Document Detail

Exercise training corrects control of spontaneous calcium waves in hearts from myocardial infarction heart failure rats.
MedLine Citation:
PMID:  21465470     Owner:  NLM     Status:  MEDLINE    
Impaired cardiac control of intracellular diastolic Ca(2+) gives rise to arrhythmias. Whereas exercise training corrects abnormal cyclic Ca(2+) handling in heart failure, the effect on diastolic Ca(2+) remains unstudied. Here, we studied the effect of exercise training on the generation and propagation of spontaneous diastolic Ca(2+) waves in failing cardiomyocytes. Post-myocardial infarction heart failure was induced in Sprague-Dawley rats by coronary artery ligation. Echocardiography confirmed left ventricular infarctions of 40 ± 5%, whereas heart failure was indicated by increased left ventricular end-diastolic pressures, decreased contraction-relaxation rates, and pathological hypertrophy. Spontaneous Ca(2+) waves were imaged by laser linescanning confocal microscopy (488 nm excitation/505-530 nm emission) in 2 µM Fluo-3-loaded cardiomyocytes at 37°C and extracellular Ca(2+) of 1.2 and 5.0 mM. These studies showed that spontaneous Ca(2+) wave frequency was higher at 5.0 mM than 1.2 mM extracellular Ca(2+) in all rats, but failing cardiomyocytes generated 50% (P < 0.01) more waves compared to sham-operated controls at Ca(2+) 1.2 and 5.0 mM. Exercise training reduced the frequency of spontaneous waves at both 1.2 and 5.0 mM Ca(2+) (P < 0.05), although complete normalization was not achieved. Exercise training also increased the aborted/completed ratio of waves at 1.2 mM Ca(2+) (P < 0.01), but not 5.0 mM. Finally, we repeated these studies after inhibiting the nitric oxide synthase with L-NAME. No differential effects were found; thus, mediation did not involve the nitric oxide synthase. In conclusion, exercise training improved the cardiomyocyte control of diastolic Ca(2+) by reducing the Ca(2+) wave frequency and by improving the ability to abort spontaneous Ca(2+) waves after their generation, but before cell-wide propagation.
Ole J Kemi; Niall MacQuaide; Morten A Hoydal; Oyvind Ellingsen; Godfrey L Smith; Ulrik Wisloff
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  227     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2011-10-25     Completed Date:  2011-12-08     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  20-6     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Wiley Periodicals, Inc.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Calcium / metabolism*
Heart / physiopathology
Heart Failure / metabolism,  physiopathology,  rehabilitation
Microscopy, Confocal
Myocardial Infarction / metabolism,  physiopathology,  rehabilitation*
Myocytes, Cardiac / metabolism*
Physical Conditioning, Animal / physiology*
Rats, Sprague-Dawley
Grant Support
PG/09/107/28154//British Heart Foundation; //British Heart Foundation
Reg. No./Substance:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Cementum protein 1 (CEMP1) induces a cementoblastic phenotype and reduces osteoblastic differentiati...
Next Document:  Nuclear gamma-tubulin associates with nucleoli and interacts with tumor suppressor protein C53.