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European Journal of Sport Science
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Lack of association of the ACE genotype with the
muscle strength response to resistance training
Paulo Gentil a , Ricardo M. Lima a , Rinaldo Wellerson Pereira b , Julia Mourot b , Tailce
Kaley Leite b & Martim Bottaro a
a Faculdade de Educação Física, Universidade de Brasilia, Brasilia, Brazil
b Ciências Genômicas e Biotecnologia, Universidade Católica de Brasília, Brasilia, Brazil
Available online: 09 Dec 2011
To cite this article: Paulo Gentil, Ricardo M. Lima, Rinaldo Wellerson Pereira, Julia Mourot, Tailce Kaley Leite & Martim
Bottaro (2011): Lack of association of the ACE genotype with the muscle strength response to resistance training, European
Journal of Sport Science, DOI:10.1080/17461391.2011.573581
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ORIGINAL ARTICLE
Lack of association of the ACE genotype with the muscle strength
response to resistance training
PAULO GENTIL
1
, RICARDO M. LIMA
1
, RINALDO WELLERSON PEREIRA
2
,
JULIA MOUROT
2
, TAILCE KALEY LEITE
2
, & MARTIM BOTTARO
1
1
Faculdade de Educac
¸a
˜oFı
´sica, Universidade de Brasilia, Brasilia, Brazil, and
2
Cie
ˆncias Geno
ˆmicas e Biotecnologia,
Universidade Cato
´lica de Brası
´lia, Brasilia, Brazil
Abstract
Introduction: Previous studies have attempted to link the insertion/deletion (I/D) polymorphism in the angiotensin-
converting enzyme (ACE ) gene with the variability in muscle strength responses to resistance training (RT); however, the
literature is inconclusive. The purpose of the present study was to investigate the association between the ACE I/D genotype
and muscle strength response to a RT program in young men.
Methods: 124 men (2292.6 years; 174.896.5cm; 71.5913.8 kg) without resistance training experience were tested before
and after 11 weeks of five whole-body RTexercises (bench press, seated row, knee extension, knee flexion and sit ups). The
bench press 1RM test was used to assess upper-body muscle strength and the isokinetic knee extensor peak torque (PT) was
used as a measure of lower-body strength.
Results: At baseline, there were no differences among AC E genotype for 1RM load (54911.7 kg for II, 58.598.9 kg for ID
and 52.3912.2 kg for DD) or knee extensor peak torque (PT) (220.1936.8 N ×m for II, 209.4 944.4 N ×m for ID and
199.7932.4 N×m for DD). Moreover, ACE genotype was not associated with lower-body (7.1910.5%, 15.7910.4% and
14.1922.7% for II, ID and DD, respectively) or upper-body strength gains (16.298.9%, 14.5911.3% and 21.9917.1%
for II, ID and DD, respectively) in response to RT.
Conclusion: The ACE I/D genotype was not associated with the muscle strength responses to RT.
Keywords: Genetics, exercise, candidate gene, muscle strength, peak torque, strength training
Introduction
Although environmental factors are important in
determining muscle strength, it is well recognized
that genetic factors have an important influence on
this phenotype (Bray et al., 2009; Maes et al., 1996;
Reed, Fabsitz, Selby, & Carmelli, 1991; Stewart &
Rittweger, 2006). One of the most studied candidate
genes is the angiotensin-converting enzyme (ACE)
gene. ACE is a key enzyme in the renin-angiotensin
system which converts angiotensin I to angiotensin
II. A functional polymorphism of the ACE gene is
defined as the presence (insertion, I-allele) or ab-
sence (deletion, D-allele) of a 287 base pair (bp) Alu
repeat sequence within intron 16 (Rigat et al., 1990).
This polymorphism has been found to be responsible
for half of the variation in ACE enzyme activity (Rigat
et al., 1990; Woods, D.R., Humphries, & Montgom-
ery, 2000), with those carrying the D-allele (D)
presenting an increased ACE enzyme activity (Dan-
ser et al., 1995; McCauley, Mastana, Hossack,
Macdonald, & Folland, 2009; Tiret et al., 1992;
Williams et al., 2005). The renin-angiotensin system
also exists in diverse tissues; in particular, the ACE
gene is expressed in skeletal muscle (Jones & Woods,
2003). The description of ACE activity in skeletal
muscle (Reneland & Lithell, 1994) and the increased
muscle tension development after angiotensin II
infusion in rats (Rattigan, Dora, Tong, & Clark,
1996) introduced the ACE gene as candidate in
association studies with muscle-related phenotypes.
A higher proportion of the DD genotype has been
reported in elite sprint athletes when compared to
Correspondence: Paulo Gentil, Universidade de Brasilia, Faculdade de Educac
¸a
˜oFı´sica, Campus Universitario Darcy Ribeiro Brasilia,
Brazil. E-mail: paulogentil@hotmail.com
European Journal of Sport Science
2011, 17, iFirst article
ISSN 1746-1391 print/ISSN 1536-7290 online #2011 European College of Sport Science
http://dx.doi.org/10.1080/17461391.2011.573581
Downloaded by [Paulo Gentil] at 18:17 11 December 2011
endurance athletes and controls (Jones, Montgomery,
& Woods, 2002; Myerson et al., 1999; Nazarov et al.,
2001; Woods, D. et al., 2001). This genotype has been
associated with a greater proportion of fast twitch
fibres (Zhang et al., 2003), suggesting that this
polymorphism may influence skeletal muscle func-
tion, although contradictory evidence also exists
(Akhmetov et al., 2006). However, studies investigat-
ing the association between ACE I/D genotype and
skeletal muscle strength phenotypes have yielded
inconsistent results. Although the D-allele has been
previously associated with greater isometric and
isokinetic strength (Williams, et al., 2005), most
studies have found no association of this allelic variant
with muscle strength (Folland et al., 2000; McCauley,
et al., 2009; Pescatello et al., 2006; Thomis, M.A.
et al., 2004; Woods, D., et al., 2001).
Resistance training (RT) is regarded as an effective
mean of increasing muscle strength (ACSM, 2009);
however, adaptations to RT are highly variable
between individuals. Neuromuscular adaptations to
RT have been shown to be partially determined by
genetic factors (Beunen & Thomis, 2004; Brutsaert
& Parra, 2006; Thomis, M. et al., 1998; Thomis,
M.A., et al., 2004). Some candidate genes have been
investigated but agreement on important contribu-
tors has not been reached. In this regard, the ACE
gene has been pointed as a potential candidate.
Folland et al. (2000) and Giaccaglia et al. (2008)
showed ACE I/D genotype RT interaction in
young and older persons, respectively, with the
D-allele carriers presenting higher training-induced
increases in muscle strength compared with the II
genotype. In contrast, Lima et al. (2011), Charbon-
neau et al. (2008), Thomis, M.A. et al. (2004) and
Williams et al. (2005) failed to show significant
association between ACE I/D genotype and the
response of muscle strength to RT, while Pescatello
et al. (2006) observed that the I-allele carriers
showed greater gains. Therefore, although the bio-
logical rationale suggests an advantage for the
D-allele with regard to muscle strength, the literature
is inconclusive. The purpose of the present study was
to investigate the association between the ACE I/D
genotype and muscle strength response to an RT
program in young men. The hypothesis is that the
ACE I/D genotype would not influence the response
to RT.
Methods
Experiment overview
Participants undertook two days per week of whole-
body resistance training, with a minimum of 48 hours
between sessions, during 11 weeks. All volunteers
performed the same exercises and were instructed to
complete 812 repetitions until volitional fatigue at a
speed of four seconds per repetition (two seconds for
the concentric phase and two seconds for the
eccentric phase). The RT program characteristics
were selected based on literature recommendations
(ACSM, 2009; Kraemer et al., 2002).
Participants were initially required to attend three
to four sessions in order to become familiarized with
the RT program. Maximal knee extensor peak
torque (PT) in an isokinetic dynamometer as well
as bench press one repetition maximum (1RM) were
measured before and after the 11 weeks of training.
The initial tests were performed between the third
and fourth familiarization sessions and the final tests
were performed five to seven days after the last
training session. For genotype analyses, 4 ml of
venous blood were collected from all the volunteers
at the end of the study period in the fed state.
Participants
One hundred and sixty college non-resistance
trained men volunteered to participate in the study.
Participants were selected at random from respon-
dents to fliers distributed over the university campus,
and by word of mouth. The training classes were
part of college activities. The criteria for entering the
analysis included being at least 18 years of age, no
previous resistance training experience and being
free of clinical problems that could be aggravated by
the study procedures. To be included in the statis-
tical analysis, participants were permitted to miss
only four training sessions during the 12-week
program. Final training adherence was 89%. The
volunteers were oriented not to change their nutri-
tional habits during the study period; if a relevant
change were detected (i.e. becoming a vegetarian,
taking nutritional supplements or ergogenic aids,
etc.) the participant’s data were excluded from the
analysis. Although they were untrained in a resis-
tance training sense, all were physically active, with
involvement in other activities such as walking,
jogging, martial arts and team sports. At the end of
the study, 124 participants met the criterions to
be included in the analysis (21.9892.63 years;
174.8496.51cm; 71.49913.81 kg).
All participants were notified of the research
procedures, requirements, benefits and risks before
providing informed consent. The Institutional Re-
search Ethics Committee granted approval for the
study.
Procedures
One repetition maximum test. In the week before the
experiment and 57 days after the last training
session, the load for 1RM was determined for each
2P. Gentil et al.
Downloaded by [Paulo Gentil] at 18:17 11 December 2011
participant in the bench press exercise using the
protocol suggested by Kraemer and Fry (1995). The
initial tests were repeated after 25 days in all
participants and the intraclass correlation coefficient
(ICC) was calculated as 0.98.
Measurement of isokinetic peak torque (PT). Subjects
warmed up on a cycle ergometer at 2550 Watts for
5 min. After the cycle warm-up, they were seated on
the isokinetic dynamometer and actively warmed up
the involved quadriceps muscles by performing 10
12 submaximal knee extension repetitions at
3008×s
1
(Bottaro, Russo, & Oliveira, 2005). For
familiarization with isokinetic exercise, subjects per-
formed two sets of four maximal repetitions at
608×s
1
with 1-min rest between sets (Parcell,
Sawyer, Tricoli, & Chinevere, 2002). The familiar-
ization session was performed between 48 and 72
hours before the first isokinetic training protocol.
Knee extensor isokinetic PT was measured on the
Biodex System 3 Isokinetic Dynamometer (Biodex
Medical, Inc., Shirley, NY, USA). Calibration of the
dynamometer was performed according to the man-
ufacturer’s specifications before every testing session.
The participants sat upright with the axis of rotation
of the dynamometer arm oriented with the lateral
femoral condyle of the right knee. Belts were used to
secure the thigh, pelvis and trunk to the dynam-
ometer chair to prevent additional body movement.
The chair and dynamometer settings were recorded
to ensure the same positioning for all tests. The
flexor torque produced by the relaxed segment was
used for gravity correction. Subjects were instructed
to fully extend and flex the knee and to work
maximally during each set of exercises. Verbal
encouragement was given throughout the testing
session. The tests comprised two sets of four
repetitions at 608s
1
(Bottaro, et al., 2005; Parcell,
et al., 2002). Participants were instructed to fully
extend and flex the knee and to work maximally
during each set. After each set, participants were
required to take 60 s of rest before the onset of the
next set (Bottaro, et al., 2005; Parcell, et al., 2002).
The knee strap was released during each rest period
to ensure unrestricted blood flow to the lower limb.
The procedures were administered to all participants
by the same investigator. Knee extensor PT baseline
test and retest ICC and standard error of the mean
were 0.98 and 2.3% respectively.
Resistance training intervention. A whole-body multi-
ple-set resistance training program was implemented
using a combination of free weights and machines.
The sessions consisted of five exercises, two for the
upper body (bench press and seated row), two for
the lower body (one for the knee extensors and one
for the knee flexors) and one for the midsection
(sit ups). To improve external validity, and follow
literature recommendations (ACSM, 2009; Kraemer
et al., 2002), participants performed two sets of 812
repetitions. Participants were instructed to adjust
training loads carefully; if participants could not
perform eight repetitions or could lift the load more
than 12 times, they were instructed to adjust the load
in order to ensure the completion of the required
number of repetitions.
Training was conducted two days a week, with a
minimum of 48 hours between sessions, for 11
weeks. Twice-weekly training sessions were chosen
because the current physical activity guidelines state
that adults should do at least 150 minutes per week
of moderate intensity physical activity and also two
or more days per week of muscle-strengthening
activities (USDHHS, 2008). The sets started every
three minutes, leading to a rest interval of approxi-
mately two minutes. During the training sessions,
music tracks with 120 bpm were played in order to
facilitate control of movement speed. Each partici-
pant kept a training log where the loads used and the
numbers of repetitions performed in each exercise
were recorded. Training sessions were closely super-
vised, in a ratio of five volunteers per supervisor,
because previous research has demonstrated greater
gains in supervised versus unsupervised training
(Gentil & Bottaro, 2010).
Genotypes. For genotype analysis, blood samples were
obtained using EDTA vacutainer tubes from each
volunteer in the fed state. High molecular weight
DNA was extracted from peripheral venous blood
leukocytes using a salting out protocol. The ACE I/D
polymorphism was identified by polymerase chain
reaction (PCR) using the forward (5?-CTGGAGAC-
CACTCCCATCCTTTCT-3?) and reverse (5?-GA
TGTGGCCATCACATTCGTCAGAT-3?) primers
described by Zhao et al. (2003). Amplicons were
electrophoresed on 1% agarose gel and fragments
were visualized by ethidium bromide staining and
ultraviolet transillumination. The PCR product is a
190 bp fragment in the presence of the deletion (D)
allele and a 490 bp fragment in the presence of the
insertion (I) allele. Therefore, three ACE I/D geno-
types were possible: II a 490 bp band; DD a 190
bp band; and heterozygote ID the presence of both
490 and 190 bp bands. As an attempt to avoid
mistyping of ID as DD, all samples classified as
homozygous DD were subjected to a second ampli-
fication reaction using forward (5?-TGGGACCA-
CAGCGCCCGCCACTAC-3?) and reverse (5?-T
CGCCAGCCCTCCCATGCCCATAA-3?) primers
that anneal to an insertion-specific sequence as
described by Gonzalez et al. (2006). Negative and
positive controls were included in this second PCR
and the presence of a 335 bp fragment demonstrates
ACE genotype and response to resistance training 3
Downloaded by [Paulo Gentil] at 18:17 11 December 2011
mistyping whereas a real DD genotype shows no
amplification. All genotypes were determined by two
independent investigators.
Statistical analyses
Distribution of ACE I/D genotypes was analysed by
Pearson chi-square test to verify agreement with the
HardyWeinberg equilibrium. The data were in
normal distribution, according to the Kolmogorov
Smirnov test. To test for differences in age, height,
weight, initial bench press 1RM and knee extensor
PT, one-way analysis of variance (ANOVA) was
performed. To examine the association between the
ACE I/D genotypes and the RT-induced adaptations,
a repeated measures ANOVA (genotypetime) was
performed, in which the within-subject factors were
pre and post values of the phenotypes under study
and the between-subject factors were the genotypes
(DD, ID and II). Relative percentage change was
calculated for the knee extensor PT and bench press
1RM using the following equation: [(post values
pre values)/pre values100]. The two-step cluster
analysis was used to create homogenous groups
according to increases in bench press 1RM and
knee extensor PT. Cluster analysis was performed
because it seeks to identify homogeneous subgroups
of cases in a population, minimizing within-group
and maximizing between-group variations. Whereas
the use of fixed values for classifying groups may
create heterogeneous groups, with relatively large
within-group variations Pearson chi-square was used
to analyse association between the distribution of
muscle strength gains and ACE I/D genotype.
A sample size of 114 subjects (23 for II, 68 for ID,
and 33 for DD groups) provided 0.85% statistical
power at an alevel of 0.05 (2-tailed) for both
outcomes (PT and 1RM). All statistical analyses
were performed using the Statistical Package for the
Social Sciences 16.0 software (SPSS, Chicago, IL,
USA). Data are expressed as means9standard
deviation.
Results
Participants’characteristics according to ACE I/D
genotype are shown in Table I. The genotype
distribution was in expected HardyWeinberg equi-
librium (P0.05). At baseline, no significant differ-
ences were found for any variable (P0.05).
There were no genotype by time interactions for
knee extensor PT or bench press 1RM (P0.05).
According to the results, all genotypes significantly
increased bench press 1RM and knee extensor
isokinetic PT, with no difference between groups
(PB0.05). Additional comparisons between carriers
of the D allele (IDDD) and the II genotype
revealed no difference between groups for baseline
values or changes in knee extensors PT and bench
press 1RM (P0.05).
Two clusters were formed for knee extensor PT:
(1) HPT high response (25.8914.9%; 22 partici-
pants); and (2) LPT low response (3.397.1%; 94
participants). The analysis of bench press 1RM data
led to the formation of three clusters: (1) HBP high
response (30.199.6%; 21 participants); (2) IBP
intermediate response (16.193.3 g ×cm
2
; 51 parti-
cipants); and (3) low response (3.394.8%; 42
participants). According to the Pearson chi-square
results, there was no significant association between
the distribution of ACE I/D genotypes and knee
extensor PT (Figure 1) or bench press 1RM
response (Figure 2).
Discussion
Genotype distribution was in expected HardyWein-
berg equilibrium in the present study sample. ACE
genotype frequencies have been shown to differ
among race groups. Commonly, the allele frequency
among Caucasian individuals is approximately 50%
for both the I and D alleles, compared with 41% and
59% for the I and D alleles, respectively, in black
individuals (Mathew, Basheeruddin, & Prabhakar,
2001). In the USA, racial groups are relatively well
Table I. Subject characteristics and muscle strength indexes according to ACE I/D genotype (mean9standard deviation).
Variable II ID DD
n23 68 33
Age (years) 20.9 91.9 21.9 93.2 20.9 91.4
Height (cm) 174.7 99.6 175.6 96.8 174.2 96.6
Body mass (kg) 68.6 917 71.6 914.4 67.3 96.9
Knee extensor PT pre (N×m) 220.1 936.8 209.4 944.4 199.7 932.4
Knee extensor PT post (N×m) 235.1 940.6* 239.3 940.8* 223.3 929.2*
Dknee extensor PT (%) 7.1 910.5 15.7 910.4 14.1 922.7
Bench press 1RM pre (kg) 54 911.7 58.5 98.9 52.3 912.2
Bench press 1RM post (kg) 62 910.1* 66.4 98.9* 62.7 910.5*
Dbench press 1RM (%) 16.7 98.9 14.5 911.3 21.9 917.1
PT peak torque, 1RM one repetition maximum
*PB0.05 pre versus post
4P. Gentil et al.
Downloaded by [Paulo Gentil] at 18:17 11 December 2011
defined and easily identified. In Brazil, however,
such subgroups are much less well defined. Most
Brazilians are of mixed European, African and
Amerindian ancestry. Despite that, ACE ID geno-
type distribution of the present study was in Hardy
Weinberg equilibrium, with frequencies of 18.6, 54.8
and 26.6% for the ACE II, ID, and DD genotypes,
respectively. Pescatello et al. (2006) reported similar
frequencies for the white population for the ACE II
(23.1%), ID (46.1%), and DD (30.8%) genotypes.
The results of the present study provide no
evidence of an association between ACE I/D geno-
type and baseline upper- and lower-body muscle
strength. These results are in agreement with pre-
vious cross-sectional results (Charbonneau, et al.,
2008; Folland, et al., 2000; Giaccaglia, et al., 2008;
McCauley, et al., 2009; Pescatello, et al., 2006;
Thomis, M. A., et al., 2004; Williams, et al., 2005)
and, in conjunct with them, indicate that the genetic
variant under investigation does not play a pivotal
role in determining muscle strength phenotypes.
The results of experimental designed studies
analysing the effects of the ACE genotype in resis-
tance training adaptations are controversial. Giacca-
glia et al. (2008) studied a population of older adults
before and after 18 months of walking and light RT,
and reported that the DD homozygous presented
greater gains in knee extensor isokinetic strength
than the II homozygous. Earlier, Folland
et al. (2000) found that the knee extensor isometric
strength gains was associated with ACE I/D geno-
type, with young men that carry the D-allele
presenting greater strength increases than II homo-
zygous after 9 weeks of RT. However the baseline
results for 1RM and isokinetic strength were similar
among genotypes.
Williams et al. (2005) examined the ACE I/D
genotype associations with quadriceps muscle
strength in 81 young Caucasian men. Baseline
isometric strength was significantly associated with
the ACE genotype, with I-allele homozygous show-
ing the lowest strength values. On the other hand, no
association was found with changes in strength in 44
men who completed an 8-week RT program. The
lack of association between strength gains and ACE
genotype in the Williams study could be due to small
statistical power. However, with regard to training
adaptations, this issue is not likely for the present
study that reported the same results. In agreement
with the present study, Charbonneau et al. (2008)
found no difference in knee extensor 1RM response
between different ACE I/D genotypes after 10 weeks
of unilateral knee extensor RT. Similarly, a recent
study by Lima et al. (2011) did not find a pivotal role
for the ACE I/D polymorphism in determining
muscle strength response to RT in older women.
In contrast to the present study, Pescatello et al.
(2006) reported greater increases in maximal iso-
metric voluntary (MVC) contraction after 12 weeks
(twice a week) of unilateral RT in young people
carrying the I allele than in DD homozygous, but
interestingly found no difference for 1RM gains.
Likewise, Thomis, M.A. et al. (2004) studied 57
young male twins who underwent 10 weeks of elbow
flexors RT and showed no association between ACE
I/D genotype and 1RM gains, but reported a border-
line significance for larger isokinetic knee flexion PT
in II homozygous. According to Pescatello et al.
(2006), it seems plausible that the exercise-induced
ACE signalling effects are greater with the ACE
I allele due to its associations with increased brady-
kinin activity compared with the ACE D allele. The
authors suggested that the bradykinin is involved in
the exercise pressor reflex, being released by high-
intensity, static muscle contractions in direct propor-
tion to lactate production and inversely related to
pH. Also it appears that differences in association
could be in some way related to the specificity of the
Figure 1. ACE I/D genotype distribution among different clusters
of knee extensors peak torque response to resistance training.
HPT high response; LPT low response.
Figure 2. ACE I/D genotype distribution among different clusters
of bench press 1RM response to resistance training. HBP high
response; IBP intermediate response; LBP low response.
ACE genotype and response to resistance training 5
Downloaded by [Paulo Gentil] at 18:17 11 December 2011
strength testing mode (1RM versus MVC) or muscle
group studied (upper versus lower body). However,
in our study we assessed strength by 1RM upper-
body isoinertial test and PT lower-body isokinetic
test, and also found no relation between ACE I/D
genotype and strength gains.
Conclusions
In summary, the present results do not suggest a
pivotal influence of the ACE I/D polymorphism in
determining dynamic muscle strength response to
RT in young men. It is true that different methodo-
logical approaches make comparisons between stu-
dies difficult; however, despite these differences, if
the ACE gene were a robust contributor of muscle
strength some agreement would be noted in the
literature. One possible explanation for the lack of
congruent results is that the ACE I/D polymorphism
is one of many genetic variants contributing to the
variance in the muscle strength response to RT, and
that only a small part of the variability in these
phenotype may be attributable to the ACE I/D
genotype (Pescatello et al., 2006). According to
this assumption, future investigators should not
focus their effort in designing studies to examine
the ACE gene individually in association with muscle
strength. It is important that upcoming studies
investigate the interaction between different genes,
which we believe will lead to a better understanding
of the genetic contribution of muscle strength in
response to RT.
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