Document Detail


Impact of the human circadian system, exercise, and their interaction on cardiovascular function.
MedLine Citation:
PMID:  21059915     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The risk of adverse cardiovascular events peaks in the morning (≈9:00 AM) with a secondary peak in the evening (≈8:00 PM) and a trough at night. This pattern is generally believed to be caused by the day/night distribution of behavioral triggers, but it is unknown whether the endogenous circadian system contributes to these daily fluctuations. Thus, we tested the hypotheses that the circadian system modulates autonomic, hemodynamic, and hemostatic risk markers at rest, and that behavioral stressors have different effects when they occur at different internal circadian phases. Twelve healthy adults were each studied in a 240-h forced desynchrony protocol in dim light while standardized rest and exercise periods were uniformly distributed across the circadian cycle. At rest, there were large circadian variations in plasma cortisol (peak-to-trough ≈85% of mean, peaking at a circadian phase corresponding to ≈9:00 AM) and in circulating catecholamines (epinephrine, ≈70%; norepinephrine, ≈35%, peaking during the biological day). At ≈8:00 PM, there was a circadian peak in blood pressure and a trough in cardiac vagal modulation. Sympathetic variables were consistently lowest and vagal markers highest during the biological night. We detected no simple circadian effect on hemostasis, although platelet aggregability had two peaks: at ≈noon and ≈11:00 PM. There was circadian modulation of the cardiovascular reactivity to exercise, with greatest vagal withdrawal at ≈9:00 AM and peaks in catecholamine reactivity at ≈9:00 AM and ≈9:00 PM. Thus, the circadian system modulates numerous cardiovascular risk markers at rest as well as their reactivity to exercise, with resultant profiles that could potentially contribute to the day/night pattern of adverse cardiovascular events.
Authors:
Frank A J L Scheer; Kun Hu; Heather Evoniuk; Erin E Kelly; Atul Malhotra; Michael F Hilton; Steven A Shea
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2010-11-08
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  107     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-24     Completed Date:  2011-01-20     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  20541-6     Citation Subset:  IM    
Affiliation:
Division of Sleep Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. fscheer@rics.bwh.harvard.edu
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MeSH Terms
Descriptor/Qualifier:
Adult
Blood Pressure
Body Temperature
Cardiovascular Diseases / etiology*
Catecholamines / blood
Circadian Rhythm / physiology*
Exercise / physiology*
Female
Heart Rate
Hemostasis / physiology
Humans
Hydrocortisone / blood
Likelihood Functions
Male
Time Factors
Grant Support
ID/Acronym/Agency:
K24 HL076446/HL/NHLBI NIH HHS; K24 HL076446-08/HL/NHLBI NIH HHS; K24 HL093218/HL/NHLBI NIH HHS; K24 HL093218-02/HL/NHLBI NIH HHS; K24-HL076446/HL/NHLBI NIH HHS; K24-HL093218/HL/NHLBI NIH HHS; K99 HL102241/HL/NHLBI NIH HHS; K99 HL102241-01/HL/NHLBI NIH HHS; K99-HL102241/HL/NHLBI NIH HHS; M01-RR02635/RR/NCRR NIH HHS; P30-HL101299/HL/NHLBI NIH HHS; R01-HL76409/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Catecholamines; 50-23-7/Hydrocortisone
Comments/Corrections

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