Can People Sleep Too Much? Effects of Extended Sleep Opportunity on Sleep Duration and Timing

Many people are concerned about whether they are getting “enough” sleep, and if they can “sleep too much.” These concerns can be approached scientifically using experiments probing long-term (i.e., multi-night) sleep homeostatic processes, since homeostatic processes move the system toward its physiological setpoint (i.e., between “not enough” and “too much”). We analyzed sleep data from two human studies with sleep opportunities much longer than people usually stay in bed (i.e., conditions in which sleep homeostatic responses could be documented): sleep opportunities were 14–16 h per day for 3–28 days. Across the nights of the extended sleep opportunities, total sleep duration, Rapid Eye Movement (REM) sleep duration and non-REM sleep durations decreased and sleep latency increased. Multiple nights were required to reach approximately steady-state values. These results suggest a multi-day homeostatic sleep process responding to self-selected insufficient sleep duration prior to the study. Once steady state-values were reached, there were large night-to-night variations in total sleep time and other sleep metrics. Our results therefore answer these concerns about sleep amount and are important for understanding the basic physiology of sleep and for two sleep-related topics: (i) the inter-individual and intra-individual variability are relevant to understanding “normal” sleep patterns and for people with insomnia and (ii) the multiple nights of sleep required for recovery from insufficient sleep from self-selected sleep loss is important for public health and other efforts for reducing the adverse effects of sleep loss on multiple areas of physiology.

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Abstract 15080: Chronic Mild Sleep Curtailment Increases Markers of Adiposity While Maintained Healthy Sleep Reduces These Measures in Women

Circulation ◽

10.1161/circ.142.suppl_3.15080 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Faris M Zuraikat ◽

Samantha E Scaccia ◽

Arindam RoyChoudhury ◽

Marie-Pierre St-Onge

Keyword(s):

Skeletal Muscle ◽

Body Weight ◽

Sleep Duration ◽

Cardiovascular Health ◽

Sleep Time ◽

Whole Body ◽

Body Volume ◽

Insufficient Sleep ◽

Wrist Actigraphy ◽

Sleep Condition

Introduction: Over one-third of US adults do not achieve adequate sleep duration of 7 or more h per night. Short sleep is linked to higher odds of cardiometabolic diseases, including obesity. However, whether prolonged insufficient sleep causes increased body weight or adiposity remains unclear. Objective: To compare, in women, changes in body weight and composition in response to prolonged mild sleep restriction (SR) vs maintenance of healthy, habitual sleep (HS). Methods: Women (n=55; age: 35±13 y; BMI: 25.5±3.5 kg/m 2 ) with average adequate sleep duration (total sleep time [TST]=455±23 min) took part in a randomized crossover study with two 6-wk phases: HS and SR. In HS, usual bed and wake times (determined from 2 wk wrist actigraphy and sleep logs) were maintained. In SR, TST was reduced by 1.5 h/night. Sleep was measured continuously and verified weekly for compliance. Body weight and composition were measured at 0 and 6 wk using magnetic resonance imaging (MRI). Linear-mixed models tested interactions of sleep condition with week on outcome measures. Results: Average TST was reduced in SR and unchanged in HS (-87±19 vs -7±26 min, P<0.01). Significant study condition by week interactions were observed for whole-body volume (WBV), waist circumference (WC), and skeletal muscle. In HS, WBV and WC decreased while these measures increased in SR (WBV: -0.47±0.22 vs 0.27±0.05 L, P=0.02; WC: -1.04 ± 0.78 vs 1.16 ± 0.54 cm, P=0.04). Results were similar for skeletal muscle (-0.19 ± 0.07 vs 0.17 ± 0.01 L, P<0.01). A trend for a reduction in weight was observed in HS relative to SR (-0.39±0.31 vs 0.34±0.09 kg, P=0.09). Conclusions: This is the first evidence that prolonged insufficient sleep leads to increased body size in women. Conversely, maintaining adequate sleep may improve body composition. Our data suggest that healthy sleep duration should be a key component of strategies to improve cardiovascular health in women.

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Abstract P545: Insufficient Sleep and Nitric Oxide-Mediated Endothelium-Dependent Vasodilation in Adults With Elevated Blood Pressure

Circulation ◽

10.1161/circ.141.suppl_1.p545 ◽

2020 ◽

Vol 141 (Suppl_1) ◽

Author(s):

Kelly A Stockelman ◽

Anthony R Bain ◽

Dana M Withrow ◽

Tracey A Larson ◽

Elizabeth M Boland ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Blood Pressure ◽

Sleep Duration ◽

Elevated Blood Pressure ◽

Elevated Blood ◽

Short Sleep Duration ◽

Insufficient Sleep ◽

Short Sleep ◽

Normal Sleep

Elevated blood pressure (BP ≥130/80 mmHg) is associated with increased risk for myocardial infarction, heart failure, stroke and vascular disease. Insufficient nightly sleep (<7 h/night) has been linked not only to the etiology of elevated blood pressure but is a prevalent, often ignored, comorbidity. Indeed, short sleep duration is now considered to be a plausible risk factor for elevated blood pressure and a harbinger of increased cardiovascular risk. A high prevalence of insufficient nightly sleep has been reported in adults with elevated blood pressure. The influence of insufficient sleep on endothelial vasodilator function in adults with elevated blood pressure is unknown. We tested the hypotheses that chronic insufficient sleep is associated with diminished nitric oxide (NO)-mediated endothelium-dependent vasodilation in adults with elevated blood pressure. Moreover, the insufficient sleep-related reduction in endothelial vasodilator function is due, at least in part to increased oxidative stress. Thirty-five middle-aged and older adults with elevated blood pressure were studied: 15 with normal nightly sleep duration (11M/4F; age: 58±2 yr; BP: 136/82±1/2 mmHg; sleep: 7.6±0.2 h/night) and 20 with short nightly sleep duration (14M/6F; 58±1 yr; BP: 138/84±1/1 mmHg; sleep: 6.0±0.1 h/night). Forearm blood flow (FBF) responses to intra-arterial infusion of acetylcholine (ACh), in the absence and presence of the endothelial NO synthase inhibitor N G -monomethyl-L-arginine (L-NMMA) and the antioxidant vitamin C were determined by venous occlusion plethysmography. The FBF response to ACh was significantly lower (~20%) in the short sleep (from 3.8±0.2 to 11.0±0.6 ml/100 ml tissue/min) compared with the normal sleep duration group (from 4.2±0.2 to 13.6±0.6 ml/100 ml tissue/min). L-NMMA significantly reduced (~25%) the FBF response to ACh in the normal sleep but not the short sleep group. Vitamin C markedly increased (~35%; P<0.05) the vasodilator response to ACh in short sleepers only. In summary, habitual short sleep duration worsens NO-mediated endothelium-dependent vasodilation in adults with elevated blood pressure. Furthermore, the sleep-related diminishment in endothelial vasodilator function is due, in part, to increased oxidative stress.

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Sleep deprivation amplifies striatal activation to monetary reward

Psychological Medicine ◽

10.1017/s0033291712002875 ◽

2013 ◽

Vol 43 (10) ◽

pp. 2215-2225 ◽

Cited By ~ 56

Author(s):

B. C. Mullin ◽

M. L. Phillips ◽

G. J. Siegle ◽

D. J. Buysse ◽

E. E. Forbes ◽

...

Keyword(s):

Young Adults ◽

Sleep Deprivation ◽

Sleep Time ◽

Sleep Loss ◽

Monetary Reward ◽

Late Adolescents ◽

Compulsive Gambling ◽

Reward Seeking ◽

Normal Sleep ◽

Reinforcing Stimuli

BackgroundSleep loss produces abnormal increases in reward seeking but the mechanisms underlying this phenomenon are poorly understood. The present study examined the influence of one night of sleep deprivation on neural responses to a monetary reward task in a sample of late adolescents/young adults.MethodUsing a within-subjects crossover design, 27 healthy, right-handed late adolescents/young adults (16 females, 11 males; mean age 23.1 years) underwent functional magnetic resonance imaging (fMRI) following a night of sleep deprivation and following a night of normal sleep. Participants' recent sleep history was monitored using actigraphy for 1 week prior to each sleep condition.ResultsFollowing sleep deprivation, participants exhibited increased activity in the ventral striatum (VS) and reduced deactivation in the medial prefrontal cortex (mPFC) during the winning of monetary reward, relative to the same task following normal sleep conditions. Shorter total sleep time over the five nights before the sleep-deprived testing condition was associated with reduced deactivation in the mPFC during reward.ConclusionsThese findings support the hypothesis that sleep loss produces aberrant functioning in reward neural circuitry, increasing the salience of positively reinforcing stimuli. Aberrant reward functioning related to insufficient sleep may contribute to the development and maintenance of reward dysfunction-related disorders, such as compulsive gambling, eating, substance abuse and mood disorders.

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Insomnia and sleep state misperception: Clinical features, diagnosis, management and implications

European Psychiatry ◽

10.1016/j.eurpsy.2017.01.1696 ◽

2017 ◽

Vol 41 (S1) ◽

pp. s853-s853

Author(s):

J. Isaac ◽

C. Santos ◽

A. Matos Pires

Keyword(s):

Sleep Duration ◽

Clinical Features ◽

Mental Disease ◽

Sleep Time ◽

Sleep State ◽

Short Sleep Duration ◽

Short Sleep ◽

Psychological Therapies ◽

Normal Sleep ◽

Competing Interest

BackgroundInsomnia is a highly prevalent complaint, largely associated with mental disease. Clinical evidence classifies insomnia in 2 subtypes: with sleep misperception (WSM) and without sleep misperception (wSM). That presents distinctive pathophysiologic pathways and different public health implications.ObjectivesDescribe the main differences between primary insomnia WSM and wSM regarding:– clinical features;– diagnosis;– management;– implications.MethodsWe conducted a systematic review. PubMed, Embase and PsycInfo were searched from 2000–2016. The reference lists of systematic reviews, narrative synthesis and some important articles were included. Following the inclusion criteria, we selected 25 studies from 59 articles.ResultsThe prevalence of sleep-state misperception in primary insomniacs (total sleep time > 6.5 h and sleep efficiency > 85%) is around 26%. Insomniacs with normal sleep duration showed a profile of high depression and anxiety and low ego strength, whereas insomniacs with short sleep duration showed a profile of a medical disorder.Cortical hyperarousal is higher in insomniacs and could be related to an alteration in sleep protection mechanisms. The sleep architecture was relatively normal for the WSM comparing with the group wSM. Risk of cardiometabolic, neurocognitive morbidity and mortality, and responses to treatment are different between these two insomnia phenotypes. Patients with short sleep duration may respond better to biological treatments, whereas insomnia with normal sleep duration may respond primarily to psychological therapies.ConclusionsThe clinical characteristics of patients with sleep-state misperception differed from those without this condition. Available research related to these conditions is expanding rapidly, but many questions remain unanswered.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Disorders of sleep

10.1093/med/9780199568741.003.0054 ◽

2018 ◽

Author(s):

Sophie West

Keyword(s):

Chronic Disease ◽

Eye Movement ◽

Rem Sleep ◽

Excessive Daytime Sleepiness ◽

Slow Wave Sleep ◽

Total Sleep Time ◽

Sleep Time ◽

Sleep Stages ◽

Normal Sleep ◽

Sedative Drugs

Typically, disorders of sleep cause disturbance either to the sufferer or to their bed partner. If total sleep time is reduced, this may lead to problems with excessive daytime sleepiness, which can affect work, driving, concentration, and relationships. ‘Sleepiness’ implies an intrusive desire to fall asleep, caused by some form of sleep deprivation or sedative drugs; this is different from ‘tiredness’, which implies general fatigue, lethargy, and exhaustion and is caused by a range of conditions, including depression, chronic disease, or a busy lifestyle. Adults sleep on average for 8 hours a night. Normal sleep consists of periods of deep or slow-wave sleep, interspersed with shorter periods of dreaming or rapid-eye-movement (REM) sleep. Periods of REM sleep lengthen towards the morning and hence some people remember their dreams on waking. Different disorders of sleep can affect any of these sleep stages.

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Abstract 2455: Short Sleep Duration is an Independent Predictor of Cardiovascular Events in Hypertensive Patients

Circulation ◽

10.1161/circ.118.suppl_18.s_728-c ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Kazuo Eguchi ◽

Thomas G Pickering ◽

Joseph E Schwartz ◽

Satoshi Hoshide ◽

Joji Ishikawa ◽

...

Keyword(s):

Sleep Duration ◽

Short Duration ◽

Cardiovascular Events ◽

Sleep Time ◽

Cvd Risk ◽

Short Sleep Duration ◽

Hypertensive Patients ◽

Short Sleep ◽

Multivariable Analyses ◽

Normal Sleep

We aimed this study to test the hypothesis that short duration of sleep is independently associated with incident cardiovascular diseases (CVD) in hypertensive patients. We performed ambulatory BP monitoring (ABPM) in 1255 subjects with hypertension (mean age: 70.4 ± 9.9 years) and they were followed for an average of 50 ± 23 months. Short sleep duration was defined as <7.5 hrs (20 th percentile). Multivariable Cox hazard models predicting CVD events were used to estimate the adjusted hazard ratio (HR) and 95% CI for short sleep duration. A riser pattern was defined when average nighttime SBP exceeded daytime SBP. The end point was cardiovascular events: stroke, fatal or non-fatal myocardial infarction (MI), and sudden cardiac death. In multivariable analyses, short duration of sleep (<7.5 hrs) was associated with incident CVD (HR=1.68; 1.06 –2.66, P=.03). A synergistic interaction was observed between short sleep duration and the riser pattern (P=.089). When subjects were categorized on the basis of their sleep time and riser/non-riser patterns, the shorter sleep+riser group had a highest incidence of CVD among the 4 groups ( Figure ), and substantially and significantly higher incidence of CVD than the predominant normal sleep+non-riser group (HR=4.43; 2.09 –9.39, P<0.001), independent of covariates. Short duration of sleep is associated with incident CVD risk, and the combination of riser pattern and short duration of sleep that is most strongly predictive of future CVD, independent of ambulatory BP levels. Physicians should inquire about sleep duration in the risk assessment of hypertensive patients.

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Abstract P183: Influence of Insufficient Sleep on Endothelial Fibrinolytic Capacity in Adults With Elevated Blood Pressure

Hypertension ◽

10.1161/hyp.70.suppl_1.p183 ◽

2017 ◽

Vol 70 (suppl_1) ◽

Author(s):

Anthony R Bain ◽

Caitlin A Dow ◽

Kyle J Diehl ◽

Tyler D Bammert ◽

Jared J Greiner ◽

...

Keyword(s):

Sleep Duration ◽

Tissue Type ◽

Short Sleep Duration ◽

Insufficient Sleep ◽

Short Sleep ◽

Type Plasminogen Activator ◽

Increased Risk ◽

Normal Sleep ◽

Middle Aged Adults

The capacity of the endothelium to release tissue-type plasminogen activator (t-PA) is impaired in adults with elevated BP, leading to an increased risk of thrombotic events. Insufficient sleep is independently associated with elevated BP and impaired t-PA release. However, the compounded influence of insufficient sleep on t-PA release in adults with elevated BP is unknown. We tested the hypothesis that impairments in the capacity of the endothelium to release t-PA in adults with elevated BP is worse in those who sleep <7 h/night (short sleep duration) compared with those who sleep 7 to 9 h/night (normal sleep duration). We studied 38 sedentary, middle-aged adults: 10 with normal BP and normal nightly sleep duration (6M/4F; age: 55±2 yr; BP: 114/94±2/3 mmHg, sleep duration: 7.4±0.2 h); 14 with elevated BP and normal nightly sleep duration (8M/6F; 60±2 yr; 141/87±2/2 mmHg; 7.8±0.1 h); and 14 with elevated BP and short nightly sleep duration (10M/4F; 57±2 yr; 139/85±2/2 mmHg; 6.1±0.2 h). All subjects were free of overt metabolic and coronary disease. Net endothelial release of t-PA was determined, in vivo, in response to intra-brachial infusions of bradykinin (BK: 125-500 ng/min) and sodium nitroprusside (SNP: 2.0-8.0 μg/min). In the normal sleep groups, as expected, endothelial t-PA release in response to BK was significantly blunted (~30%) in the adults with elevated BP (from -1.2±0.8 to 50.2±4.8 ng/100mL tissue/min) compared with normal BP (from 0.9±3.4 to 73.0±8.0 ng/100mL tissue/min); and total t-PA release (area under the BK curve) was ~25% lower (p<0.05) in the adults with elevated (307±33 ng/100mL tissue) vs. normal (396±27 ng/100mL tissue) BP. Importantly, net endothelial release rate (from -1.5±1.0 to 40.6±4.3 ng/100mL tissue/min) and total amount of t-PA released (222±28 ng/100mL tissue) in response to BK were markedly lower (~25% and 30%, respectively, P<0.05) in the elevated BP and short sleep duration group compared with the elevated BP and normal sleep duration group. In the elevated BP population, sleep duration was positively correlated with total t-PA release (r=0.46, P<0.05). There was no effect of SNP on t-PA release in any group. In summary, insufficient sleep is associated with exacerbated impairments in t-PA release in adults with elevated BP.

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Abstract 28: Regular Aerobic Exercise Counteracts Endothelial Vasomotor Dysfunction Associated With Insufficient Sleep

Circulation ◽

10.1161/circ.141.suppl_1.28 ◽

2020 ◽

Vol 141 (Suppl_1) ◽

Author(s):

Kelly A Stockelman ◽

Anthony R Bain ◽

Caitlin A Dow ◽

Jared J Greiner ◽

Brian L Stauffer ◽

...

Keyword(s):

Exercise Training ◽

Aerobic Exercise ◽

Sleep Duration ◽

Middle Aged ◽

Short Sleep Duration ◽

Insufficient Sleep ◽

Short Sleep ◽

Vasomotor Regulation ◽

Normal Sleep ◽

Middle Aged Adults

Insufficient sleep, defined as chronic short sleep duration (<7 h/night), is an independent risk factor for cardiovascular disease (CVD). We have previously demonstrated that insufficient sleep is associated with reduced endothelium-dependent vasodilation and enhanced endothelin (ET)-1-mediated vasoconstrictor tone. Impaired endothelial vasomotor regulation is thought to contribute mechanistically to the increased risk of atherosclerotic vascular disease incurred with chronic insufficient sleep. Regular aerobic exercise is an effective lifestyle strategy for improving endothelial function and, in turn reducing cardiovascular risk. It is currently unknown if regular aerobic exercise can counteract the negative impact of insufficient sleep on endothelial vasomotor regulation. We tested the hypotheses that regular aerobic exercise would: 1) improve endothelial vasodilation; and 2) decrease ET-1-mediated vasoconstrictor tone in middle-aged adults who chronically sleep less than 7 h/night. We studied 36 healthy, middle-aged adults: 16 with normal sleep duration (10M/6F; age: 57±2 yr; sleep duration: 7.4±0.1 h/night) and 20 with short sleep duration (11M/9F; 56±1 yr; sleep duration: 6.2±0.1 h/night). The 20 short sleepers completed a 3-month aerobic exercise training intervention. Forearm blood flow (FBF; plethysmography) was determined in response to intra-arterial doses of acetylcholine (ACh), sodium nitroprusside (SNP), BQ-123 (ET A receptor antagonist) and ACh + BQ-123 in both groups and after the exercise intervention in the short sleepers. As expected, forearm vasodilator responses to ACh were lower (20%; P<0.05) in the short (from 4.2±0.2 to 10.5±0.6 mL/100 mL tissue/min) vs normal (4.2±0.2 to 12.7±0.6 mL/100 mL tissue/min) sleepers. FBF responses to SNP were comparable between the groups. In response to BQ-123, short sleep group had a greater increase in resting FBF than normal sleep group (~25% vs ~8%; P< 0.05). ACh+BQ-123 resulted in an ~25% increase in the ACh-vasodilation in the short sleep group only. After exercise training, although nightly sleep duration was not affected (6.4±0.1 h/night), ACh-mediated vasodilation was ~20% higher (P<0.05), ET-1-mediated vasoconstriction was ~90% lower (P<0.05) and vasodilator response to ACh was not significantly increased with ET A receptor blockade. These results indicate that regular aerobic exercise can reverse the negative influence of insufficient sleep on endothelial vasomotor function, independent of changes in nightly sleep duration.

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0992 Prevalence Of Insufficient Sleep Duration And Consequences On Daytime Sleepiness, Mood And Academic Performance In Thai Adolescents

SLEEP ◽

10.1093/sleep/zsaa056.988 ◽

2020 ◽

Vol 43 (Supplement_1) ◽

pp. A377-A377

Author(s):

R Rojrattanadumrong ◽

K K Sudnawa ◽

W Areekul ◽

R Jaroenying

Keyword(s):

Depressive Symptoms ◽

Sleep Duration ◽

Daytime Sleepiness ◽

Child Anxiety ◽

Sleep Time ◽

Poor Sleep ◽

Insufficient Sleep ◽

Grade Point ◽

Thai Adolescents ◽

Sleep Length

Abstract Introduction Insufficient sleep duration in adolescents is key public health concerns in many societies. This study aims to assess the prevalence of insufficient sleep duration and the association between short sleep with daytime sleepiness, depressive symptoms, and anxiety among Thai adolescents. Methods Thai adolescents aged 11 -18 years completed a self-administered questionnaire including Phramongkutklao Hospital Sleep disorders center Questionnaire, Pittsburg Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), The Children depress Inventory (CDI) scale and Child Anxiety Related Emotional Disorder (SCARED). Results 232 adolescents with the mean age of 14.58 (range 11-18) years participated in this survey. The average total sleep time was 7.44 hours. The overall prevalence of insufficient sleep duration (sleep duration <8 hours) was 37.5% and the small difference was found between males (42.0%) and females (32.7%). Compared with those who had a sleep length of 8 hours and more, insufficient sleep duration group exhibited higher in BMI and less in Grade Point Average (GPA). Subjective sleep insufficiency among Thai adolescent also had higher percentage of subjects with ESS ≥10 (43.2% vs 21.3%, P <0.001), depressive symptoms (56.3% vs 39.3%, P 0.012) and anxiety (54.0% vs 38.6%, P 0.022) compare to those with adequate sleep duration. Conclusion High amount of Thai adolescents with poor sleep duration were observed in the study, consistency with prior surveys. Insufficiency sleep duration group had significantly increased daytime sleepiness, mood and anxiety problems among Thai adolescents. These findings emphasized the development of interventions to improve sleep duration in Thai adolescents and more sample size should be achieved in the future. Support None

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Regular Aerobic Exercise Counteracts Endothelial Vasomotor Dysfunction Associated With Insufficient Sleep

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00615.2020 ◽

2021 ◽

Author(s):

Kelly A. Stockelman ◽

Anthony R. Bain ◽

Caitlin A. Dow ◽

Kyle J. Diehl ◽

Jared J. Greiner ◽

...

Keyword(s):

Blood Flow ◽

Cardiovascular Risk ◽

Aerobic Exercise ◽

Sleep Duration ◽

Forearm Blood Flow ◽

Insufficient Sleep ◽

Short Sleep ◽

Normal Sleep ◽

Middle Aged Adults ◽

Vasomotor Dysfunction

Insufficient sleep is associated with endothelial vasomotor dysfunction and increased cardiovascular risk. Regular aerobic exercise is an effective lifestyle strategy for improving endothelial function and, in turn, reducing cardiovascular risk. We tested the hypotheses that regular aerobic exercise would: 1) improve endothelial vasodilation; and 2) decrease ET-1-mediated vasoconstrictor tone in middle-aged adults who chronically sleep <7 h/night. Thirty-six healthy, middle-aged adults were studied: 16 with normal sleep duration (age: 57±2 yr; sleep duration: 7.4±0.1 h/night) and 20 with short sleep duration (56±1 yr; 6.2±0.1 h/night). The 20 short sleepers completed a 3-month aerobic exercise training intervention. Forearm blood flow was determined (via plethysmography) in response to intra-arterial acetylcholine (ACh), BQ-123 (ETAreceptor antagonist), ACh+BQ-123 and sodium nitroprusside. Forearm blood flow responses to ACh were lower (20%; P<0.05) in the short (from 4.2±0.2 to 10.5±0.6 mL/100 mL tissue/min) vs normal (4.2±0.2 to 12.7±0.6 mL/100 mL tissue/min) sleepers. In response to BQ-123, the short sleep group had a significantly greater increase in resting forearm blood flow than the normal sleep group (~25% vs ~8%). ACh+BQ-123 resulted in a significant (~25%) increase in the ACh-vasodilation in the short sleep group only. After exercise training, although nightly sleep duration was unchanged (6.4±0.1 h/night), ACh-mediated vasodilation was significantly higher (~20%), ET-1-mediated vasoconstriction was significantly lower (~80%) and the vasodilator response to ACh was not increased with ETAreceptor blockade. Regular aerobic exercise, independent of changes in nightly sleep duration, can counteract insufficient sleep-related endothelial vasomotor dysfunction.

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