Purpose: The association of ACE IID polymorphism with changes in LV mass in
response to physical training has been observed, but no association has be
en found with AT1R A1166C polymorphism. We investigated the ACE I/D, AT1R A
1166C, and AT1R CA microsatellite polymorphisms genotype distribution in el
ite athletes and whether the presence of AT1R C1166 variant, in addition to
ACE D allele affects the training-induced LV mass alterations in elite tra
ined athletes. Methods: The study population comprised 38 healthy players r
ecruited from an Italian elite male soccer team and 155 healthy male subjec
ts. LV mass, LV mass adjusted for body surface area, septal thickness, post
erior wall, end-diastolic and end-systolic ventricular dimension, and eject
ion fraction were determined by echocardiography in pretrained period, at r
est and 7 months later during the training. All subjects were genotyped for
ACE I/D, AT1R A1166C, and CA microsatellite polymorphisms. Results: Traini
ng induced an LV mass increase in all but six athletes. The percentage of a
thletes in whom an increase of LV mass was found after training was statist
ically different in relation to the ACE D allele: no increase was observed
in three of 24 D allele carriers and in three of four ll genotype players (
Fisher's exact test, P = 0.02). As AT1R is concerned, no increase was obser
ved in 4 of 15 C allele carriers and in 2 of 13 AA genotype athletes (Fishe
r's exact test, P > 0.05). The contemporary presence of ACE D and AT1R C al
lele did not affect the changes after training. No difference has been obse
rved in the CA microsatellite marker allele frequencies between athletes an
d controls (P = 0.46). Conclusion: In this study, we provide the evidence t
hat soccer play does not select athletes on genotype basis. Training-induce
d LV mass changes in male elite athletes are significantly associated with
the presence of ACE D allele, but not of AT1R C allele.