scholarly journals Regular Aerobic Exercise Counteracts Endothelial Vasomotor Dysfunction Associated With Insufficient Sleep

Author(s):  
Kelly A. Stockelman ◽  
Anthony R. Bain ◽  
Caitlin A. Dow ◽  
Kyle J. Diehl ◽  
Jared J. Greiner ◽  
...  

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.

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Kelly A Stockelman ◽  
Anthony R Bain ◽  
Caitlin A Dow ◽  
Jared J Greiner ◽  
Brian L Stauffer ◽  
...  

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.


Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Anthony R Bain ◽  
Caitlin A Dow ◽  
Kyle J Diehl ◽  
Tyler D Bammert ◽  
Jared J Greiner ◽  
...  

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.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Kelly A Stockelman ◽  
Anthony R Bain ◽  
Dana M Withrow ◽  
Tracey A Larson ◽  
Elizabeth M Boland ◽  
...  

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.


2010 ◽  
Vol 88 (8) ◽  
pp. 777-781 ◽  
Author(s):  
Brian R. Weil ◽  
Michael L. Mestek ◽  
Christian M. Westby ◽  
Gary P. Van Guilder ◽  
Jared J. Greiner ◽  
...  

Short sleep duration is associated with increased cardiovascular disease (CVD) morbidity. Endothelial vasomotor dysfunction represents a potential mechanism contributing to the increased CVD risk associated with habitual short sleep duration. Endothelin (ET)-1 is a potent vasoconstrictor peptide that is associated with endothelial vasomotor dysfunction and increased CVD risk. Currently, there is no information regarding the influence of short sleep duration on ET-1 vasoconstrictor activity in adults. We tested the hypothesis that ET-1-mediated vasoconstrictor activity is greater in adults who sleep less than 7 h/night (short sleep duration) compared with those who sleep 7–9 h/night (normal sleep duration). Forearm blood flow (FBF) responses to intra-arterial infusion of BQ-123 (100 nmol/min for 60 min), a selective ETAreceptor antagonist, were determined in 80 adults: 50 with normal sleep duration (32 males and 18 females; age: 56.6 ± 1.2 years; sleep: 7.6 ± 0.1 h/night) and 30 with short sleep duration (17 males and 13 females; age: 56.5 ± 1.2 years; sleep: 6.1 ± 0.1 h/night). In response to BQ-123, adults reporting short sleep duration had a greater increase in resting FBF compared with adults reporting normal sleep duration (~20% vs. ~8%; P < 0.05). There was an inverse relation between mean nightly sleep duration and the FBF response to BQ-123 at 60 min (r = –0.29, P < 0.05). These findings indicate that habitual short sleep duration is associated with greater ET-1-mediated vasoconstrictor tone. Increased ET-1 vasoconstrictor activity may contribute to the elevated CVD risk associated with chronic reductions in sleep duration.


2015 ◽  
Vol 16 (12) ◽  
pp. 1482-1488 ◽  
Author(s):  
Kenneth Anujuo ◽  
Karien Stronks ◽  
Marieke B. Snijder ◽  
Girardin Jean-Louis ◽  
Femke Rutters ◽  
...  

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A425-A426
Author(s):  
R Peprah ◽  
D Jenkins ◽  
T Donley ◽  
A Sexias ◽  
G Jean-Louis

Abstract Introduction Sleep duration can have important effects on health. Long and short sleep has been associated with negative health outcomes in women. Depression may aggravate an already impaired sleep quality. This study explored associations between sleep duration and depression in pregnant women. Methods We analyzed data for adult women (n=9,372) from the 2017 and 2018 National Health Interview Survey (NHIS), which is a nationally representative study of the US civilian non-institutionalized population. Sleep was categorized by short (≤6 hrs), normal/healthy (7-8 hrs), and long (≥9 hrs) sleep. Using STATA 15.0 for Windows, we report weighted frequencies and Chi-and square tests. Alpha of 0.05 was used for all significance levels. Results Of the sample, 81.7% of the women were White, 10.6% were Black and 7.7% were other minorities. The mean age was 51.4±18.3. We found that the proportion of women who reported short sleep increased with age (p&lt;0.000). Current drinkers (37%) had higher numbers of normal sleep than those who were former drinkers or abstainers (p&lt;0.000). With respect to BMI, more obese women were short and sleepers (17% and 4% respectively), but women with normal BMI (19%) were normal sleepers (p&lt;0.000). In short sleepers, more women had trouble falling asleep (13%) and staying asleep (17%), but reported not using medication and never feeling rested. Similar results were found for long sleepers. Higher proportions of normal sleepers reported not have trouble falling asleep (27%), staying asleep (26%), or using medication for sleep (40%) (p&lt;0.000). However, of those who reported normal sleep, greater frequencies of working up feeling rested occurred only 3-6 times in the past week (p&lt;0.000). Conclusion In this study, women with depression self-reported more normal sleep duration. This finding is inconsistent with previous research. Whether this association is causal and what pathways explain this association is unknown. Support This study was supported by funding from the NIH: R01MD007716, R01HL142066, K01HL135452, and K07AG052685.


Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2103 ◽  
Author(s):  
Jing Sun ◽  
Hong Jiang ◽  
Weijing Wang ◽  
Xue Dong ◽  
Dongfeng Zhang

Current evidence on the relationship of phytoestrogens with sleep is limited and contradictory. In particular, studies on individual phytoestrogens and sleep have not been reported. Thus, this study aimed to appraise the associations of individual phytoestrogens with sleep disorders and sleep duration. This cross-sectional study comprising 4830 adults utilized data from the National Health and Nutrition Examination Survey 2005–2010. Phytoestrogens were tested in urine specimens. Sleep disorders and sleep duration were based on a self-reported doctor’s diagnosis and usual sleep duration. The main analyses utilized logistic and multinomial logistic regression models and a restricted cubic spline. In the fully adjusted model, compared with tertile 1 (lowest), the odds ratios (95% confidence intervals (CIs)) of sleep disorders for the highest tertile of urinary concentrations of enterolactone, enterodiol, and O-desmethylangolensin were 0.64 (0.41–1.00), 1.54 (1.07–2.21), and 1.89 (1.26–2.85), respectively. Linear inverse, approximatively linear positive, and inverted L-shaped concentration–response relationships were found between enterolactone, enterodiol, and O-desmethylangolensin and sleep disorders, respectively. Compared with normal sleep (7–8 h/night), the relative risk ratio (RRR) (95% CI) of very short sleep for enterolactone was 0.56 (0.36–0.86), and the RRR (95% CI) of long sleep risk for genistein was 0.62 (0.39–0.99). Furthermore, negative associations of genistein with sleep disorders and enterolactone with long sleep risk, as well as positive associations of enterodiol with both long and very short sleep, were observed in the stratified analysis by age or gender. Finally, a notable finding was that urinary O-desmethylangolensin concentration was positively related to sleep disorders in both females aged 40–59 years and non-Hispanic Whites but inversely associated with sleep disorders in both females aged 60 years or over and other Hispanics. Our findings suggested that enterolactone and genistein might be beneficial for preventing sleep disorders or non-normal sleep duration among adults, and enterodiol might be adverse toward this goal. However, the association of O-desmethylangolensin with sleep disorders might be discrepant in different races and females of different ages.


2013 ◽  
Vol 110 (5) ◽  
pp. 949-959 ◽  
Author(s):  
Sarah Bel ◽  
Nathalie Michels ◽  
Tineke De Vriendt ◽  
Emma Patterson ◽  
Magdalena Cuenca-García ◽  
...  

Evidence has grown supporting the role for short sleep duration as an independent risk factor for weight gain and obesity. The purpose of the present study was to examine the relationship between sleep duration and dietary quality in European adolescents. The sample consisted of 1522 adolescents (aged 12·5–17·5 years) participating in the European multi-centre cross-sectional ‘Healthy Lifestyle in Europe by Nutrition in Adolescence’ study. Sleep duration was estimated by a self-reported questionnaire. Dietary intake was assessed by two 24 h recalls. The Diet Quality Index for Adolescents with Meal index (DQI-AM) was used to calculate overall dietary quality, considering the components dietary equilibrium, dietary diversity, dietary quality and a meal index. An average sleep duration of ≥ 9 h was classified as optimal, between 8 and 9 h as borderline insufficient and < 8 h as insufficient. Sleep duration and the DQI-AM score were positively associated (β = 0·027, r 0·130, P< 0·001). Adolescents with insufficient (62·05 (sd 14·18)) and borderline insufficient sleep (64·25 (sd 12·87)) scored lower on the DQI-AM than adolescents with an optimal sleep duration (64·57 (sd 12·39)) (P< 0·001; P= 0·018). The present study demonstrated in European adolescents that short sleep duration was associated with a lower dietary quality. This supports the hypothesis that the health consequences of insufficient sleep may be mediated by the relationship of insufficient sleep to poor dietary quality.


2017 ◽  
Vol 41 (S1) ◽  
pp. s853-s853
Author(s):  
J. Isaac ◽  
C. Santos ◽  
A. Matos Pires

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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Elizabeth B. Klerman ◽  
Giuseppe Barbato ◽  
Charles A. Czeisler ◽  
Thomas A. Wehr

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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