Sleep deprivation increases blood pressure in healthy normotensive elderly and attenuates the blood pressure response to orthostatic challenge.

Center for Advanced Research in Sleep Medicine, Hôpital du Sacré-Coeur de Montréal, Montréal, Canada.
Sleep (Impact Factor: 5.06). 01/2011; 34(3):335-9.
Source: PubMed

ABSTRACT To determine how aging affects the impact of sleep deprivation on blood pressure at rest and under orthostatic challenge.
Subjects underwent a night of sleep and 24.5 h of sleep deprivation in a crossover counterbalanced design.
Sleep laboratory.
Sixteen healthy normotensive men and women: 8 young adults (mean 24 years [SD 3.1], range 20-28 years) and 8 elderly adults (mean 64.1 years [SD 3.4], range 60-69 years).
Sleep deprivation.
Brachial cuff arterial blood pressure and heart rate were measured in semi-recumbent and upright positions. These measurements were compared across homeostatic sleep pressure conditions and age groups. Sleep deprivation induced a significant increase in systolic and diastolic blood pressure in elderly but not young adults. Moreover, sleep deprivation attenuated the systolic blood pressure orthostatic response in both age groups.
Our results suggest that sleep deprivation alters the regulatory mechanisms of blood pressure and might increase the risk of hypertension in healthy normotensive elderly.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Self-reported short or long sleep duration has been associated with adverse cardiometabolic health outcomes in laboratory and epidemiologic studies, but interpretation of such data has been limited by methodologic issues. Adult respondents of the 2007-2008 US National Health and Nutrition Examination Survey (NHANES) were examined in a cross-sectional analysis (N=5649). Self-reported sleep duration was categorized as very short (<5h), short (5-6h), normal (7-8h), or long (⩾9h). Obesity, diabetes mellitus (DM), hypertension, and hyperlipidemia were objectively assessed by self-reported history. Statistical analyses included univariate comparisons across sleep duration categories for all variables. Binary logistic regression analyses and cardiometabolic factor as outcome, with sleep duration category as predictor, were assessed with and without covariates. Observed relationships were further assessed for dependence on race/ethnicity. In adjusted analyses, very short sleep was associated with self-reported hypertension (odds ratio [OR], 2.02, [95% confidence interval {CI},1.45-2.81]; P<0.0001), self-reported hyperlipidemia (OR, 1.96 [95% CI, 1.43-2.69]; P<0.0001), objective hyperlipidemia (OR, 1.41 [95% CI, 1.04-1.91]; P=0.03), self-reported DM (OR, 1.76 [95% CI, 1.13-2.74]; P=0.01), and objective obesity (OR, 1.53 [95% CI, 1.03-1.43]; P=0.005). Regarding short sleep (5-6h), in adjusted analyses, elevated risk was seen for self-reported hypertension (OR, 1.22 [95% CI, 1.02-1.45]; P=0.03) self-reported obesity (OR, 1.21 [95% CI, 1.03-1.43]; P=0.02), and objective obesity (OR, 1.17 [95% CI, 1.00-1.38]; P<0.05). Regarding long sleep (⩾9h), no elevated risk was found for any outcomes. Interactions with race/ethnicity were significant for all outcomes; race/ethnicity differences in patterns of risk varied by outcome studied. In particular, the relationship between very short sleep and obesity was strongest among blacks and the relationship between short sleep and hypertension is strongest among non-Hispanic whites, blacks, and non-Mexican Hispanics/Latinos. Short sleep duration is associated with self-reported and objectively determined adverse cardiometabolic outcomes, even after adjustment for many covariates. Also, these patterns of risk depend on race/ethnicity.
    Sleep Medicine 10/2013; DOI:10.1016/j.sleep.2013.09.012 · 3.10 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Sleep loss is suspected to induce endothelial dysfunction, a key factor in cardiovascular risk. We examined whether sympathetic activity is involved in the endothelial dysfunction caused by total sleep deprivation (TSD). TWO GROUPS: TSD (24-h wakefulness), using slowly rotating wheels, and wheel control (WC). Seven-month-old male Wistar rats. Pharmacological sympathectomy (reserpine, 5 mg/kg, intraperitoneal), nitric oxide synthase (NOS) inhibition (N (G)-nitro-L-arginine, 20 mg/kg, intraperitoneally 30 min before experiment) and cyclooxygenase (COX) inhibition (indomethacin, 5 mg/kg, intraperitoneally 30 min before experiment). In protocol 1, changes in heart rate (HR) and blood pressure were continuously recorded in the sympathectomized and non-sympathectomized rats. Blood pressure and HR increased during TSD in non-sympathectomized rats. In protocol 2, changes in skin blood flow (vasodilation) were assessed in the sympathectomized and non-sympathectomized rats using laser-Doppler flowmetry coupled with iontophoretic delivery of acetylcholine (ACh), sodium nitroprusside (SNP), and anodal and cathodal currents. ACh- and cathodal current-induced vasodilations were significantly attenuated after TSD in non-sympathectomized and sympathectomized rats (51% and 60%, respectively). In protocol 3, ACh-induced vasodilation was attenuated after NOS and COX inhibition (66% and 49%, respectively). Cathodal current-induced vasodilation decreased by 40% after COX inhibition. In TSD compared to WC a decrease in ACh-induced vasodilation was still observed after COX inhibition. No changes in SNP- and anodal current-induced vasodilation were detected. These results demonstrate that total sleep deprivation induces a reduction in endothelial-dependent vasodilation. This endothelial dysfunction is independent of blood pressure and sympathetic activity but associated with nitric oxide synthase and cyclooxygenase pathway alterations. Sauvet F; Florence G; Van Beers P; Drogou C; Lagrume C; Chaumes C; Ciret S; Leftheriotis G; Chennaoui M. Total sleep deprivation alters endothelial function in rats: a nonsympathetic mechanism. SLEEP 2014;37(3):465-473.
    Sleep 03/2014; 37(3):465-73. DOI:10.5665/sleep.3476 · 5.06 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Sleep-wake disturbances are among the most persistent sequelae after traumatic brain injury (TBI) and probably arise during the hospital stay following TBI. These disturbances are characterized by difficulties sleeping at night and staying awake during the day. The aim of the present study was to document rest-activity cycle consolidation in acute moderate/severe TBI using actigraphy and to assess its association with injury severity and outcome. In all, 16 hospitalized patients (27.1 ± 11.3 years) with moderate/severe TBI wore actigraphs for 10 days, starting in the intensive care unit (ICU) when continuous sedation was discontinued and patients had reached medical stability. Activity counts were summed for daytime (7:00-21:59 hours) and nighttime periods (22:00-6:59 hours). The ratio of daytime period activity to total 24-hour activity was used to quantify rest-activity cycle consolidation. An analysis of variance was carried out to characterize the evolution of the daytime activity ratio over the recording period. Rest-activity cycle was consolidated only 46.6% of all days; however, a significant linear trend of improvement was observed over time. Greater TBI severity and longer ICU and hospital lengths of stay were associated with poorer rest-activity cycle consolidation and evolution. Patients with more rapid return to consolidated rest-activity cycle were more likely to have cleared posttraumatic amnesia and have lower disability at hospital discharge. Patients with acute moderate/severe TBI had an altered rest-activity cycle, probably reflecting severe fragmentation of sleep and wake episodes, which globally improved over time. A faster return to rest-activity cycle consolidation may predict enhanced brain recovery.
    Neurorehabilitation and neural repair 12/2013; 28(5). DOI:10.1177/1545968313517756 · 4.62 Impact Factor

Full-text (2 Sources)

Available from
Oct 22, 2014