Exercise training improves muscle vasodilatation in individuals with T786C polymorphism of endothelial nitric oxide synthase gene


Autoria(s): Negrão, Marcelo V.; Alves, Cleber R.; Alves, Guilherme B.; Pereira, Alexandre C.; Dias, Rodrigo G.; Laterza, Mateus C.; Mota, Gloria F.; Oliveira, Edilamar Menezes; Bassaneze, Vinicius; Krieger, Jose E.; Negrão, C. E.; Rondon, Maria Urbana Pinto Brandão
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

18/10/2012

18/10/2012

2010

Resumo

Negrão M.V, Alves CR, Alves G.B, Pereira A.C, Dias R.G, Laterza M.C, Mota G.F, Oliveira E.M, Bassaneze V, Krieger J.E, Negrão C.E, Rondon M.U.P. Exercise training improves muscle vasodilatation in individuals with T786C polymorphism of endothelial nitric oxide synthase gene. Physiol Genomics 42A: 71-77, 2010. First published July 6, 2010; doi:10.1152/physiolgenomics.00145.2009.-Allele T at promoter region of the eNOS gene has been associated with an increase in coronary disease mortality, suggesting that this allele increases susceptibility for endothelial dysfunction. In contrast, exercise training improves endothelial function. Thus, we hypothesized that: 1) Muscle vasodilatation during exercise is attenuated in individuals homozygous for allele T, and 2) Exercise training improves muscle vasodilatation in response to exercise for TT genotype individuals. From 133 preselected healthy individuals genotyped for the T786C polymorphism, 72 participated in the study: TT (n = 37; age 27 +/- 1 yr) and CT + CC (n = 35; age 26 +/- 1 yr). Forearm blood flow (venous occlusion plethysmography) and blood pressure (oscillometric automatic cuff) were evaluated at rest and during 30% handgrip exercise. Exercise training consisted of three sessions per week for 18 wk, with intensity between anaerobic threshold and respiratory compensation point. Resting forearm vascular conductance (FVC, P = 0.17) and mean blood pressure (P = 0.70) were similar between groups. However, FVC responses during handgrip exercise were significantly lower in TT individuals compared with CT + CC individuals (0.39 +/- 0.12 vs. 1.08 +/- 0.27 units, P = 0.01). Exercise training significantly increased peak VO(2) in both groups, but resting FVC remained unchanged. This intervention significantly increased FVC response to handgrip exercise in TT individuals (P = 0.03), but not in CT + CC individuals (P = 0.49), leading to an equivalent FVC response between TT and CT + CC individuals (1.05 +/- 0.18 vs. 1.59 +/- 0.27 units, P = 0.27). In conclusion, exercise training improves muscle vasodilatation in response to exercise in TT genotype individuals, demonstrating that genetic variants influence the effects of interventions such as exercise training.

Fundação de Amparo a Pesquisa do Estado de São Paulo (FAPESP)[2005/59740-7]

Fundação de Amparo a Pesquisa do Estado de São Paulo (FAPESP)[2007/52784-4]

Fundação Zerbini

Conselho Nacional de Pesquisa (CNPq)[302146/2007-5]

Conselho Nacional de Pesquisa (CNPq)[303518/2008-1]

Identificador

PHYSIOLOGICAL GENOMICS, v.42A, n.1, p.71-77, 2010

1094-8341

http://producao.usp.br/handle/BDPI/17416

10.1152/physiolgenomics.00145.2009

http://dx.doi.org/10.1152/physiolgenomics.00145.2009

Idioma(s)

eng

Publicador

AMER PHYSIOLOGICAL SOC

Relação

Physiological Genomics

Direitos

restrictedAccess

Copyright AMER PHYSIOLOGICAL SOC

Palavras-Chave #genetics #CORONARY-ARTERY-DISEASE #REGULAR PHYSICAL-ACTIVITY #HEART-FAILURE #DEPENDENT RELAXATION #METABOREFLEX CONTROL #ANAEROBIC THRESHOLD #NEOINTIMA FORMATION #AEROBIC CAPACITY #PROGENITOR CELLS #SKELETAL-MUSCLE #Cell Biology #Genetics & Heredity #Physiology
Tipo

article

original article

publishedVersion