Endothelial Nitric Oxide Synthase Polymorphisms and Adaptation of Parasympathetic Modulation to Exercise Training

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dc.contributor Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.author SILVA, Bruno M.
NEVES, Fabricia J.
NEGRAO, Marcelo V. FMUSP-HC
ALVES, Cleber R. FMUSP-HC
DIAS, Rodrigo G. FMUSP-HC
ALVES, Guilherme B.
PEREIRA, Alexandre C. FMUSP-HC
RONDON, Maria U. FMUSP-HC
KRIEGER, Jose E. FMUSP-HC
NEGRAO, Carlos E. FMUSP-HC
NOBREGA, Antonio Claudio Lucas da
dc.date.issued 2011
dc.identifier.citation MEDICINE AND SCIENCE IN SPORTS AND EXERCISE, v.43, n.9, p.1611-1618, 2011
dc.identifier.issn 0195-9131
dc.identifier.uri http://observatorio.fm.usp.br/handle/OPI/22810
dc.description.abstract SILVA, B. M., F. J. NEVES, M. V. NEGRAO, C. R. ALVES, R. G. DIAS, G. B. ALVES, A. C. PEREIRA, M. U. RONDON, J. E. KRIEGER, C. E. NEGRAO, and A. C. DA NOBREGA. Endothelial Nitric Oxide Synthase Polymorphisms and Adaptation of Parasympathetic Modulation to Exercise Training. Med. Sci. Sports Exerc., Vol. 43, No. 9, pp. 1611-1618, 2011. Purpose: There is a large interindividual variation in the parasympathetic adaptation induced by aerobic exercise training, which may be partially attributed to genetic polymorphisms. Therefore, we investigated the association among three polymorphisms in the endothelial nitric oxide gene (-786T>C, 4b4a, and 894G>T), analyzed individually and as haplotypes, and the parasympathetic adaptation induced by exercise training. Methods: Eighty healthy males, age 20-35 yr, were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis, and haplotypes were inferred using the software PHASE 2.1. Autonomic modulation (i.e., HR variability and spontaneous baroreflex sensitivity) and peak oxygen consumption ((V) over dotO(2peak)) were measured before and after training (running, moderate to severe intensity, three times per week, 60 min.day(-1), during 18 wk). Results: Training increased (V) over dotO(2peak) (P < 0.05) and decreased mean arterial pressure (P < 0.05) in the whole sample. Subjects with the -786C polymorphic allele had a significant reduction in baroreflex sensitivity after training (change: wild type (-786TT) = 2% +/- 89% vs polymorphic (-786TC/CC) = -28% +/- 60%, median +/- quartile range, P = 0.03), and parasympathetic modulation was marginally reduced in subjects with the 894T polymorphic allele (change: wild type (894GG) = 8% +/- 67% vs polymorphic (894GT/TT) = -18% +/- 59%, median +/- quartile range, P = 0.06). Furthermore, parasympathetic modulation percent change was different between the haplotypes containing wild-type alleles(-786T/4b/894G) and polymorphic alleles at positions -786 and 894 (-786C/4b/894T) (-6% +/- 56% vs -41% +/- 50%, median T quartile range, P = 0.04). Conclusions: The polymorphic allele at position -786 and the haplotype containing polymorphic alleles at positions -786 and 894 in the endothelial nitric oxide gene were associated with decreased parasympathetic modulation after exercise training.
dc.description.sponsorship · Sao Paulo Research Foundation (FAPESP) [2005/59740-7, 2007/52784-4]
· CNPq [474621/2004-9]
· Fundacao Zerbini
· Coordination for the Improvement of Higher Education Personnel (CAPES) [0723-09-6, 2690/09-8]
· Brazilian National Council of Scientific and Technological Development (CNPq) [307251/2009-8, 303518/2008-1, 302146/2007-5]
· Foundation of Research Support of Rio de Janeiro State (FAPERJ) [E-26/102.378/2009]
dc.language.iso eng
dc.publisher LIPPINCOTT WILLIAMS & WILKINS
dc.relation.ispartof Medicine and Science in Sports and Exercise
dc.rights restrictedAccess
dc.subject GENETIC VARIATION; NOS3; AUTONOMIC NERVOUS SYSTEM; PHYSICAL TRAINING
dc.subject.other heart-rate-variability; coronary-artery-disease; baroreflex sensitivity; myocardial-infarction; gene haplotypes; blood-pressure; muscle vasodilatation; healthy-men; enos gene; genotype
dc.title Endothelial Nitric Oxide Synthase Polymorphisms and Adaptation of Parasympathetic Modulation to Exercise Training
dc.type article
dc.rights.holder Copyright LIPPINCOTT WILLIAMS & WILKINS
dc.description.group LIM/13
dc.identifier.doi 10.1249/MSS.0b013e3182152197
dc.identifier.pmid 21364486
dc.type.category original article
dc.type.version publishedVersion
hcfmusp.author NEGRAO, Marcelo V.:FM:
hcfmusp.author ALVES, Cleber R.:FM:
hcfmusp.author DIAS, Rodrigo G.:HC:LIM/13
hcfmusp.author PEREIRA, Alexandre C.:HC:INCOR
hcfmusp.author RONDON, Maria U.:HC:INCOR
hcfmusp.author KRIEGER, Jose E.:FM:MCP
hcfmusp.author NEGRAO, Carlos E.:HC:INCOR
hcfmusp.author.external · SILVA, Bruno M.:Univ Fed Fluminense, Dept Physiol & Pharmacol, Niteroi, RJ, Brazil; Univ Fed Fluminense, Grad Program Cardiovasc Sci, Niteroi, RJ, Brazil; Univ Estado Rio De Janeiro, Grad Program Clin & Expt Pathophysiol, Rio De Janeiro, Brazil
· NEVES, Fabricia J.:Univ Fed Fluminense, Dept Physiol & Pharmacol, Niteroi, RJ, Brazil; Univ Fed Fluminense, Grad Program Cardiovasc Sci, Niteroi, RJ, Brazil
· ALVES, Guilherme B.:Univ Sao Paulo, Sch Med, Heart Inst InCor, Sao Paulo, Brazil
· NOBREGA, Antonio Claudio Lucas da:Univ Fed Fluminense, Dept Physiol & Pharmacol, Niteroi, RJ, Brazil; Univ Fed Fluminense, Grad Program Cardiovasc Sci, Niteroi, RJ, Brazil; Univ Estado Rio De Janeiro, Grad Program Clin & Expt Pathophysiol, Rio De Janeiro, Brazil
hcfmusp.origem.id 2-s2.0-79952081886
hcfmusp.origem.id WOS:000293951800002
hcfmusp.publisher.city PHILADELPHIA
hcfmusp.publisher.country USA
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dc.description.index MEDLINE
hcfmusp.citation.scopus 9
hcfmusp.citation.wos 9
hcfmusp.affiliation.country Brasil


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