Impact of mental stress, the circadian system and their interaction on human cardiovascular function.
Impact of mental stress, the circadian system and their interaction on human cardiovascular function.
The risk for adverse cardiovascular events (e.g., myocardial infarction, sudden cardiac death) peaks in the morning, possibly due to the effects of the endogenous circadian system on cardiovascular risk factors, or the occurrence in the morning of specific triggers, such as mental stress. To assess any interacting effects on cardiovascular function of mental stress and the circadian system, 12 healthy adults underwent a 240-h protocol with all measurements and behaviors scheduled evenly across the circadian cycle. Mental stress was repeatedly induced by performance-motivated serial addition tasks. Cardiovascular measures included hemodynamic function (heart rate, blood pressure), circulating catecholamines (epinephrine, norepinephrine), and estimates of sympathovagal balance and cardiac vagal modulation derived from heart rate variability analyses. Mental stress increased hemodynamic function, sympathovagal balance and epinephrine, and decreased cardiac vagal modulation. Endogenous circadian variation occurred in all cardiovascular measures: sympathovagal balance peaked in the circadian morning (∼9 AM), cardiac vagal modulation in the circadian night (∼4 AM), and heart rate and circulating catecholamines in the late circadian morning/early afternoon (∼12 PM). Importantly, the effects of mental stress and the endogenous circadian system on cardiovascular function occurred in conjunction, such that mental stress in the circadian morning caused greatest sympathovagal balance. This summation of effects could contribute to the increased morning cardiovascular vulnerability.
125-129
Scheer, FAJL
91fea554-bacb-4008-ae58-8fd2bbc5d0fe
Chellappa, SL
516582b5-3cba-4644-86c9-14c91a4510f2
Hu, K
83c5e569-46c4-4947-a5eb-e0388b2d4378
Shea, SA
66ca5794-8481-4f4e-a5b3-8117841c8693
May 2019
Scheer, FAJL
91fea554-bacb-4008-ae58-8fd2bbc5d0fe
Chellappa, SL
516582b5-3cba-4644-86c9-14c91a4510f2
Hu, K
83c5e569-46c4-4947-a5eb-e0388b2d4378
Shea, SA
66ca5794-8481-4f4e-a5b3-8117841c8693
Scheer, FAJL, Chellappa, SL, Hu, K and Shea, SA
(2019)
Impact of mental stress, the circadian system and their interaction on human cardiovascular function.
Psychoneuroendocrinology, 103, .
(doi:10.1016/j.psyneuen.2019.01.016).
Abstract
The risk for adverse cardiovascular events (e.g., myocardial infarction, sudden cardiac death) peaks in the morning, possibly due to the effects of the endogenous circadian system on cardiovascular risk factors, or the occurrence in the morning of specific triggers, such as mental stress. To assess any interacting effects on cardiovascular function of mental stress and the circadian system, 12 healthy adults underwent a 240-h protocol with all measurements and behaviors scheduled evenly across the circadian cycle. Mental stress was repeatedly induced by performance-motivated serial addition tasks. Cardiovascular measures included hemodynamic function (heart rate, blood pressure), circulating catecholamines (epinephrine, norepinephrine), and estimates of sympathovagal balance and cardiac vagal modulation derived from heart rate variability analyses. Mental stress increased hemodynamic function, sympathovagal balance and epinephrine, and decreased cardiac vagal modulation. Endogenous circadian variation occurred in all cardiovascular measures: sympathovagal balance peaked in the circadian morning (∼9 AM), cardiac vagal modulation in the circadian night (∼4 AM), and heart rate and circulating catecholamines in the late circadian morning/early afternoon (∼12 PM). Importantly, the effects of mental stress and the endogenous circadian system on cardiovascular function occurred in conjunction, such that mental stress in the circadian morning caused greatest sympathovagal balance. This summation of effects could contribute to the increased morning cardiovascular vulnerability.
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e-pub ahead of print date: 22 January 2019
Published date: May 2019
Identifiers
Local EPrints ID: 479754
URI: http://eprints.soton.ac.uk/id/eprint/479754
ISSN: 0306-4530
PURE UUID: cdb1b75f-e268-4e64-8825-2e66ee72664f
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Date deposited: 26 Jul 2023 16:56
Last modified: 17 Mar 2024 04:20
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Author:
FAJL Scheer
Author:
SL Chellappa
Author:
K Hu
Author:
SA Shea
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