title: Influence of angiotensinogen and angiotensin-converting enzyme polymorphisms on cardiac hypertrophy and improvement on maximal aerobic capacity caused by exercise training.
abstract: BACKGROUND
  The allele threonine (T) of the angiotensinogen has been associated with ventricular hypertrophy in hypertensive patients and soccer players. However, the long-term effect of physical exercise in healthy athletes carrying the T allele remains unknown. We investigated the influence of methionine (M) or T allele of the angiotensinogen and D or I allele of the angiotensin-converting enzyme on left-ventricular mass index (LVMI) and maximal aerobic capacity in young healthy individuals after long-term physical exercise training.
  
  
  METHODS
  Prospective clinical trial.
  
  
  METHODS
  Eighty-three policemen aged between 20 and 35 years (mean+/-SD 26+/-4.5 years) were genotyped for the M235T gene angiotensinogen polymorphism (TT, n = 25; MM/MT, n = 58) and angiotensin-converting enzyme gene insertion/deletion (I/D) polymorphism (II, n = 18; DD/DI, n = 65). Left-ventricular morphology was evaluated by echocardiography and maximal aerobic capacity (VO2peak) by cardiopulmonary exercise test before and after 17 weeks of exercise training (50-80% VO2peak).
  
  
  RESULTS
  Baseline VO2peak and LVMI were similar between TT and MM/MT groups, and II and DD/DI groups. Exercise training increased significantly and similarly VO2peak in homozygous TT and MM/MT individuals, and homozygous II and DD/DI individuals. In addition, exercise training increased significantly LVMI in TT and MM/MT individuals (76.5+/-3 vs. 86.7+/-4, P = 0.00001 and 76.2+/-2 vs. 81.4+/-2, P = 0.00001, respectively), and II and DD/DI individuals (77.7+/-4 vs. 81.5+/-4, P = 0.0001 and 76+/-2 vs. 83.5+/-2, P = 0.0001, respectively). However, LVMI in TT individuals was significantly greater than in MM/MT individuals (P = 0.04). LVMI was not different between II and DD/DI individuals.
  
  
  CONCLUSIONS
  Left-ventricular hypertrophy caused by exercise training is exacerbated in homozygous TT individuals with angiotensinogen polymorphism.
authors.affiliation: Heart Institute (InCor), University of São Paulo, São Paulo, Brazil. gui_barreto@uol.com.br
authors.forename: Guilherme B
authors.initials: GB
authors.lastname: Alves
authors.forename: Edilamar M
authors.initials: EM
authors.lastname: Oliveira
authors.forename: Cleber R
authors.initials: CR
authors.lastname: Alves
authors.forename: Heron R S
authors.initials: HR
authors.lastname: Rached
authors.forename: Glória F A
authors.initials: GF
authors.lastname: Mota
authors.forename: Alexandre C
authors.initials: AC
authors.lastname: Pereira
authors.forename: Maria U
authors.initials: MU
authors.lastname: Rondon
authors.forename: Nara Y
authors.initials: NY
authors.lastname: Hashimoto
authors.forename: Luciene F
authors.initials: LF
authors.lastname: Azevedo
authors.forename: José Eduardo
authors.initials: JE
authors.lastname: Krieger
authors.forename: Carlos Eduardo
authors.initials: CE
authors.lastname: Negrão
mesh_terms: D000328:Adult; D000483:Alleles; D000704:Analysis of Variance; D000808:Angiotensinogen / Q000235:genetics*; D001938:Brazil; D005080:Exercise Test; D005081:Exercise Therapy / Q000379:methods*; D005838:Genotype; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000235:genetics* / Q000503:physiopathology / Q000534:rehabilitation*; D008297:Male; D010101:Oxygen Consumption / Q000502:physiology; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D016896:Treatment Outcome
chemical_list: D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A