Document Detail

Angiotensin-converting enzyme genotype predicts cardiac and autonomic responses to prolonged exercise.
MedLine Citation:
PMID:  16875979     Owner:  NLM     Status:  MEDLINE    
OBJECTIVES: The purpose of this study was to investigate the phenomenon of left ventricular (LV) dysfunction after ultraendurance exercise. BACKGROUND: Subclinical LV dysfunction in response to endurance exercise up to 24 h duration has been described, but its mechanism remains elusive. METHODS: We tested 86 athletes before and after the Adrenalin Rush Adventure Race using echocardiography, impedance cardiography, and plasma immunoassay. RESULTS: At baseline, athletes demonstrated physiology characteristic of extreme endurance training. After 90 to 120 h of almost-continuous exercise, LV systolic and diastolic function declined (fractional shortening before the race, 39.6 +/- 0.65%; after, 32.2 +/- 0.84%, p < 0.001; mitral inflow E-wave deceleration time before the race, 133 +/- 5 ms; after, 160 +/- 5 ms, n = 48, p < 0.001) without change in loading conditions as defined by LV end-diastolic dimension and total peripheral resistance estimated by thoracic impedance. There was a compensatory increase in heart rate (before, 55 +/- 1.3 beats/min; after, 59 +/- 1.5 beats/min, p = 0.05), which left cardiac output unchanged, as well as significant-but-subclinical increases in brain natriuretic peptide and troponin I. In addition, we found that athletes who were homozygous for the intron-16 insertion polymorphism of the angiotensin-converting enzyme (ACE) gene exhibited a significantly greater decrease in fractional shortening than athletes who were homozygous for the deletion allele. Heterozygotes showed an intermediate phenotype. In addition, the deletion group manifest an enhanced sympathovagal balance after the race, as evidenced by greater power in the low-frequency component of blood pressure variability. CONCLUSIONS: The ACE genotype predicts the extent of reversible subclinical LV dysfunction after prolonged exercise and is associated with a differential postactivity augmentation of sympathetic nervous system function that may explain it.
Euan A Ashley; Attila Kardos; Ewan S Jack; Walter Habenbacher; Mathew Wheeler; Young M Kim; Jeffrey Froning; Jonathan Myers; Gregory Whyte; Victor Froelicher; Pamela Douglas
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Publication Detail:
Type:  Journal Article     Date:  2006-07-12
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  48     ISSN:  1558-3597     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-07-31     Completed Date:  2006-08-16     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  523-31     Citation Subset:  AIM; IM    
Division of Cardiology, Stanford University, Stanford, California 94305, USA.
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MeSH Terms
Autonomic Nervous System / physiology*
Biological Markers / blood
Exercise / physiology*
Fatigue / etiology,  physiopathology
Heart / physiology*,  physiopathology
Peptidyl-Dipeptidase A / genetics*
Physical Endurance*
Predictive Value of Tests
Time Factors
Ventricular Dysfunction, Left / etiology*,  genetics*,  physiopathology
Ventricular Function, Left
Reg. No./Substance:
0/Biological Markers; EC A

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

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