title: Differential response to resistance training in CHF according to ACE genotype.
abstract: BACKGROUND
  The Angiotensin Converting Enzyme (ACE) gene may influence the risk of heart disease and the response to various forms of exercise training may be at least partly dependent on the ACE genotype. We aimed to determine the effect of ACE genotype on the response to moderate intensity circuit resistance training in chronic heart failure (CHF) patients.
  
  
  METHODS
  The relationship between ACE genotype and the response to 11weeks of resistance exercise training was determined in 37 CHF patients (New York Heart Association Functional Class=2.3±0.5; left ventricular ejection fraction 28±7%; age 64±12years; 32:5 male:female) who were randomised to either resistance exercise (n=19) or inactive control group (n=18). Outcome measures included V˙O(2peak), peak power output and muscle strength and endurance. ACE genotype was determined using standard methods.
  
  
  RESULTS
  At baseline, patients who were homozygous for the I allele had higher V˙O(2peak) (p=0.02) and peak power (p=0.003) compared to patients who were homozygous for the D allele. Patients with the D allele, who were randomised to resistance training, compared to non-exercising controls, had greater peak power increases (ID p<0.001; DD p<0.001) when compared with patients homozygous for the I allele, who did not improve. No significant genotype-dependent changes were observed in V˙O(2peak), muscle strength, muscle endurance or lactate threshold.
  
  
  CONCLUSIONS
  ACE genotype may have a role in exercise tolerance in CHF and could also influence the effectiveness of resistance training in this condition.
authors.affiliation: School of Human Life Sciences, University of Tasmania, Launceston, Australia. Andrew.Williams@utas.edu.au
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Williams
authors.forename: Mitchell J
authors.initials: MJ
authors.lastname: Anderson
authors.forename: Steve
authors.initials: S
authors.lastname: Selig
authors.forename: Michael F
authors.initials: MF
authors.lastname: Carey
authors.forename: Mark A
authors.initials: MA
authors.lastname: Febbraio
authors.forename: Alan
authors.initials: A
authors.lastname: Hayes
authors.forename: Deidre
authors.initials: D
authors.lastname: Toia
authors.forename: Stephen B
authors.initials: SB
authors.lastname: Harrap
authors.forename: David L
authors.initials: DL
authors.lastname: Hare
mesh_terms: D000368:Aged; D002908:Chronic Disease; D005260:Female; D005838:Genotype; D006333:Heart Failure / Q000235:genetics / Q000503:physiopathology / Q000534:rehabilitation; D006801:Humans; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption / Q000235:genetics; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010807:Physical Endurance / Q000235:genetics; D055070:Resistance Training / Q000379:methods*; D012720:Severity of Illness Index
chemical_list: C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A