title: High plasmatic angiotensin-converting enzyme (ACE) activity is not correlated with training-induced left ventricular growth in ACE congenic rats.
abstract: OBJECTIVE
  The aim of this study was to determine the influence of angiotensin-converting enzyme (ACE) genotype on left ventricular growth after endurance training, in ACE congenic rats with plasma ACE activity twice as high as the donor strain (LOU), thus mimicking the ACE I/D polymorphism observed in humans.
  
  
  METHODS
  LOU and congenic rats (n = 12) were submitted to an endurance training on a treadmill for 7 weeks, while similar LOU and congenic rats (n = 10) constituted the control groups. Blood pressure, skeletal muscle citrate synthase activity, plasma and left ventricular ACE activity were assessed, and echocardiography was performed before and after the training.
  
  
  RESULTS
  Angiotensin-converting enzyme plasmatic activity of congenic rats (188.2 +/- 26.6 in controls and 187.1 +/- 22.6 IU in trained rats respectively) was twofold that of the LOU strain (91.9 +/- 23.3 in controls, and 88.3 +/- 18.1 IU in trained rats respectively). After training, congenic and LOU rats showed a similar significant increase in citrate synthase activity (P < 0.05), and in the left ventricular mass/body mass ratio x 10(3): 3.7 +/- 0.3 and 3.6 +/- 0.6 in the trained congenic and LOU groups, respectively, vs. 3.0 +/- 0.1 and 2.9 +/- 0.2 in the control congenic and LOU groups respectively (P < 0.05). There was no significant correlation between ACE plasma activity and left ventricular mass in trained or untrained congenic rats.
  
  
  CONCLUSIONS
  We conclude that training-induced left ventricular growth is not associated with plasma ACE activity in congenic rats.
authors.affiliation: Physiology of Cardiovascular Incoherencies, EA 2992, Montpellier 1 University, Montpellier, France. s.zalvide@montp.inserm.fr
authors.forename: S
authors.initials: S
authors.lastname: Zalvidea
authors.forename: G
authors.initials: G
authors.lastname: Py
authors.forename: K
authors.initials: K
authors.lastname: Lambert
authors.forename: B
authors.initials: B
authors.lastname: Jover
authors.forename: M
authors.initials: M
authors.lastname: Dauzat
authors.forename: D
authors.initials: D
authors.lastname: Le Gallais
mesh_terms: D000818:Animals; D001835:Body Weight; D002950:Citrate (si)-Synthase / Q000378:metabolism; D004195:Disease Models, Animal; D005838:Genotype; D006352:Heart Ventricles / Q000201:enzymology / Q000254:growth & development / Q000473:pathology; D006824:Hybridization, Genetic; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology; D009043:Motor Activity / Q000502:physiology; D009929:Organ Size; D007703:Peptidyl-Dipeptidase A / Q000097:blood* / Q000235:genetics / Q000502:physiology; D010807:Physical Endurance / Q000502:physiology*; D011110:Polymorphism, Genetic; D051381:Rats; D014463:Ultrasonography
chemical_list: D002950:Citrate (si)-Synthase; D007703:Peptidyl-Dipeptidase A