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      Effects of Angiotensin-Converting Enzyme Polymorphism on Aortic Elastic Parameters in Athletes

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          Abstract

          Background: Physiologic adaptations in an athlete’s heart include increased left and right ventricular chamber size, left ventricular wall thickness and mass. Angiotensin-converting enzyme (ACE) is a key enzyme in angiotensin II production causing cardiac hypertrophy. The cloning of the ACE gene has made it possible to identifya deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. Therefore, the ACE genes, which have been shown to be polymorphic, could be candidate genes for large-artery stiffness. Methods: 56 endurance athletes and 46 sedentary subjects were included in this study, and they underwent both complete echocardiographic examination, and analysis of ACE insertion (I) and deletion (D) allele frequencies in peripheral blood. The aortic diameter was recorded by M-mode echocardiography at a level 3 cm above the aortic valve. Aortic systolic diameter was measured at the time of full opening of the aortic valve, and diastolic diameter was measured at the peak of QRS. Aortic strain, stiffness index and distensibility were calculated. Results: Left ventricular mass index and left ventricular ejection fraction were significantly higher in athletes than controls (p < 0.001). The aortic distensibility index and strain were significantly greater in athletes compared with controls (respectively: 5.8 ± 2.7 vs. 4.7 ± 1.8 cm<sup>–2</sup> dyn<sup>–1</sup> 10<sup>–6</sup>, p = 0.017; 12.3 ± 2.4 vs. 9.3 ± 3.1, p < 0.001). The aortic stiffness index was significantly lower in athletes than in controls (4.8 ± 1.9 vs. 6.1 ± 2.1, p < 0.001). The aortic distensibility index and strain were statistically different in ACE DD vs. DI groups and DD vs. II groups of athletes. The aortic stiffness index was statistically different in ACE DD vs. II groups of athletes. Aortic parameters were similar according to ACE genotypes in controls. Conclusion: The results of this study indicate that aortic distensibility was increased by prolonged training in endurance athletes, particularly in those with the ACE II genotype. This effect represents an extracardiac adaptation to chronic prolonged training in athletes.

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          Most cited references 23

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          Two putative active centers in human angiotensin I-converting enzyme revealed by molecular cloning.

          The amino-terminal amino acid sequence and several internal peptide sequences of angiotensin I-converting enzyme (ACE; peptidyl-dipeptidase A, kininase II; EC 3.4.15.1) purified from human kidney were used to design oligonucleotide probes. The nucleotide sequence of ACE mRNA was determined by molecular cloning of the DNA complementary to the human vascular endothelial cell ACE mRNA. The complete amino acid sequence deduced from the cDNA contains 1306 residues, beginning with a signal peptide of 29 amino acids. A highly hydrophobic sequence located near the carboxyl-terminal extremity of the molecule most likely constitutes the anchor to the plasma membrane. The sequence of ACE reveals a high degree of internal homology between two large domains, suggesting that the molecule resulted from a gene duplication. Each of these two domains contains short amino acid sequences identical to those located around critical residues of the active site of other metallopeptidases (thermolysin, neutral endopeptidase, and collagenase) and therefore bears a putative active site. Since earlier experiments suggested that a single Zn atom was bound per molecule of ACE, only one of the two domains should be catalytically active. The results of genomic DNA analysis with the cDNA probe are consistent with the presence of a single gene for ACE in the haploid human genome. Whereas the ACE gene is transcribed as a 4.3-kilobase mRNA in vascular endothelial cells, a 3.0-kilobase transcript was detected in the testis, where a shorter form of ACE is synthesized.
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            Human gene for physical performance.

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              Elite endurance athletes and the ACE I allele--the role of genes in athletic performance.

              Genetic markers that might contribute to the making of an elite athlete have not been identified. Potential candidate genes might be found in the renin-angiotensin pathway, which plays a key role in the regulation of both cardiac and vascular physiology. In this study, DNA polymorphisms derived from the angiotensin converting enzyme (ACE), the angiotensin type 1 receptor (AT1) and the angiotensin type 2 receptor (AT2) were studied in 64 Australian national rowers. Compared with a normal population, the rowers had an excess of the ACE I allele (P<0.02) and the ACE II genotype (P=0.03). The ACE I allele is a genetic marker that might be associated with athletic excellence. It is proposed that the underlying mechanism relates to a healthier cardiovascular system.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2005
                September 2005
                15 September 2005
                : 104
                : 3
                : 113-119
                Affiliations
                Departments of aCardiology, bPhysiology, and cBiostatistics, Medical Faculty, Pamukkale University, Denizli, and dPamukkale University Research Center for Genetic Engineering and Biotechnology, Denizli, Turkey
                Article
                87243 Cardiology 2005;104:113–119
                10.1159/000087243
                16088128
                © 2005 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 2, Tables: 4, References: 56, Pages: 7
                Categories
                General Cardiology

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