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dc.contributor.authorJames, Jack E
dc.date.accessioned2009-11-23T15:10:09Z
dc.date.available2009-11-23T15:10:09Z
dc.date.issued2009
dc.date.submitted2009
dc.identifier.citationSálfræðiritið 2009, Fylgirit 1. 14:85-9en
dc.identifier.issn1607-8326
dc.identifier.urihttp://hdl.handle.net/2336/86715
dc.descriptionNeðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/Openen
dc.description.abstractThe reactivity hypothesis of hypertension states that persistent and exaggerated blood pressure (BP) responses to common stressful events may lead to the development of hypertension and cardiovascular disease. This experiment aimed to examine hemodynamic profile induced by behavioural challenges in the form of sleep restriction and psychosocial stress induced by time-pressured cognitive performance. Participants were 96 healthy male and female adults who received 40% of their usual overnight sleep on 2 of 4 nights preceding 4 morning visits to the research laboratory. Consistent with previous studies, sleep restriction had no appreciable effect on BP level. However, Finapres measurements of CO and TPR showed that the null effect of sleep restriction on BP concealed a pronounced vascular response in the form of marked increases in TPR, suggesting that a lifestyle characterised by persistent sleep loss could contribute significantly to the development of cardiovascular disease.
dc.language.isoenen
dc.publisherSálfræðingfélag Íslandsen
dc.relation.urlhttp://www.sal.isen
dc.subject.meshSleep Deprivationen
dc.subject.meshCardiovascular Diseasesen
dc.titleHemodynamic effects of sleep restriction and laboratory stressen
dc.typeArticleen
dc.identifier.journalSálfræðiritið : Fylgiriten
refterms.dateFOA2018-09-12T18:58:31Z
html.description.abstractThe reactivity hypothesis of hypertension states that persistent and exaggerated blood pressure (BP) responses to common stressful events may lead to the development of hypertension and cardiovascular disease. This experiment aimed to examine hemodynamic profile induced by behavioural challenges in the form of sleep restriction and psychosocial stress induced by time-pressured cognitive performance. Participants were 96 healthy male and female adults who received 40% of their usual overnight sleep on 2 of 4 nights preceding 4 morning visits to the research laboratory. Consistent with previous studies, sleep restriction had no appreciable effect on BP level. However, Finapres measurements of CO and TPR showed that the null effect of sleep restriction on BP concealed a pronounced vascular response in the form of marked increases in TPR, suggesting that a lifestyle characterised by persistent sleep loss could contribute significantly to the development of cardiovascular disease.


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