Exercise-induced expression of cardiac ATP-sensitive potassium channels promotes action potential shortening and energy conservation

Leonid V Zingman; Zhiyong Zhu; Ana Sierra; Elizabeth Stepniak; Colin M-L Burnett; Gennadiy Maksymov; Mark E Anderson; William A Coetzee; Denice M Hodgson-Zingman

doi:10.1016/j.yjmcc.2011.03.010

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Exercise-induced expression of cardiac ATP-sensitive potassium channels promotes action potential shortening and energy conservation

Journal article

Peer reviewed

Exercise-induced expression of cardiac ATP-sensitive potassium channels promotes action potential shortening and energy conservation

Leonid V Zingman, Zhiyong Zhu, Ana Sierra, Elizabeth Stepniak, Colin M-L Burnett, Gennadiy Maksymov, Mark E Anderson, William A Coetzee and Denice M Hodgson-Zingman

Journal of molecular and cellular cardiology, Vol.51(1), pp.72-81

07/2011

DOI: 10.1016/j.yjmcc.2011.03.010

PMCID: PMC3103621

PMID: 21439969

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https://www.ncbi.nlm.nih.gov/pmc/articles/3103621View

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Abstract

Physical activity is one of the most important determinants of cardiac function. The ability of the heart to increase delivery of oxygen and metabolic fuels relies on an array of adaptive responses necessary to match bodily demand while avoiding exhaustion of cardiac resources. The ATP-sensitive potassium (K ATP ) channel has the unique ability to adjust cardiac membrane excitability in accordance with ATP and ADP levels, and up-regulation of its expression that occurs in response to exercise could represent a critical element of this adaption. However, the mechanism by which K ATP channel expression changes result in a beneficial effect on cardiac excitability and function remains to be established. Here, we demonstrate that an exercise-induced rise in K ATP channel expression enhanced the rate and magnitude of action potential shortening in response to heart rate acceleration. This adaptation in membrane excitability promoted significant reduction in cardiac energy consumption under escalating workloads. Genetic disruption of normal K ATP channel pore function abolished the exercise-related changes in action potential duration adjustment and caused increased cardiac energy consumption. Thus, an expression-driven enhancement in the K ATP channel-dependent membrane response to alterations in cardiac workload represents a previously unrecognized mechanism for adaptation to physical activity and a potential target for cardioprotection.

KATP

exercise

remodeling

heart rate

oxygen consumption

K-ATP

Details

Title: Subtitle: Exercise-induced expression of cardiac ATP-sensitive potassium channels promotes action potential shortening and energy conservation
Creators: Leonid V Zingman - Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA
Zhiyong Zhu - Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA
Ana Sierra - Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA
Elizabeth Stepniak - Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA
Colin M-L Burnett - Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA
Gennadiy Maksymov - Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA
Mark E Anderson - Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA
William A Coetzee - Department of Pediatrics, NYU School of Medicine, New York, New York 10016, USA
Denice M Hodgson-Zingman - Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA
Resource Type: Journal article
Publication Details: Journal of molecular and cellular cardiology, Vol.51(1), pp.72-81
DOI: 10.1016/j.yjmcc.2011.03.010
PMID: 21439969
PMCID: PMC3103621
NLM abbreviation: J Mol Cell Cardiol
ISSN: 0022-2828
eISSN: 1095-8584
Grant note: K08 HL093368-04 || HL / National Heart, Lung, and Blood Institute : NHLBI L30 HL085940-03 || HL / National Heart, Lung, and Blood Institute : NHLBI K08 HL092286-05 || HL / National Heart, Lung, and Blood Institute : NHLBI R01 HL085820-04 || HL / National Heart, Lung, and Blood Institute : NHLBI
Language: English
Date published: 07/2011
Academic Unit: Roy J. Carver Department of Biomedical Engineering; Cardiovascular Medicine; Internal Medicine
Record Identifier: 9984094367302771

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