Sleep Regulation and Insomnia: Many effective strategies for improving insomnia symptoms work, in part, through their impact on how sleep is regulated. The Figure depicts the two-process model of sleep regulation that governs the timing and quality of sleep through the coordination of a sleep homeostatic and circadian process (17). A homeostatic sleep drive builds across wakefulness, exerting an intensifying pressure on the brain to fall asleep, and this drive dissipates with sleep. Thus, the longer an individual remains awake, the higher the pressure to fall asleep.
Circadian rhythms are generated by a master clock located in the suprachiasmatic nucleus (SCN) of the anterior hypothalamus. The SCN receives light signals from the eyes via the retinohypothalamic tract and uses this information to coordinate the timing of all internal activities with the external light/dark cycle, including the sleep/wake rhythm. Light can either advance or delay a person’s internal clock depending on when exposure occurs, and it is primarily through this mechanism that adjustment to a new time zone and light/dark cycle occurs.
In an ideal situation, the internal clock is synchronized to the environmental light/dark cycle such that the internal clock promotes rest and sleepiness at a clock time when sleep is desired and when the homeostatic drive for sleep is high. Under this set of circumstances, sleep onset occurs quickly and sleep quality is high. Conversely, if synchronization between these systems is not optimal, individuals may attempt to sleep at a biologically inappropriate time for sleep. Insomnia can manifest in these situations as delayed sleep onset (trouble falling asleep), increased awakenings (trouble staying asleep), and early termination of sleep (waking up before desired).
Physiological and psychological states that result in elevated central nervous system (CNS) activity can override an otherwise well-coordinated sleep regulatory system. Physical pain and stress as well as excessive worry and anxiety can activate the hypopituitary axis (HPA), making it more difficult to fall or stay asleep. Thus, individuals suffering from physical injuries and/or stress or psychological trauma may experience symptoms of insomnia. These conditions and settings are considered as precipitating factors to the development of chronic sleep problems in the Speilman “3P” model of insomnia (18). Predisposing factors and perpetuating attitudes or practices refer to the other two ‘Ps’ in the Spielman model of insomnia. Predisposing factors are acquired or inherited characteristics that render individuals more susceptible to develop a particular type of insomnia. Perpetuating attitudes or practices refer to the behavioral practices that maintain sleep difficulty, mental worrying about sleeplessness, etc.
With this background as a primer, the following sections discuss helpful strategies to improve sleep for those who may struggle with insomnia symptoms from time to time or are considering seeking clinical treatment for their insomnia. The focus is on behavioral approaches that are evidence based. Special attention is given to the role of exercise in a behavioral approach to managing insomnia.
Sleep Hygiene Intervention: Experts in the field have developed a set of recommendations for promoting sleep and preventing insomnia, and these recommendations often are used as a behavioral insomnia intervention (19). These are available on the National Sleep Foundation Web site www.sleepfoundation.org, American Sleep Association Web site www.sleepassociation.org, and elsewhere. For someone initially struggling with insomnia, these recommendations may be a good place to start for resolving sleep issues and are reviewed here in more depth. Many are rooted in sleep physiology and based on the principles of cognitive behavioral therapy for insomnia (CBT-I), which is discussed later. Table 2 includes a list of these recommendations.
In general, keeping a consistent sleep/wake schedule, even on the weekends, is important. Staying up and sleeping in much later on nonwork days changes the pattern of light exposure and can delay the circadian clock, making it harder to fall asleep and wake up on subsequent workdays. This desynchrony between
In general, keeping a consistent sleep/wake schedule, even on the weekends, is important. Staying up and sleeping in much later on nonwork days changes the pattern of light exposure and can delay the circadian clock, making it harder to fall asleep and wake up on subsequent work days.
biological and social time is like switching back and forth between time zones and often is referred to as social jet lag (20), which is itself associated with a higher risk for cancer, obesity, impaired glucose regulation, and depressed mood (21–25). To assist with getting to sleep, establishing a bedtime routine can help transition the brain for sleep by winding down approximately 30 to 45 minutes before bedtime. This can be accomplished through the ritualization of activities that begin to slow down CNS activity and prepare the brain for transition to sleep. Examples of a bedtime routine include the following: turning off bright lights and disengaging from stimulating activities, meditating, reading, listening to relaxing music, brushing teeth, and getting into sleeping clothes.
Light exposure also is critical to achieving high-quality sleep. Exposure to sunlight helps anchor internal circadian rhythms to the environmental light/dark cycle. Early morning light exposure will advance circadian rhythms, making it easier to fall asleep at night (26). Reducing light at night also is important to maintaining healthy circadian rhythms. The internal clock responds to bright light at night by delaying the release of melatonin, an important hormone involved in priming the body for sleep (27,28). Furthermore, if light exposure occurs after melatonin onset, melatonin levels are suppressed, and these changes have been shown to increase the time it takes to fall asleep (27). In particular, light of the blue green spectral band (such as that found in the afternoon sky, but also in high intensities from overhead lighting and in electronic devices), can more profoundly impact circadian rhythms. Sleep experts recommend putting away smartphone devices and computers, switching off TVs, and turning down ambient lighting within an hour of bedtime. If electronics absolutely must be used, there are now a variety of downloadable blue light filters available for reducing blue light exposure.
Avoid stimulants and alcohol too close to bedtime. Caffeine and nicotine both increase CNS activity. Caffeine has been shown to cause sleep disruption if taken within 6 hours of bedtime (29). Although alcohol can make it easier to fall asleep, it can severely disrupt sleep by increasing awakenings and altering sleep stages. This can greatly reduce sleep quality, and increase next-day fatigue, particularly when consumed in high doses and close to bedtime (30).
Getting routine physical activity is helpful for obtaining high-quality sleep. Furthermore, when physical activity is conducted outside under a bright sky, the additional light exposure can help synchronize internal circadian rhythms. The role of exercise will be expanded on in the next section.
Pay attention to the amount of time in bed (TIB) spent lying awake. Sleep experts advise that the bed should be used only for sleeping and not for activities such as reading, watching television, browsing the Internet, texting, and talking on the phone. It should be noted that for some people, reading or watching television in bed is an effective bedtime ritual that helps prepare them for sleep. For individuals with insomnia, however, these activities are not advised because they can strengthen a maladaptive association with the bed and wakefulness. If unable to sleep within 15 to 30 minutes, it is recommended to get out of bed both at the start of the sleep period as well as after an awakening during the night. Conditioning the brain to connect the bed with sleep and not with wake and/or struggling to fall asleep will facilitate faster transition to sleep. Unfortunately, many individuals with insomnia believe that more TIB will lead to more sleep and thus move bedtime earlier, a practice that further perpetuates poor sleep because bedtime then occurs at a biological time not sufficient for sleep. Instead, engaging in a relaxing activity away from the bedroom, such as reading or meditating, and heading to bed when sleepy can help reinforce a positive association between the bed and falling asleep quickly. Avoiding prolonged time in bed also is good for physical health reasons. As National Aeronautics and Space Administration (NASA) bed rest studies have shown, prolonged bed rest also can have negative health consequences including muscle wasting, decreases in bone density, and cardiovascular complications (31).
Cognitive Behavioral Therapy for Insomnia. CBT-I was developed as a 6- to 8-week intervention requiring several face-to-face appointments with a trained clinician such as a cognitive psychologist or a physician. The efficacy is well documented in the research literature (32), and it is recommended by the American Academy of Sleep Medicine (33) as well as the American College of Physicians (34) as the first-line treatment for addressing chronic insomnia. CBT-I is a multicomponent therapy that includes sleep education, sleep restriction therapy, stimulus control principles, cognitive therapy, and relaxation strategies.
Sleep restriction therapy, first advanced by Arthur Spielman in 1987 (35), operates on the understanding that insomniacs often spend extended periods of time lying in bed awake during the night instead of sleeping. Using information from sleep diaries, the patient’s actual total sleep time (TST) is subtracted from the TIB, and this extra time spent lying in bed is removed from future sleep opportunities. This helps reassociate the bed with sleep, and not with struggling to sleep. For example, an individual might spend 8 hours in bed, but if he or she is actually sleeping 5 hours, then TIB is restricted to 5 hours. This process can help consolidate sleep by increasing sleep efficiency (SE) through reductions in sleep onset and the number and duration of awakenings. After several days, the clinician reevaluates the person’s SE (defined as the percentage of TST divided by TIB from lights out until lights on). If SE is 90% or greater, then the TIB is extended by 15 to 30 minutes per night, and either the bedtime or awakening time is adjusted. If, however, the SE remains less than 90%, then TIB is decreased by 15 to 30 minutes per night, and either the bedtime or awakening time is adjusted. This progressive lengthening of TIB continues until patients feel they are getting adequate sleep, at which point TIB is not extended any further.
Stimulus control treatment of insomnia, first advanced by Richard Bootzin in 1972 (36), involves the principle of conditioning, such that the bed is associated only with sleeping and not for other waking activities. For this reason, individuals are instructed to get out of bed if unable to fall sleep or return to sleep after 15 to 30 minutes. An interesting phenomenon observed in some people with insomnia is that they sleep better when away from home, presumably because they are removed from the home bed and bedroom factors that they have learned to associate with insomnia.
The cognitive therapy component of CBT-I involves addressing irrational concerns about the consequences of poor sleep and getting patients to focus less on trying to go to sleep. For example, some individuals with insomnia fear that poor sleep will render them completely unable to function the next day. This worry contributes to their sleep problems. Cognitive therapy helps insomnia patients to restructure their thoughts. Patients are reminded that we all have poor sleep, at least occasionally, and we manage to function nonetheless.
In clinical trials, CBT-I has been found to be superior to sleeping pills for chronic treatment of insomnia (37–39). The drawbacks of this therapy are that it is expensive, labor intensive, and skilled clinicians are in short supply. Fortunately, there has been much progress in making this treatment more accessible. Several studies have found that Internet-delivered CBT-I is effective for improving insomnia symptoms in patients with diagnosed insomnia (for review see (40)). Furthermore, modified versions of CBT-I can now be given over an accelerated timeline and require less face-to-face meetings with providers (41,42). Some versions focus only on the behavioral components of the therapy and thus are able to be delivered by clinicians with less specialized education such as clinical nurses and junior-level therapists. One example is termed brief behavioral treatment for insomnia and has been shown to be effective for resolving short-term insomnia in older adults (43,44). Versions of self-directed CBT-I are even available now via smartphone and Web-based applications as a nonclinical tool for addressing insomnia. One recent program was tested in a large sample of college students that screened positive for insomnia. In this population, Internet-based CBT-I led to marked improvements in insomnia symptoms and mental health outcomes (45). Table 3 includes a list of online resources for learning more about CBT-I.
Exercise as a Behavioral Treatment for Insomnia. Historically, exercise has been considered one of the most helpful behaviors for promoting sleep. Epidemiologic research has shown that regular light, moderate, or vigorous exercise or increased levels of daily physical activity are associated with better sleep and decreased risk of insomnia (46,47). Experimental research has supported that both acute (48) and chronic exercise are associated with significant improvements in sleep in individuals with insomnia (48–51). This has been shown predominantly for aerobic exercise of moderate or high intensity in individuals with insomnia, although other research has indicated that acute (52) and chronic resistance exercise (53) can improve sleep.
Mechanisms. The mechanisms by which exercise promotes sleep are not clear. Exercise can have both acute and chronic effects that can promote sleep. The most tenable hypotheses include thermogenic and anxiety reduction effects. Other theories such as effects of exercise on serotonin levels or effects of systemic inflammation are still being studied. The thermogenic effect was largely advanced by Horne et al. (54). They found an increase in deep sleep after acute exercise, which was reversed when temperature elevation was blunted with body cooling. An important trigger for sleep onset is the decline in body temperature in the evening mediated primarily by increased blood flow and increased heat loss from the peripheral skin, an effect similar to that seen after acute exercise. Because there is some evidence that insomniacs have impaired nocturnal temperature regulation (55), a thermogenic effect may be a valid mechanism for improving sleep. The thermogenic effect includes the participation of neurons in the anterior hypothalamus/preoptic area of the brain, which has been associated with sleep onset and deep sleep. Anxiety reduction is another plausible explanation for the sleep-promoting effects of exercise. Insomnia has been linked to physiological hyperarousal as evidenced by increased sympathetic activation and cortisol excretion during sleep, elevated basal metabolic rate during wakefulness and sleep, and reports of distress and inability to stay calm when attempting to sleep (56). It is well established that exercise has anxiolytic effects, which could facilitate sleep (48,57,58).
When to Exercise. It is commonly stated that exercising at night will disturb sleep. Experimental studies have consistently shown that moderate or vigorous exercise completed within 2 hours of bedtime does not disturb sleep in most subjects (58,59). Moreover, results from surveys support these experimental studies (60–62). However, for those with insomnia, exercise too close to bedtime may have the potential to negatively impact sleep, possibly through activation of the HPA axis, which can occur following high-intensity exercise (63). It is for this reason that recommendations for good sleep habits usually discourage high-intensity exercise within 2 hours of bedtime. However, this hypothesis should be rigorously tested with experimental studies.
If exercise is conducted under bright lights, such as at a gym, this light exposure may further disrupt sleep by delaying the circadian clock and suppressing melatonin levels as discussed previously. If insomnia and poor sleep is not a concern, then the recommendation to avoid exercise at night is not warranted. For many individuals, the evening may be best time or the only time of day in which they can consistently exercise.
Type, Duration, and Intensity of Exercise. Benefits of acute exercise on sleep have been observed for light, moderate, and vigorous aerobic exercise. Chronic aerobic exercise has elicited significant sleep-promoting effects, including interventions that follow public health guidelines of 150 min/wk of moderate/vigorous exercise (61). Chronic strength training also has had significant benefits for sleep. Moderate exercise training also has had significant benefits for sleep apnea (64,65) and restless legs syndrome (64), which are two sleep disorders that often interact with insomnia.
SUMMARY AND CONCLUSIONS
For unresolved insomnia, CBT-I is a demonstrated effective intervention. Although it was developed to be delivered face to face by trained clinicians over 6 to 8 weeks, unguided CBT-I is now becoming available remotely via Web- and smartphone-based applications and under accelerated timelines. For addressing initial insomnia symptoms, incorporating good sleep habits and practices (sleep hygiene recommendations) may be tried first before seeing a medical doctor. If symptoms are still unresolved, a doctor visit is necessary to rule out the presence of other sleep disorders, such as sleep apnea, which may be causing some symptoms similar to insomnia. Exercise is another effective intervention for addressing insomnia. Future clinical trials are needed to directly compare the effects of CBT-I with exercise interventions for improving insomnia and to investigate the use of both interventions in parallel.
BRIDGING THE GAP
Cognitive behavioral therapy for insomnia (CBT-I) involves sleep restriction, stimulus control, and cognitive restructuring and is demonstrated effective for improving sleep. Epidemiologic and experimental evidence indicate that exercise also is effective for insomnia, suggesting the need for comparative efficacy trials.
1. Gradisar M, Wolfson AR, Harvey AG, Hale L, Rosenberg R, Czeisler CA. The sleep and technology use of Americans: findings from the National Sleep Foundation’s 2011 Sleep in America poll. J Clin Sleep Med
2. Ito E, Inoue Y. The international classification of sleep disorders, third edition. American Academy of Sleep Medicine. Includes bibliographies and index. Nihon Rinsho
3. Morin CM, LeBlanc M, Belanger L, Ivers H, Merette C, Savard J. Prevalence of insomnia
and its treatment in Canada. Can J Psychiatry
4. Ohayon MM. Epidemiology of insomnia
: what we know and what we still need to learn. Sleep Med Rev
5. Edinger JD, Buysse DJ, Deriy L, et al. Quality measures for the care of patients with insomnia
. J Clin Sleep Med
6. Carney CE, Ulmer C, Edinger JD, Krystal AD, Knauss F. Assessing depression symptoms in those with insomnia
: an examination of the Beck depression inventory second edition (BDI-II). J Psychiatr Res
7. Ouellet MC, Beaulieu-Bonneau S, Morin CM. Insomnia
in patients with traumatic brain injury: frequency, characteristics, and risk factors. J Head Trauma Rehabil
8. Bahouq H, Allali F, Rkain H, Hmamouchi I, Hajjaj-Hassouni N. Prevalence and severity of insomnia
in chronic low back pain patients. Rheumatol Int
9. Irwin MR. Why sleep is important for health
: a psychoneuroimmunology perspective. Annu Rev Psychol
10. Parthasarathy S, Vasquez MM, Halonen M, et al. Persistent insomnia
is associated with mortality risk. Am J Med
11. Chilcott LA, Shapiro CM. The socioeconomic impact of insomnia
. An overview. Pharmacoeconomics
. 1996;10(Suppl 1):1–14.
12. Kessler RC, Berglund PA, Coulouvrat C, et al. Insomnia
, comorbidity, and risk of injury among insured Americans: results from the America Insomnia
13. Shahly V, Berglund PA, Coulouvrat C, et al. The associations of insomnia
with costly workplace accidents and errors: results from the America Insomnia
Survey. Arch Gen Psychiatry
14. Maher MJ, Rego SA, Asnis GM. Sleep disturbances in patients with post-traumatic stress disorder: epidemiology, impact and approaches to management. CNS Drugs
15. Chen LJ, Steptoe A, Chen YH, Ku PW, Lin CH. Physical activity, smoking, and the incidence of clinically diagnosed insomnia
. Sleep Med
16. Kripke DF. Hypnotic drug risks of mortality, infection, depression, and cancer: but lack of benefit. F1000Res
17. Borbely AA. A two process model of sleep regulation. Hum Neurobiol
. 1982;1(3): 195–204.
18. Yang CM, Spielman AJ, Glovinsky P. Nonpharmacologic strategies in the management of insomnia
. Psychiatr Clin North Am
. 2006;29(4):895–919; abstract viii.
19. Stepanski EJ, Wyatt JK. Use of sleep hygiene in the treatment of insomnia
. Sleep Med Rev
20. Wittmann M, Dinich J, Merrow M, Roenneberg T. Social jetlag: misalignment of biological and social time. Chronobiol Int
21. Kantermann T, Duboutay F, Haubruge D, Kerkhofs M, Schmidt-Trucksäss A, Skene DJ. Atherosclerotic risk and social jetlag in rotating shift-workers: first evidence from a pilot study. Work
22. Levandovski R, Dantas G, Fernandes LC, et al. Depression scores associate with chronotype and social jetlag in a rural population. Chronobiol Int
23. Parsons MJ, Moffitt TE, Gregory AM, et al. Social jetlag, obesity and metabolic disorder: investigation in a cohort study. Int J Obes (Lond)
24. Roenneberg T, Allebrandt KV, Merrow M, Vetter C. Social jetlag and obesity. Curr Biol
25. Wong PM, Hasler BP, Kamarck TW, Muldoon MF, Manuck SB. Social jetlag, chronotype, and cardiometabolic risk. J Clin Endocrinol Metab
26. Rosenthal NE, Joseph-Vanderpool JR, Levendosky AA, et al. Phase-shifting effects of bright morning light as treatment for delayed sleep phase syndrome. Sleep
27. Chang AM, Aeschbach D, Duffy JF, Czeisler CA. Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness. Proc Natl Acad Sci U S A
28. Zeitzer JM, Dijk DJ, Kronauer R, Brown E, Czeisler C. Sensitivity of the human circadian pacemaker to nocturnal light: melatonin phase resetting and suppression. J Physiol
. 2000;526(Pt 3):695–702.
29. Drake C, Roehrs T, Shambroom J, Roth T. Caffeine effects on sleep taken 0, 3, or 6 hours before going to bed. J Clin Sleep Med
30. Roehrs T, Roth T. Sleep, sleepiness, and alcohol use. Alcohol Res Health
31. Meck JV, Dreyer SA, Warren LE. Long-duration head-down bed rest: project overview, vital signs, and fluid balance. Aviat Space Environ Med
. 2009;80(5 Suppl):A1–8.
32. Hofmann SG, Asnaani A, Vonk IJ, Sawyer AT, Fang A. The efficacy of cognitive behavioral therapy
: a review of meta-analyses. Cognit Ther Res
33. Schutte-Rodin S, Broch L, Buysse D, Dorsey C, Sateia M. Clinical guideline for the evaluation and management of chronic insomnia
in adults. J Clin Sleep Med
34. Qaseem A, Kansagara D, Forciea MA, et al. Management of chronic insomnia
disorder in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med
35. Spielman AJ, Saskin P, Thorpy MJ. Treatment of chronic insomnia
by restriction of time in bed. Sleep
36. Bootzin R. Stimulus control treatment for insomnia
. Proceedings of the 80th Anuual Convention of the American Psychological Association
37. Morin CM, Culbert JP, Schwartz SM. Nonpharmacological interventions for insomnia
: a meta-analysis of treatment efficacy. Am J Psychiatry
38. Sivertsen B, Omvik S, Pallesen S, et al. Cognitive behavioral therapy
vs zopiclone for treatment of chronic primary insomnia
in older adults: a randomized controlled trial. JAMA
39. Turner RM, Ascher LM. Controlled comparison of progressive relaxation, stimulus control, and paradoxical intention therapies for insomnia
. J Consult Clin Psychol
40. Seyffert M, Lagisetty P, Landgraf J, et al. Internet-delivered cognitive behavioral therapy
to treat insomnia
: a systematic review and meta-analysis. PLoS One
. 2016;11(2): e0149139.
41. Edinger JD, Sampson WS. A primary care "friendly" cognitive behavioral insomnia
42. Ellis JG, Cushing T, Germain A. Treating acute insomnia
: a randomized controlled trial of a "single-shot" of cognitive behavioral therapy
43. Buysse DJ, Germain A, Moul DE, et al. Efficacy of brief behavioral treatment for chronic insomnia
in older adults. Arch Intern Med
44. Germain A, Moul DE, Franzen PL, et al. Effects of a brief behavioral treatment for late-life insomnia
: preliminary findings. J Clin Sleep Med
45. Freeman D, Sheaves B, Goodwin GM, et al. The effects of improving sleep on mental health
(OASIS): a randomised controlled trial with mediation analysis. Lancet Psychiatry
46. Benloucif S, Orbeta L, Ortiz R, et al. Morning or evening activity improves neuropsychological performance and subjective sleep quality in older adults. Sleep
47. Reid KJ, Baron KG, Lu B, Naylor E, Wolfe L, Zee PC. Aerobic exercise
improves self-reported sleep and quality of life in older adults with insomnia
. Sleep Med
48. Passos GS, Poyares D, Santana MG, Garbuio SA, Tufik S, Mello MT. Effect of acute physical exercise
on patients with chronic primary insomnia
. J Clin Sleep Med
49. Hartescu I, Morgan K, Stevinson CD. Increased physical activity improves sleep and mood outcomes in inactive people with insomnia
: a randomized controlled trial. J Sleep Res
50. Passos GS, Poyares D, Santana MG, et al. Effects of moderate aerobic exercise
training on chronic primary insomnia
. Sleep Med
51. Tan X, Alén M, Wiklund P, Partinen M, Cheng S. Effects of aerobic exercise
on home-based sleep among overweight and obese men with chronic insomnia
symptoms: a randomized controlled trial. Sleep Med
52. Viana VA, Esteves AM, Boscolo RA, et al. The effects of a session of resistance training on sleep patterns in the elderly. Eur J Appl Physiol
53. Singh NA, Clements KM, Fiatarone MA. A randomized controlled trial of the effect of exercise
on sleep. Sleep
54. Horne JA, Staff LH. Exercise
and sleep: body-heating effects. Sleep
55. Lack LC, Gradisar M, Van Someren EJ, Wright HR, Lushington K. The relationship between insomnia
and body temperatures. Sleep Med Rev
56. Fernandez-Mendoza J, Li Y, Vqontzas AN, et al. Insomnia
is associated with cortical hyperarousal as early as adolescence. Sleep
57. Herring MP, O’Connor PK, Dishman RK. The effect of exercise
training on anxiety symptoms among patients: a systematic review. Arch Intern Med
58. Youngstedt SD. Effects of exercise
on sleep. Clin Sports Med
. 2005;24(2):355–65, xi.
59. O’Connor PJ, Breus MJ, Youngstedt SD. Exercise
-induced increase in core temperature does not disrupt a behavioral measure of sleep. Physiol Behav
60. Buman MP, Phillips BA, Youngstedt SD, Kline CE, Hirshkowitz M. Does nighttime exercise
really disturb sleep? Results from the 2013 National Sleep Foundation Sleep in America Poll. Sleep Med
61. Vuori I, Urponen H, Hasan J, Partinen M. Epidemiology of exercise
effects on sleep. Acta Physiol Scand Suppl
62. Flausino NH, Da Silva Prado JM, de Queiroz SS, Tufik S, de Mello MT. Physical exercise
performed before bedtime improves the sleep pattern of healthy young good sleepers. Psychophysiology
63. Hill EE, Zack E, Battaglini C, Viru M, Viru A, Hackney AC. Exercise
and circulating cortisol levels: the intensity threshold effect. J Endocrinol Invest
64. Kline CE, Crowley EP, Ewing GB, et al. The effect of exercise
training on obstructive sleep apnea and sleep quality: a randomized controlled trial. Sleep
65. Servantes DM, Pelcerman A, Salvetti XM, et al. Effects of home-based exercise
training for patients with chronic heart failure and sleep apnoea: a randomized comparison of two different programmes. Clin Rehabil
Keywords:© 2018 American College of Sports Medicine.
Insomnia; Sleep Problems; Cognitive Behavioral Therapy; Health; Exercise