantly, social jetlag specifically (the difference in sleep timing between work days and free days) was associated with elevated markers of cardiovascular and metabolic risk even after accounting for total sleep duration.
A 2023 National Sleep Foundation consensus statement, based on a review of 63 published studies, concluded that consistency of sleep onset and offset timing is important for health, safety, and performance [2]. A 2025 systematic review specifically on sleep regularity, covering 59 studies, found moderate-certainty evidence linking irregular sleep timing to higher rates of depression, anxiety, insulin resistance, hypertension, and incident cardiovascular events [3].
One caution I would add, because I see this in clinical practice, is the risk of becoming too rigid about sleep schedule as a source of anxiety in itself. The research on orthosomnia (the pursuit of perfect sleep metrics) applies equally to the pursuit of perfect bedtime consistency. Desperately forcing yourself to lie in bed at exactly 10pm every night when you are not sleepy, lying awake worrying that you have not fallen asleep at the right time, is counterproductive. Consistency is a guide, not a constraint to enforce through willpower. Broadly regular is better than desperately precise. And as I discussed in the sleep tracker article, normal night-to-night variability in sleep duration is around 77 minutes even in completely healthy adults, which means some variation is expected and normal.
A Dark Room: Blackout Curtains and Light Exposure
The relationship between light and sleep is ancient, and the mechanism is among the best understood in sleep science. The human circadian system was calibrated over millions of years to the natural light-dark cycle of the planet. Darkness in the evening triggers the release of melatonin from the pineal gland, signalling to the brain that night has arrived and sleep should begin. Light suppresses melatonin, which is why shift workers, people in high latitudes in summer, and anyone spending evenings in brightly lit environments can struggle to sleep at a socially conventional time.
Since the invention of the incandescent light bulb in the late nineteenth century, and accelerating dramatically with the spread of artificial lighting throughout the twentieth century, humans have on average slept less than their pre-industrial ancestors. Analysis of sleep duration data across cultures without artificial lighting suggests pre-industrial humans typically slept around seven hours per night, often in a consolidated pattern, but with the timing governed entirely by sunlight and darkness rather than social schedules. Artificial light decouples those biological triggers from social time in ways we are still understanding.
The sensitivity of the melatonin system to light is striking. Research has shown that even relatively dim evening light exposure can significantly suppress melatonin. A 2022 study by Hartstein and colleagues at the University of Colorado found that preschool-aged children (aged 3 to 5) experienced an average melatonin suppression of 85.4 per cent during a single hour of light exposure in the hour before bedtime, across a range of light intensities from 5 to 5,000 lux [4]. Even at the lowest light levels tested (5 to 40 lux, roughly equivalent to a dimly lit room), melatonin was suppressed by an average of 77.5 per cent. And critically, melatonin levels remained below 50 per cent of baseline for at least 50 minutes after the light was extinguished in the majority of children. Children appear considerably more sensitive to evening light than adults, which has significant implications for screen use and room lighting in the hours before bedtime.
For adults, the practical implication is clear enough: dimmer, warmer-toned lighting in the two to three hours before your intended sleep time gives the melatonin system the conditions it needs to begin signalling sleep onset. Blackout curtains are particularly valuable in the UK during summer, when ambient light can persist late into the evening, and in urban environments where street lighting and neighbouring buildings create meaningful light exposure through windows.
A Cool Room
As discussed in the physical interventions article, core body temperature needs to fall to initiate and maintain sleep, and a bedroom that is too warm disrupts this process. The well-evidenced recommendation is a room temperature of roughly 15 to 19 degrees Celsius, which provides the ambient conditions that allow the body's natural thermoregulation to support sleep onset.
The effect on sleep onset is real but should not be overstated. Research on room temperature and sleep suggests that moving from a warm environment (above 25 degrees Celsius) to the optimal range can shorten sleep onset latency and reduce night waking. The magnitude of this effect in people already sleeping in a reasonably cool environment is smaller, probably in the range of a few minutes of sleep onset latency.
The evidence strongly supports a cool bedroom for sleep. It says rather less about whether that needs to be achieved with a two-thousand-pound mattress rather than an open window.
What the evidence does not support is the idea that actively cooling the body below its natural temperature throughout the night is beneficial. The body naturally adjusts its core temperature during different sleep stages, and what the research shows is that a cool ambient environment facilitates, rather than forces, that natural process. Humans evolved to self-regulate temperature during sleep, moving limbs outside covers when warm, pulling them back when cool. A cool room with good bedding supports this; an actively chilled mattress imposes a thermal environment regardless of the body's natural adjustments. I am not aware of robust evidence that the latter produces superior sleep outcomes compared to the former.
Screens Before Bed
The blue light story, which dominated sleep advice for many years, deserves some reconsideration. The mechanism is real: high-energy blue wavelengths suppress melatonin more effectively than other parts of the visible spectrum, via specialised photoreceptors in the retina called intrinsically photosensitive retinal ganglion cells. Devices that emit blue-rich light, including most smartphones and laptops, do therefore have the capacity to affect the circadian system.
However, the clinical evidence for blue light blocking glasses as a specific remedy is weak. A 2025 systematic review and meta-analysis by Luna-Rangel and colleagues identified three randomised controlled crossover trials (49 participants in total) examining whether blue light blocking glasses improved sleep onset latency, total sleep time, sleep efficiency, and wake after sleep onset compared to clear lenses [5]. The reduction in sleep onset latency with blue light blocking glasses was minus 4.86 minutes, and this did not reach statistical significance. There were no significant effects on any other sleep parameter. The authors concluded that current evidence does not support significant effects from blue light blocking glasses.
The more important point about screens is probably not the wavelength of light they emit but the content they deliver and the cognitive engagement they demand. Stimulating social media, news consumption, competitive gaming, and emotionally activating content all increase cognitive arousal at a time when the nervous system needs to be winding down. This is a more consistent finding in the screen time research than the blue light mechanism, and it applies regardless of whether you are wearing orange glasses.
A 2024 National Sleep Foundation consensus statement concluded that screen use impairs sleep health in children and adolescents, and that the content of screen use before sleep — not just the light emitted — is a meaningful contributor.
A systematic review by Hale and Guan, covering 67 studies published between 1999 and 2014, found that screen time was adversely associated with sleep outcomes (primarily shorter duration and later bedtimes) in 90 per cent of studies, with the strongest associations for interactive screen use (gaming, social media) rather than passive viewing (television) [6]. A 2024 National Sleep Foundation consensus statement, based on review of 35 experimental and intervention studies, concluded that screen use impairs sleep health in children and adolescents, that the content of pre-bedtime screen use impairs sleep health of children and adolescents, and that behavioural strategies may attenuate these effects [7].
The practical advice from this evidence is to manage the content and timing of screen use in the evening rather than obsessing over wavelength filtering. Dimming screens, selecting less stimulating content, and stopping active engagement with screens an hour before bed are all reasonable steps. A blue light filter on your phone used late at night is probably a small additional benefit, but it is not the primary mechanism driving the effect.
Caffeine Timing
Caffeine is the world's most widely consumed psychoactive substance, and its effects on sleep are among the best characterised in the pharmacological literature. Understanding why it disrupts sleep also explains one of the more counterintuitive aspects of caffeine biology.
During wakefulness, a chemical called adenosine accumulates in the brain. Adenosine is a byproduct of neuronal activity, and as it builds up across the day it creates an increasing drive to sleep, what scientists call homeostatic sleep pressure. Caffeine works by blocking adenosine receptors, which prevents the brain from detecting the accumulated adenosine. This is why caffeine makes you feel alert. It is also why you experience the familiar caffeine crash when the drug wears off: the adenosine that has been building up all day is suddenly able to bind to its receptors simultaneously, creating a rapid reversal from alert to fatigued.
The critical point for sleep is that caffeine's half-life in the human body is approximately five to seven hours, meaning that six hours after drinking a cup of coffee, roughly half of the caffeine is still circulating. For the caffeine to be essentially cleared, you are looking at around fourteen hours. A double espresso at 2pm therefore still has a meaningful concentration of caffeine in the bloodstream at midnight.
Caffeine reduces total sleep time by an average of 45 minutes, reduces sleep efficiency by 7 per cent, increases sleep onset latency by 9 minutes, and reduces deep sleep by over 11 minutes. These are not trivial numbers.
A 2023 systematic review and meta-analysis by Gardiner and colleagues identified 24 studies for analysis [8]. Caffeine consumption reduced total sleep time by an average of 45 minutes and sleep efficiency by 7 per cent, increased sleep onset latency by 9 minutes and wake after sleep onset by 12 minutes. The duration of light sleep (N1) increased by about 6 minutes and the duration of deep sleep (N3 and N4 combined) decreased by over 11 minutes. A separate dose-timing study by the same research group, published in 2024, randomised 23 young men to placebo or caffeine at 100mg or 400mg at 4, 8, or 12 hours before bedtime [9]. A standard coffee (approximately 100mg caffeine) consumed up to 4 hours before bedtime produced no significant effect on objective sleep. However, 400mg (roughly equivalent to a strong pre-workout supplement or four to five espresso shots) disrupted sleep even when consumed 12 hours before bed.
Individual sensitivity to caffeine varies substantially, driven partly by genetic variation in the genes encoding adenosine receptors and caffeine-metabolising enzymes. Some people can drink coffee after dinner and sleep without apparent difficulty; others are profoundly sensitive to caffeine consumed in the afternoon. What is consistent across the research is that most people underestimate how much their afternoon and evening caffeine is affecting their sleep quality, even when they do not notice a clear effect on falling asleep, because the disruption shows up primarily as reduced deep sleep rather than difficulty with sleep onset.
Alcohol and Sleep
Alcohol is perhaps the most widely misunderstood sleep substance. The perception that a drink or two in the evening helps you sleep is almost universal, and it contains a grain of truth: alcohol does reduce the time it takes to fall asleep at sufficient doses. What it does to the rest of the night is a different story.
A 2024 systematic review and meta-analysis by Gardiner and colleagues, covering 27 studies, found that even a low dose of alcohol, defined as approximately two standard drinks, was sufficient to significantly reduce REM sleep and delay its onset [10]. A dose-response relationship was clear: disruptions to REM sleep worsened progressively with increasing alcohol intake. Reductions in sleep onset latency and time to reach deep sleep were only observed with high doses (approximately five or more standard drinks). In other words, the sleep-inducing effect of alcohol requires a lot of it, while the sleep-disrupting effects begin at very modest amounts.
REM sleep is particularly important for emotional memory processing, learning consolidation, and mood regulation. The suppression of REM sleep by alcohol is one reason why people who drink regularly and then stop often experience vivid, disturbing dreams in the nights following abstinence: REM sleep rebounds dramatically when its suppression is removed. The novelist and sleep researcher Matthew Walker describes a study in which students who learned material on a Monday and then drank alcohol on the Friday before the weekend retained significantly less of the material the following Monday compared to those who did not drink, because REM sleep during those intervening nights consolidates the memory traces laid down during learning. The biological disruption to memory caused by suppressed REM is not limited to the night of drinking.
Two standard drinks is enough to meaningfully reduce REM sleep. You may fall asleep faster after alcohol, but the quality and architecture of that sleep is compromised from the very first drink.
From the perspective of my clinical practice, the interaction between alcohol and obstructive sleep apnoea is particularly important. A 2018 meta-analysis by Kolla and colleagues analysed 14 randomised controlled trials in 422 participants and found that alcohol administration increased the apnoea-hypopnea index (the number of breathing events per hour of sleep) by an average of 2.33 events per hour [11]. In people who snore or already have OSA, the increase was considerably larger, at 4.20 events per hour in snorers and 7.10 events per hour in those with a diagnosed OSA. A separate systematic review and meta-analysis by Burgos-Sanchez and colleagues found an increase of 3.98 events per hour compared to control conditions, alongside a 2.72 per cent reduction in minimum overnight oxygen saturation [12]. Alcohol relaxes the muscles of the upper airway, reducing the tone that keeps the airway patent during sleep, and it also reduces the arousal response that would normally terminate an apnoea event. In a person with undiagnosed OSA, drinking before bed meaningfully worsens a condition they do not know they have.
Wind-Down Routines
The evidence for pre-sleep wind-down routines operates primarily through the psychology of cognitive arousal. One of the most reliable findings in sleep research is that excessive cognitive and emotional engagement close to bedtime increases sleep onset latency and reduces sleep quality. Anxious thinking, planning, problem-solving, and emotional activation all compete with the physiological process of sleep initiation.
What we know is that consistent pre-sleep routines that signal to the brain that the transition to sleep is approaching are genuinely helpful. Every parent learns this eventually: the bedtime routine with a young child, a bath, a story, dim lights, a consistent sequence in a consistent order, works not because any single element is magical but because the consistency trains the brain to associate that sequence with sleep. There is no reason to think this mechanism stops working in adulthood.
The research on specific wind-down activities is less prescriptive than you might expect. Mindfulness meditation, reading, gentle stretching, and journalling have all been studied with generally positive results for sleep quality, but the effect sizes are modest and it is difficult to disentangle the specific activity from the general effect of simply not doing something stimulating. My suggestion would be to build a consistent sequence rather than optimising the specific content of it. Forty-five minutes of dim lights, no work, and quiet activity in whatever form suits you is likely to produce a similar benefit regardless of whether that activity is a novel, a podcast, or a warm bath.
Exercise
The evidence that regular exercise improves sleep quality is among the most consistent in the behavioural sleep medicine literature. A 2015 meta-analysis by Kredlow and colleagues, covering 66 studies examining both acute and regular exercise, found that regular physical activity was associated with small beneficial effects on total sleep time and sleep efficiency, small to medium effects on sleep onset latency, and moderate effects on subjective sleep quality [13].
A more recent 2021 meta-analysis by Xie and colleagues, specifically examining randomised controlled trials in adults, analysed 22 trials and found that exercise interventions significantly improved subjective sleep quality as measured by the Pittsburgh Sleep Quality Index, with a mean improvement of 2.19 points compared to control conditions [14]. Both aerobic exercise (walking, running, cycling) and mind-body exercise (yoga, tai chi) produced improvements of similar magnitude. The effect was more pronounced in the first three months of an exercise programme, which may reflect the transition from sedentary to active rather than a waning benefit with continued exercise.
Exercise is one of the most reliable non-pharmacological tools for improving sleep quality. The timing of exercise matters less than people commonly assume, and the idea that vigorous evening exercise will inevitably disrupt sleep is not well supported by the clinical evidence.
The commonly stated advice to avoid exercise in the evening is less firmly evidenced than it is commonly presented. While very high-intensity exercise immediately before bed may elevate heart rate, body temperature, and adrenaline in ways that temporarily interfere with sleep onset, the research shows that moderate to vigorous exercise conducted in the hours before bed does not significantly disrupt sleep for most people. A study examining exercise at different times of day found that the negative effects on sleep required very strenuous exercise (greater than 90 per cent maximal effort) conducted within an hour of intended sleep. For most people with a conventional schedule who exercise in the evening out of necessity, the benefits of the exercise almost certainly outweigh any minor effect on sleep onset timing.
Exercise also directly reduces OSA severity in some patients. A 2011 randomised trial found that a 12-week aerobic exercise programme in sedentary adults with moderate to severe OSA reduced the apnoea-hypopnea index significantly compared to a stretching control, with improvements in objective sleep quality and deep sleep time, all without significant weight loss [15]. This is important because it suggests exercise contributes to airway muscle tone and respiratory function beyond simply its weight-related effects.
Eating Late at Night
The evidence on meal timing and sleep is less developed than for the other interventions in this section, but there are several mechanisms worth understanding. Late meals delay gastric emptying, and for people prone to gastro-oesophageal reflux, lying down within two to three hours of a meal increases the likelihood of acid reflux into the oesophagus and throat, which can cause arousal from sleep without the person being aware that reflux was the trigger. For this group, a later mealtime is specifically relevant.
There is also emerging research on blood glucose variability and sleep. Higher postprandial blood glucose responses in the evening appear to be associated with poorer sleep quality, and interventions that reduce post-meal glucose spikes (including timing of eating and meal composition) may improve sleep onset. This is a mechanistically interesting area but the direct clinical trials are limited. From a practical standpoint, avoiding very large, high-fat meals in the two to three hours before bed is a reasonable habit with biological plausibility, particularly for people who already notice that late eating disrupts their sleep.
A Note on Emerging Practices: NSDR, Polyphasic Sleep
Non-Sleep Deep Rest (NSDR), also known as yoga nidra in the Ayurvedic tradition, involves guided relaxation protocols in which the body is deeply relaxed but consciousness is maintained. It has been popularised in the context of sleep science by Andrew Huberman and others. From a clinical perspective, I think of it primarily as a structured wind-down and relaxation practice with its own independent benefits for stress and cognitive restoration, rather than as a distinct sleep intervention. Meditation more broadly has a meaningful evidence base for reducing anxiety and improving subjective sleep quality, though the effect sizes are modest and the mechanisms overlap substantially with the cognitive arousal reduction discussed in the wind-down section above.
Polyphasic sleep, the practice of splitting sleep into multiple shorter periods rather than a single consolidated night, is popular in certain performance-focused communities but is not supported by the evidence as a beneficial sleep strategy for most adults. The architecture of human sleep, with deep slow-wave sleep concentrated in the first part of the night and REM sleep in the final part, evolved for a consolidated nocturnal pattern. Fragmenting that pattern disrupts the natural progression through sleep stages and risks chronic REM deprivation, with its attendant effects on emotional regulation, memory consolidation, and cognitive function. The cultural precedent of afternoon naps (as practised in Spain, Italy, and other warm countries) likely reflects adaptation to hot midday climates rather than evidence that polyphasic sleep is inherently superior.
References
[1] Chaput J-P, et al. Sleep timing, sleep consistency, and health in adults: a systematic review. Applied Physiology, Nutrition, and Metabolism. 2020;45(10 Suppl 2):S232–S247. 41 articles, 92,340 participants from 14 countries; later sleep timing and greater variability consistently associated with adverse health outcomes; social jetlag associated with adverse outcomes independent of sleep duration.
[2] Sletten TL, et al. The importance of sleep regularity: a consensus statement of the National Sleep Foundation sleep timing and variability panel. Sleep Health. 2023;9(6):801–820. Formal consensus process; consistent evidence that sleep onset and offset timing consistency is important for health, safety, and performance; weekend catch-up sleep beneficial when weekday sleep is insufficient.
[3] Kalkanis A, et al. Sleep regularity as an important component of sleep hygiene: a systematic review. Sleep Medicine Reviews. 2025. 59 studies meeting inclusion criteria; moderate-certainty evidence linking irregular sleep timing to depression, anxiety, insulin resistance, hypertension, cardiovascular events, and higher all-cause mortality.
[4] Hartstein LE, et al. High sensitivity of melatonin suppression response to evening light in preschool-aged children. Journal of Pineal Research. 2022;72(2):e12780. 36 healthy children aged 3.0–4.9 years; randomised to 15 different light levels (5–5,000 lux); average melatonin suppression of 85.4% during exposure; levels remained below 50% baseline for 50 minutes post-exposure in 62% of children.
[5] Luna-Rangel FA, et al. Efficacy of blue-light blocking glasses on actigraphic sleep outcomes: a systematic review and meta-analysis of randomized controlled crossover trials. Frontiers in Neurology. 2025. 3 double-blind crossover RCTs, 49 participants; non-significant reduction in sleep onset latency (−4.86 min); no significant effects on total sleep time, sleep efficiency, or wake after sleep onset.
[6] Hale L, Guan S. Screen time and sleep among school-aged children and adolescents: a systematic literature review. Sleep Medicine Reviews. 2015;21:50–58. 67 studies published 1999–2014; screen time adversely associated with sleep outcomes in 90% of studies; primarily shorter duration and delayed timing.
[7] Hartstein LE, et al. The impact of screen use on sleep health across the lifespan: A National Sleep Foundation consensus statement. Sleep Health. 2024;10(2):128–136. 16-person expert panel; reviewed 35 experimental/intervention studies; consensus achieved that screen use impairs sleep health in children and adolescents, content of pre-bedtime screen use impairs sleep, and behavioural strategies can attenuate effects.
[8] Gardiner C, et al. The effect of caffeine on subsequent sleep: A systematic review and meta-analysis. Sleep Medicine Reviews. 2023;69:101764. 24 studies; caffeine reduced total sleep time by 45 minutes, sleep efficiency by 7%; increased sleep onset latency by 9 minutes, WASO by 12 minutes; reduced deep sleep duration by 11.4 minutes.
[9] Gardiner C, et al. Dose and timing effects of caffeine on subsequent sleep: a randomized clinical crossover trial. Sleep. 2024. 23 males; double-blind crossover; 100mg and 400mg caffeine at 4, 8, and 12 hours before bedtime; 100mg up to 4 hours pre-bed no significant effect; 400mg disrupted sleep even at 12 hours pre-bed.
[10] Gardiner C, et al. The effect of alcohol on subsequent sleep in healthy adults: A systematic review and meta-analysis. Sleep Medicine Reviews. 2024. 27 studies; dose-response relationship for REM suppression; even low dose (approximately 2 standard drinks) significantly reduced REM sleep duration; high dose (approximately 5 standard drinks) reduced sleep onset latency.
[11] Kolla BP, et al. The impact of alcohol on breathing parameters during sleep: A systematic review and meta-analysis. Sleep Medicine Reviews. 2018;42:59–67. 14 RCTs, 422 participants (72% male); alcohol increased apnoea-hypopnea index by 2.33 events/hour overall; 4.20/hr in snorers; 7.10/hr in OSA patients; mean oxygen saturation reduced by 0.60%.
[12] Burgos-Sanchez C, et al. Impact of Alcohol Consumption on Snoring and Sleep Apnea: A Systematic Review and Meta-analysis. Otolaryngology, Head and Neck Surgery. 2020;163(6):1078–1086. 13 manuscripts, 279 patients; pooled analysis showed mean difference in AHI of 3.98 events/hour; lowest oxygen saturation reduced by 2.72%.
[13] Kredlow MA, et al. The effects of physical activity on sleep: a meta-analytic review. Journal of Behavioral Medicine. 2015;38(3):427–449. 66 studies; regular exercise associated with small beneficial effects on total sleep time and efficiency; small-to-medium effects on sleep onset latency; moderate effects on subjective sleep quality.
[14] Xie Y, et al. Effects of Exercise on Sleep Quality and Insomnia in Adults: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Frontiers in Psychiatry. 2021;12:664499. 22 RCTs; exercise significantly improved PSQI score by mean 2.19 points compared to control; both aerobic and mind-body exercise produced similar improvements.
[15] Kline CE, et al. The effect of exercise training on obstructive sleep apnea and sleep quality: a randomized controlled trial. Sleep. 2011;34(12):1631–1640. 43 sedentary overweight/obese adults with untreated OSA; 12-week aerobic exercise programme versus stretching control; AHI significantly reduced (32.2 to 24.6 vs 24.4 to 28.9 events/hour); improvements in N3 sleep and actigraphic sleep quality.
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