Angiotensin-converting enzyme genotype predicts cardiac and autonomic responses to prolonged exercise.
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.
Ashley
Euan A
EA
Division of Cardiology, Stanford University, Stanford, California 94305, USA. euan@stanford.edu
Kardos
Attila
A
Jack
Ewan S
ES
Habenbacher
Walter
W
Wheeler
Mathew
M
Kim
Young M
YM
Froning
Jeffrey
J
Myers
Jonathan
J
Whyte
Gregory
G
Froelicher
Victor
V
Douglas
Pamela
P
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
D015415:Biomarkers; D007703:Peptidyl-Dipeptidase A