title: Association of angiotensin-converting enzyme gene I/D polymorphism with change in left ventricular mass in response to physical training.
abstract: BACKGROUND
  The absence (deletion allele [D]) of a 287-base pair marker in the ACE gene is associated with higher ACE levels than its presence (insertion allele [I]). If renin-angiotensin systems regulate left ventricular (LV) growth, then individuals of DD genotype might show a greater hypertrophic response than those of II genotype. We tested this hypothesis by studying exercise-induced LV hypertrophy.
  
  
  RESULTS
  Echocardiographically determined LV dimensions and mass (n=140), electrocardiographically determined LV mass and frequency of LV hypertrophy (LVH) (n=121), and plasma brain natriuretic peptide (BNP) levels (n=49) were compared at the start and end of a 10-week physical training period in male Caucasian military recruits. Septal and posterior wall thicknesses increased with training, and LV mass increased by 18% (all P<.0001). Response magnitude was strongly associated with ACE genotype: mean LV mass altered by +2.0, +38.5, and +42.3 g in II, ID and DD, respectively (P<.0001). The prevalence of electrocardiographically defined LVH rose significantly only among those of DD genotype (from 6 of 24 before training to 11 of 24 after training, P<.01). Plasma brain natriuretic peptide levels rose by 56.0 and 11.5 pg/mL for DD and II, respectively (P<.001).
  
  
  CONCLUSIONS
  Exercise-induced LV growth in young males is strongly associated with the ACE I/D polymorphism.
authors.affiliation: The Hatter Institute for Cardiovascular Research University College, London Medical Schools, University College Hospital, UK.
authors.forename: H E
authors.initials: HE
authors.lastname: Montgomery
authors.forename: P
authors.initials: P
authors.lastname: Clarkson
authors.forename: C M
authors.initials: CM
authors.lastname: Dollery
authors.forename: K
authors.initials: K
authors.lastname: Prasad
authors.forename: M A
authors.initials: MA
authors.lastname: Losi
authors.forename: H
authors.initials: H
authors.lastname: Hemingway
authors.forename: D
authors.initials: D
authors.lastname: Statters
authors.forename: M
authors.initials: M
authors.lastname: Jubb
authors.forename: M
authors.initials: M
authors.lastname: Girvain
authors.forename: A
authors.initials: A
authors.lastname: Varnava
authors.forename: M
authors.initials: M
authors.lastname: World
authors.forename: J
authors.initials: J
authors.lastname: Deanfield
authors.forename: P
authors.initials: P
authors.lastname: Talmud
authors.forename: J R
authors.initials: JR
authors.lastname: McEwan
authors.forename: W J
authors.initials: WJ
authors.lastname: McKenna
authors.forename: S
authors.initials: S
authors.lastname: Humphries
mesh_terms: D000328:Adult; D000483:Alleles; D015331:Cohort Studies; D004452:Echocardiography; D004562:Electrocardiography; D005838:Genotype; D006352:Heart Ventricles; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology; D008297:Male; D008887:Military Medicine; D020097:Natriuretic Peptide, Brain; D009419:Nerve Tissue Proteins / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010806:Physical Education and Training; D011110:Polymorphism, Genetic
chemical_list: D009419:Nerve Tissue Proteins; D020097:Natriuretic Peptide, Brain; D007703:Peptidyl-Dipeptidase A