Effects of Sleep Deprivation on Neural Circulatory Control

Kato, Masahiko; Phillips, Brian N.; Sigurðsson, Garðar; Narkiewicz, Krzysztof; Pesek, Catherine A.; Somers, Virend K.

doi:10.1161/01.hyp.35.5.1173

Cited by 283 publications

(219 citation statements)

References 23 publications

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“…Inadequate sleep may also have consequences for circulatory control that, in the absence of measurements of sleep quality, could be misinterpreted as changes secondary to morning fluctuations in cardiovascular physiology. 40,41 Finally, the use of nitroglycerin-induced dilation as an internal control makes more robust our findings of a selective impairment of FMD but not NFMD.…”

Section: Discussionmentioning

confidence: 67%

Early Morning Attenuation of Endothelial Function in Healthy Humans

et al. 2004

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Background-Cardiovascular events such as myocardial infarction, sudden death, and stroke have a peak incidence in the early hours after waking. The mechanisms involved in this circadian variation are not clear. Endothelial dysfunction is associated with increased risk for cardiovascular events. We tested the hypothesis that endothelial function is reduced in the early morning, around the time of waking, compared with measurements obtained both before sleep and later in the day in healthy humans. Methods and Results-We studied 30 subjects (19 men, 11 women; mean age, 41.6 years). All participants underwent polysomnography to exclude obstructive sleep apnea or other sleep disorders. Brachial artery flow-mediated endothelium-dependent vasodilation (FMD) and endothelium-independent dilation (non-FMD) were measured on 3 different occasions: before subjects went to sleep (9 PM), the next morning immediately after waking (6 AM), and during the late morning 5 hours after waking (11 AM). All subjects had normal sleep with good sleep efficiency of 84Ϯ2%. Compared with before sleep, FMD decreased markedly in the early morning after waking and recovered by late morning (9 PM, 7.5Ϯ1%; 6 AM, 4.4Ϯ0.7%; 11 AM, 7.7Ϯ1%; Pϭ0.02). Non-FMD was similar for the 3 periods of observation (9 PM, 17.3Ϯ1.6%; 6 AM, 17.2Ϯ1.3%; 11 AM, 18.5Ϯ1.7%). Conclusions-FMD is blunted in the early morning in healthy subjects. Decreased endothelial function in the early morning may have implications for our understanding of the morning peak in cardiac and vascular events. (Circulation.

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Section: Discussionmentioning

confidence: 67%

Early Morning Attenuation of Endothelial Function in Healthy Humans

et al. 2004

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“…11,2741,42 Alcoholic subjects who have a night of insufficient sleep may be particularly vulnerable to increases of blood pressure and heart rate in the morning. 11,12 Cardiovascular events are known to occur more frequently from early morning to noon, 14 and longitudinal studies have found that autonomic dysregulation is related to greater risk of cardiovascular disease. 43 …”

Section: Irwin and Ziegler Sleep Deprivation And Sympathetic Activatimentioning

confidence: 99%

“…Loss of sleep induces elevations in circulating levels of epinephrine and norepinephrine, 9,10 with attendant increases of blood pressure and heart rate the next day. 11,12 In addition, habitual sleep loss and insomnia are markers of subclinical heart disease and are independent predictors of cardiovascular disease risk, particularly in males. 13 Fluctuations in sympathetic activity across the sleep-wake cycle are thought to contribute to the low rates of sudden cardiac death, myocardial infarction, and ischemic stroke during sleep, as well as to their peak incidence at the end of sleep or in the morning after awakening.…”

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confidence: 99%

Sleep Deprivation Potentiates Activation of Cardiovascular and Catecholamine Responses in Abstinent Alcoholics

Irwin

2005

Hypertension

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Abstract-Alcohol dependence is associated with an increased incidence of hypertension and cardiac arrhythmias, but the triggering mechanisms are not known. Sleep loss, common in alcohol-dependent patients, causes an activation of the sympathetic nervous system. To determine whether sleep deprivation induces differential cardiovascular and sympathetic responses in alcohol dependence, we measured heart rate, blood pressure, and circulating sympathetic catecholamines in 36 abstinent alcohol-dependent men and 36 age-, gender-, and ethnicity-matched controls after a baseline night of sleep, in the morning after early night partial sleep deprivation, and again after a full night of recovery sleep. Subjects were on average normotensive and none was being treated for hypertension. Baseline heart rate, blood pressure, and sympathetic catecholamines were similar in the 2 groups. Administration of partial night sleep deprivation induced greater increases of heart rate (PϽ0.01) and circulating levels of norepinephrine (PϽ0.05) and epinephrine (PϽ0.05) in the alcohol-dependent men as compared with responses in controls. Even after a full night of recovery sleep, elevations in heart rate (PϽ0.05) and circulating catecholamines (PϽ0.05) persisted in the alcoholic subjects. Partial night sleep deprivation induces elevated heart rate and sympathetic catecholamine responses in alcoholic subjects as compared with controls, and this sympathetic activation is sustained after nights of partial and recovery sleep. A lcohol dependence, which exceeds a lifetime incidence of 10%, 1 is a major risk factor for cardiovascular diseases, with alcohol-dependent men showing an increased prevalence of hypertension and cardiac arrhythmias. 2,3 An increase of sympathetic nervous system activity is implicated as being one underlying mechanism of the deleterious cardiovascular effects of chronic alcohol consumption. 4 Human studies have found that acute alcohol intake induces elevations of heart rate and blood pressure via centrally mediated increases of sympathetic discharge. 5 There is also evidence that abnormalities of cardiovascular regulation persist into recovery. Abstinent alcohol-dependent male patients show exaggerated heart rate and blood pressure reactivity in response to behavioral stress, although measures of sympathetic activation have not been determined. 6 -8 In this study, we examined cardiovascular responses and circulating levels of norepinephrine and epinephrine at rest and in response to a behavioral challenge, sleep deprivation, in abstinent male alcohol-dependent patients.Experimental sleep deprivation can serve as a naturalistic probe of the homeostatic regulation of sympathetic activity. Loss of sleep induces elevations in circulating levels of epinephrine and norepinephrine, 9,10 with attendant increases of blood pressure and heart rate the next day. 11,12 In addition, habitual sleep loss and insomnia are markers of subclinical heart disease and are independent predictors of cardiovascular disease risk, particularly in ma...

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“…Short-term sleep deprivation studies suggest that acute sleep deprivation increases BP. 19,20 Furthermore, a relationship between habitual sleep duration and BP 21 and an inverse relation between sleep duration and body mass index (BMI) 22,23 have been demonstrated. Hypertension in short sleepers may then also be favored by the development of obesity.…”

Section: Introductionmentioning

confidence: 99%

Low Physical Activity Is a Determinant for Elevated Blood Pressure in High Cardiovascular Risk Obstructive Sleep Apnea

Mendelson

Tamisier

Laplaud³

et al. 2013

Respir Care

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INTRODUCTION:Obstructive sleep apnea (OSA) is associated with cardiovascular morbidity, including hypertension. Beyond the severity of nocturnal hypoxia, other factors such as metabolic abnormalities but also sedentary behaviors and insufficient physical activity may contribute to elevated blood pressure (BP). To clarify the respective role of these factors as determinants of BP in OSA patients, we examined the relationship between BP and anthropometrics, severity of sleep apnea, and objectively measured physical activity and sedentary behaviors. METHODS: Ninetyfive adults presenting with OSA (apnea-hypopnea index > 10 events/h) and high cardiovascular risk (63.3 ؎ 8.8 y; body mass index: 29.9 ؎ 4.9 kg/m 2 ; apnea-hypopnea index: 41.3 ؎ 17.5/h; cardiovascular risk score: 13.5 ؎ 3.7%) were included. Physical activity and sedentary behaviors were objectively assessed by actigraphy, and self-measured home BP monitoring was measured. Logistic regression models adjusted for sex, age, and body mass index were built to identify the predictors of self-measured morning and evening BP. RESULTS: Physical activity was significantly related to obesity but not to the severity of sleep apnea or sleepiness. Sedentary behaviors were associated with self-measured morning and evening systolic BP (r ‫؍‬ 0.32, P ‫؍‬ .002; r ‫؍‬ 0.29, P ‫؍‬ .004). Steps per day were inversely associated with evening BP (r ‫؍‬ ؊0.27, P ‫؍‬ .01). Univariate analysis identified steps/d and time spent in vigorous physical activity as determinants for evening self-measured BP. In multivariate analysis, only steps/d were identified as a significant determinant of evening BP. CONCLUSIONS: Physical activity is the major determinant for evening BP in adults with OSA presenting high cardiovascular risk. Our results emphasize the need for lifestyle counseling programs in combination with CPAP to encourage regular physical activity in OSA subjects to obtain better BP control. (ClinicalTrials.gov registration NCT01226641.)

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Effects of Sleep Deprivation on Neural Circulatory Control

Cited by 283 publications

References 23 publications

Early Morning Attenuation of Endothelial Function in Healthy Humans

Early Morning Attenuation of Endothelial Function in Healthy Humans

Sleep Deprivation Potentiates Activation of Cardiovascular and Catecholamine Responses in Abstinent Alcoholics

Low Physical Activity Is a Determinant for Elevated Blood Pressure in High Cardiovascular Risk Obstructive Sleep Apnea

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