Document Detail

Exercise-induced cardiac hypertrophy: a substrate for sudden death in athletes?
MedLine Citation:
PMID:  12955164     Owner:  NLM     Status:  MEDLINE    
Cardiac hypertrophy is a general term signifying an increase in cardiac mass in response to applied stress. In mild, early hypertrophy, cardiac myocyte contractile performance may be normal or enhanced, whereas in severe hypertrophy associated with cardiac failure, myocyte contraction is reduced in amplitude and increased in duration. In contrast to the varied contractile response, the duration of electrical excitation shows similar changes in both mild and severe hypertrophy. Action potential duration in mid-myocardial and sub-epicardial layers is increased, which is associated with ventricular arrhythmias (in a similar manner to the long QT syndromes from other causes), based on afterdepolarizations and enhanced automaticity. Single-cell studies following exercise training in animal models show that exercise-induced cardiac hypertrophy displays features similar to mild, compensated hypertrophy from other causes. Developed shortening of unloaded single cells is increased or unchanged, and developed force in single myocytes is enhanced. Action potential duration is increased, apart from in the sub-endocardial layer. As with mild hypertrophy from other causes, this will be pro-arrhythmic because of altered dispersion of repolarization and enhanced automaticity. Major abnormalities of the ECG in man include frequent and complex ventricular ectopy, ST segment changes and prolongation of repolarization. In this review a case is presented for regarding exercise-induced cardiac hypertrophy as being no different from mild cardiac hypertrophy resulting from other, pathological causes. The cellular electrophysiological changes are sufficient to account for many of the abnormalities of the ECG, including high-grade ventricular ectopy. Sudden death in trained athletes who have no evidence of specific heart disease may be a direct consequence of cardiac hypertrophy and altered repolarization.
G Hart
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Experimental physiology     Volume:  88     ISSN:  0958-0670     ISO Abbreviation:  Exp. Physiol.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-09-04     Completed Date:  2004-06-24     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  639-44     Citation Subset:  IM    
Department of Medicine, University Clinical Departments, The Duncan Building, Daulby Street, Liverpool L69 3GA, UK.
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MeSH Terms
Adaptation, Physiological
Cardiomegaly / etiology*,  physiopathology*
Death, Sudden, Cardiac / etiology*
Heart / physiopathology*
Heart Conduction System / physiopathology*
Physical Education and Training*

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

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