Related Experiment Videos
RAS genes influence exercise-induced left ventricular hypertrophy: an elite athletes study
C Fatini1, R Guazzelli, P Manetti
1Unità di Genetica Medica Dpt. Fisiopatol Clinica, Centro Medicina dello Sport, Università di Firenze, Florence, Italy.
Medicine and Science in Sports and Exercise
|November 18, 2000
Summary
Elite athletes
Area of Science:
- Cardiovascular Genetics
- Sports Science
- Molecular Biology
Background:
- The angiotensin-converting enzyme (ACE) I/D polymorphism and the angiotensin II type 1 receptor (AT1R) A1166C polymorphism are studied for their influence on cardiovascular adaptations.
- Previous research indicated an association between ACE I/D polymorphism and left ventricular (LV) mass changes in response to training, but not for AT1R A1166C polymorphism.
Purpose of the Study:
- To investigate the genotype distribution of ACE I/D, AT1R A1166C, and AT1R CA microsatellite polymorphisms in elite athletes.
- To determine if the AT1R C1166 variant, alongside the ACE D allele, influences training-induced LV mass alterations in elite trained athletes.
Main Methods:
- Echocardiography was used to assess LV mass and dimensions in 28 elite male soccer players and 155 healthy male controls.
- Measurements were taken before and after a 7-month training period.
- Genotyping was performed for ACE I/D, AT1R A1166C, and AT1R CA microsatellite polymorphisms.
Main Results:
- Training increased LV mass in most athletes. The ACE D allele was significantly associated with altered LV mass response to training (P = 0.02).
- No significant association was found between AT1R C allele carriers and LV mass changes (P > 0.05).
- The combined presence of ACE D and AT1R C alleles did not impact training-induced LV mass alterations. No differences in CA microsatellite marker frequencies were observed between athletes and controls.
Conclusions:
- Soccer participation does not appear to select athletes based on these specific genotypes.
- Training-induced changes in LV mass among elite male athletes are significantly linked to the ACE D allele, but not the AT1R C allele.