title: ACE and angiotensinogen gene genotypes and left ventricular mass in athletes.
abstract: BACKGROUND
  Genetic factors may be important in modifying heart size due to long-term athletic training. The significance of polymorphisms of genes of the renin-angiotensin system in myocardial mass in a population of athletes participating in different disciplines is not known.
  
  
  METHODS
  The angiotensin I-converting enzyme gene insertion/deletion (I/D) polymorphism, angiotensinogen gene M235T polymorphism and angiotensin II type 1 receptor gene A1166C polymorphism were determined in 83 male Caucasian endurance athletes and associated with left ventricular mass.
  
  
  RESULTS
  No association with left ventricular mass was found for the polymorphisms of angiotensin I-converting enzyme gene I/D, angiotensinogen gene M235T and angiotensin II type 1 gene A1166C when studied separately. However, combined analysis of the angiotensin I-converting enzyme gene I/D polymorphism and angiotensinogen gene M235T polymorphism genotypes suggested an association with left ventricular mass (g m(-2)) (P = 0.023). Athletes with the angiotensin I-converting enzyme gene DD/angiotensinogen gene TT genotype combination had greater left ventricular mass compared with all other genotype combinations (179.8 +/- 26.1 g m(-2) vs. 145.2 +/- 27.3 g m(-2), P = 0.003).
  
  
  CONCLUSIONS
  These results suggest an association of combined angiotensin I-converting enzyme gene I/D polymorphism genotypes, and angiotensinogen gene M235T polymorphism genotypes with left ventricular hypertrophy due to long-term athletic training. A synergistic effect of angiotensin I-converting enzyme gene DD genotype and angiotensinogen gene TT genotype on left ventricular mass in endurance athletes appears to occur.
authors.affiliation: Klinik für Innere Medizin III, Universität zu Köln, Joseph-Stelzmann-Strasse 9, 50924 Köln, Germany. f.diet@uni-koeln.de
authors.forename: F
authors.initials: F
authors.lastname: Diet
authors.forename: C
authors.initials: C
authors.lastname: Graf
authors.forename: N
authors.initials: N
authors.lastname: Mahnke
authors.forename: G
authors.initials: G
authors.lastname: Wassmer
authors.forename: H G
authors.initials: HG
authors.lastname: Predel
authors.forename: I
authors.initials: I
authors.lastname: Palma-Hohmann
authors.forename: R
authors.initials: R
authors.lastname: Rost
authors.forename: M
authors.initials: M
authors.lastname: Böhm
mesh_terms: D000293:Adolescent; D000328:Adult; D000808:Angiotensinogen / Q000235:genetics*; D004452:Echocardiography; D005838:Genotype; D006321:Heart / Q000033:anatomy & histology*; D006352:Heart Ventricles / Q000033:anatomy & histology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010807:Physical Endurance / Q000235:genetics / Q000502:physiology; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000235:genetics; D012084:Renin-Angiotensin System / Q000235:genetics / Q000502:physiology; D013177:Sports / Q000502:physiology*
chemical_list: D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A