Document Detail


Endurance exercise training normalizes repolarization and calcium-handling abnormalities, preventing ventricular fibrillation in a model of sudden cardiac death.
MedLine Citation:
PMID:  23042911     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The risk of sudden cardiac death is increased following myocardial infarction. Exercise training reduces arrhythmia susceptibility, but the mechanism is unknown. We used a canine model of sudden cardiac death (healed infarction, with ventricular tachyarrhythmias induced by an exercise plus ischemia test, VF+); we previously reported that endurance exercise training was antiarrhythmic in this model (Billman GE. Am J Physiol Heart Circ Physiol 297: H1171-H1193, 2009). A total of 41 VF+ animals were studied, after random assignment to 10 wk of endurance exercise training (EET; n = 21) or a matched sedentary period (n = 20). Following (>1 wk) the final attempted arrhythmia induction, isolated myocytes were used to test the hypotheses that the endurance exercise-induced antiarrhythmic effects resulted from normalization of cellular electrophysiology and/or normalization of calcium handling. EET prevented VF and shortened in vivo repolarization (P < 0.05). EET normalized action potential duration and variability compared with the sedentary group. EET resulted in a further decrement in transient outward current compared with the sedentary VF+ group (P < 0.05). Sedentary VF+ dogs had a significant reduction in repolarizing K(+) current, which was restored by exercise training (P < 0.05). Compared with controls, myocytes from the sedentary VF+ group displayed calcium alternans, increased calcium spark frequency, and increased phosphorylation of S2814 on ryanodine receptor 2. These abnormalities in intracellular calcium handling were attenuated by exercise training (P < 0.05). Exercise training prevented ischemically induced VF, in association with a combination of beneficial effects on cellular electrophysiology and calcium handling.
Authors:
Ingrid M Bonilla; Andriy E Belevych; Arun Sridhar; Yoshinori Nishijima; Hsiang-Ting Ho; Quanhua He; Monica Kukielka; Dmitry Terentyev; Radmila Terentyeva; Bin Liu; Victor P Long; Sandor Györke; Cynthia A Carnes; George E Billman
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-10-04
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  113     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-03     Completed Date:  2013-05-29     Revised Date:  2013-12-04    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1772-83     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Action Potentials
Animals
Calcium Signaling*
Death, Sudden, Cardiac / etiology,  prevention & control*
Disease Models, Animal
Dogs
Electrocardiography
Exercise Therapy*
Heart Rate
Myocardial Infarction / complications
Myocytes, Cardiac / metabolism*
Patch-Clamp Techniques
Phosphorylation
Physical Endurance*
Potassium / metabolism
Potassium Channels / metabolism
Ryanodine Receptor Calcium Release Channel / metabolism
Time Factors
Ventricular Fibrillation / diagnosis,  etiology,  metabolism,  physiopathology,  prevention & control*
Grant Support
ID/Acronym/Agency:
HL063043/HL/NHLBI NIH HHS; HL086700/HL/NHLBI NIH HHS; HL089836/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Potassium Channels; 0/Ryanodine Receptor Calcium Release Channel; RWP5GA015D/Potassium
Comments/Corrections

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