title: Angiotensin-converting enzyme genotype predicts cardiac and autonomic responses to prolonged exercise.
abstract: OBJECTIVE
  The purpose of this study was to investigate the phenomenon of left ventricular (LV) dysfunction after ultraendurance exercise.
  
  
  BACKGROUND
  Subclinical LV dysfunction in response to endurance exercise up to 24 h duration has been described, but its mechanism remains elusive.
  
  
  METHODS
  We tested 86 athletes before and after the Adrenalin Rush Adventure Race using echocardiography, impedance cardiography, and plasma immunoassay.
  
  
  RESULTS
  At baseline, athletes demonstrated physiology characteristic of extreme endurance training. After 90 to 120 h of almost-continuous exercise, LV systolic and diastolic function declined (fractional shortening before the race, 39.6 +/- 0.65%; after, 32.2 +/- 0.84%, p < 0.001; mitral inflow E-wave deceleration time before the race, 133 +/- 5 ms; after, 160 +/- 5 ms, n = 48, p < 0.001) without change in loading conditions as defined by LV end-diastolic dimension and total peripheral resistance estimated by thoracic impedance. There was a compensatory increase in heart rate (before, 55 +/- 1.3 beats/min; after, 59 +/- 1.5 beats/min, p = 0.05), which left cardiac output unchanged, as well as significant-but-subclinical increases in brain natriuretic peptide and troponin I. In addition, we found that athletes who were homozygous for the intron-16 insertion polymorphism of the angiotensin-converting enzyme (ACE) gene exhibited a significantly greater decrease in fractional shortening than athletes who were homozygous for the deletion allele. Heterozygotes showed an intermediate phenotype. In addition, the deletion group manifest an enhanced sympathovagal balance after the race, as evidenced by greater power in the low-frequency component of blood pressure variability.
  
  
  CONCLUSIONS
  The ACE genotype predicts the extent of reversible subclinical LV dysfunction after prolonged exercise and is associated with a differential postactivity augmentation of sympathetic nervous system function that may explain it.
authors.affiliation: Division of Cardiology, Stanford University, Stanford, California 94305, USA. euan@stanford.edu
authors.forename: Euan A
authors.initials: EA
authors.lastname: Ashley
authors.forename: Attila
authors.initials: A
authors.lastname: Kardos
authors.forename: Ewan S
authors.initials: ES
authors.lastname: Jack
authors.forename: Walter
authors.initials: W
authors.lastname: Habenbacher
authors.forename: Mathew
authors.initials: M
authors.lastname: Wheeler
authors.forename: Young M
authors.initials: YM
authors.lastname: Kim
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Froning
authors.forename: Jonathan
authors.initials: J
authors.lastname: Myers
authors.forename: Gregory
authors.initials: G
authors.lastname: Whyte
authors.forename: Victor
authors.initials: V
authors.lastname: Froelicher
authors.forename: Pamela
authors.initials: P
authors.lastname: Douglas
mesh_terms: D000328:Adult; D001341:Autonomic Nervous System / Q000502:physiology*; D015415:Biomarkers / Q000097:blood; D015444:Exercise / Q000502:physiology*; D005221:Fatigue / Q000209:etiology / Q000503:physiopathology; D005260:Female; D005838:Genotype; D006321:Heart / Q000502:physiology* / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010807:Physical Endurance; D011237:Predictive Value of Tests; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000235:genetics* / Q000503:physiopathology; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D007703:Peptidyl-Dipeptidase A