| Effects of prolonged exercise on left ventricular mechanical synchrony in long-distance runners: importance of previous exposure to endurance races. | |
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MedLine Citation:
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PMID: 20688470 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Prolonged exercise has been shown to lead to elevated levels of cardiac troponin and altered cardiac function on echocardiography. It is not known if cardiac synchrony is altered by prolonged exercise. The aims of this study were to assess changes in intra-left ventricular mechanical synchrony and circulating levels of cardiac troponin following prolonged exercise and to evaluate the importance of prior exposure to endurance racing. METHODS: Forty-three male participants in a 30-km cross-country race (20 new participants at this event [median, 3 previous endurance races] age matched against 23 repeat participants [median, 31 previous endurance events]) were assessed prospectively 1 to 2 days before and 24 hours after the race using troponin T and Doppler tissue imaging analyzing the standard deviation of time to peak myocardial systolic velocity (T(s)-SD) in a six-basal, six-midventricular segment model measuring myocardial synchrony. The insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene was also analyzed, as I allele carriers reportedly have superior endurance performance, while the D allele predisposes to renin-angiotensin system-induced cardiac remodeling. RESULTS: Prerace troponin T was undetectable in all runners, and postrace levels were higher in new runners (median, 0.03 microg/L; interquartile range [IQR], 0.01-0.04 microg/L) than in repeat runners (median, 0.01 microg/L; IQR, 0.01-0.02 microg/L) (P = .03). Although new and repeat runners had similar T(s)-SD at baseline (32 msec [IQR, 22-43 msec] vs 34 msec [IQR, 29-45 msec], P = .13), dyssynchrony increased only in new runners (40 msec [IQR, 31-47 msec], P < .001; in repeat runners, median, 38 msec [IQR, 29-43 msec], P = .30; median relative difference, +13% vs +5%, P = .02). ACE genotype distribution was similar in both groups. Multivariate analysis showed that (1) a lack of prior endurance exposure; (2) more copies of the ACE D allele; and (3) lower peak systolic velocity were independent predictors of postrace dyssynchrony (P < .05 for all). CONCLUSION: Prolonged exertion increased ventricular mechanical dyssynchrony in new endurance participants and in ACE D allele carriers. The long-term impact of such changes warrants future study. |
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Authors:
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Anders Sahlén; Kambiz Shahgaldi; Anna Aminoff; Philip Aagaard; Aristomenis Manouras; Reidar Winter; Ewa Ehrenborg; Frieder Braunschweig |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-08-05 |
Journal Detail:
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Title: Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography Volume: 23 ISSN: 1097-6795 ISO Abbreviation: J Am Soc Echocardiogr Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-08-27 Completed Date: 2011-01-11 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8801388 Medline TA: J Am Soc Echocardiogr Country: United States |
Other Details:
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Languages: eng Pagination: 977-84 Citation Subset: IM |
Copyright Information:
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2010 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved. |
Affiliation:
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Karolinska Institutet, Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden. anders.sahlen@karolinska.se |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Alleles Analysis of Variance Biological Markers / blood Echocardiography, Doppler* Heart Conduction System / physiology* Humans Linear Models Male Middle Aged Peptidyl-Dipeptidase A / genetics Polymorphism, Genetic Renin-Angiotensin System / genetics Running / physiology* Statistics, Nonparametric Troponin / blood Ventricular Function, Left / physiology* Ventricular Remodeling / genetics |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Troponin; EC 3.4.15.1/Peptidyl-Dipeptidase A |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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