Santana et al. BMC Cardiovascular Disorders 2011, 11:71
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RESEARCH ARTICLE
Open Access
The higher exercise intensity and the presence of
allele I of ACE gene elicit a higher post-exercise
blood pressure reduction and nitric oxide release
in elderly women: an experimental study
Hugo AP Santana1,2, Sérgio R Moreira3, Willson B Neto1, Carla B Silva1,4, Marcelo M Sales1, Vanessa N Oliveira6,
Ricardo Y Asano1,5*, Foued S Espíndola6, Otávio T Nóbrega7, Carmen SG Campbell1 and Herbert G Simões1†
Abstract
Background: The absence of the I allele of the angiotensin converting enzyme (ACE) gene has been associated
with higher levels of circulating ACE, lower nitric oxide (NO) release and hypertension. The purposes of this study
were to analyze the post-exercise salivary nitrite (NO2-) and blood pressure (BP) responses to different exercise
intensities in elderly women divided according to their ACE genotype.
Methods: Participants (n = 30; II/ID = 20 and DD = 10) underwent three experimental sessions: incremental test IT (15 watts workload increase/3 min) until exhaustion; 20 min exercise 90% anaerobic threshold (90% AT); and 20
min control session without exercise. Volunteers had their BP and NO2- measured before and after experimental
sessions.
Results: Despite both intensities showed protective effect on preventing the increase of BP during post-exercise
recovery compared to control, post-exercise hypotension and increased NO2- release was observed only for carriers
of the I allele (p < 0.05).
Conclusion: Genotypes of the ACE gene may exert a role in post-exercise NO release and BP response.
Background
The systemic arterial hypertension (SAH) has committed about two thirds of elderly population in several
countries [1,2]. Being considered a cardiovascular risk
factor [3] that may be associated with endothelial dysfunction and thus with a low endothelial dependent
vasodilatation [4,5].
The treatment of SAH includes pharmacological therapy and lifestyle changes, such as physical activity
enrollment and nutritional habits re-education [6].
Among cardiovascular benefits of exercise, the postexercise blood pressure reduction has been considered
an important tool for blood pressure (BP) control
[7-15]. The protective effect of exercise in lowering
* Correspondence: ricardokiu@ig.com.br
† Contributed equally
1
Programa de Pós-graduação em Educação Física e Saúde, Universidade
Católica de Brasília - UCB, Brasília-DF, Brazil
Full list of author information is available at the end of the article
blood pressure may be mainly due vasodilatation substances induced vascular resistance reduction after exercise [9].
During physical exercise the increased blood flux lead
to mechanical vessel stress and thus an endothelial NO
release [16]. The NO is involved with vascular tonus
regulation [17] and its release has been associated to
post-exercise BP reduction (e.g. post-exercise hypotension - PEH), which may even be influenced by genetic
characteristics [18].
Hypertensive people would benefit from PEH as a
non-pharmacological adjunct to the SAH treatment.
However, Hagberg et al. [19] highlighted that approximately 25% of the hypertensive individuals do not present PEH, what could be partially explained by genetic
variations.
Studies about the insertion/deletion (I/D) polymorphism of angiotensin converting enzyme (ACE) and its
© 2011 Santana et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.
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associations to functional, metabolic and cardiovascular
phenotypes have been documented [20-22], including
SAH [10,23]. The absence of I allele of ACE gene (e.g.
individuals D/D) has been associated with higher levels
of circulating ACE [24-26] leading to an increased
angiotensin II (ANG II) concentration, reduced bioavailability of bradykinin and thus to a lower NO release
[27,28].
We hypothesized that in respect to ACE gene, the D/
D carriers would present lower NO release during exercise and thus both lower vasodilatation and reduced
post-exercise blood pressure reduction than those with
the I allele. Furthermore, once the endothelial release of
NO is dependent on both metabolic and mechanical
stress (shear stress) [16], it was also hypothesized that
aerobic exercise of a greater intensity would result in a
higher NO release and thus to elicit a greater post-exercise BP reduction in elderly hypertensive women.
Therefore, the purposes of this study were to analyze
the post-exercise NO and blood pressure responses to
different exercise intensities in elderly women with or
without the I allele of ACE gene, as well as to investigate
if the NO release and post-exercise hypotension in this
population would be influenced by of the I/D polymorphism of ACE gene. Due to factors such as age and gender
affect blood pressure responses, this report poses a contribution by standardizing these variables in our sample.
Page 2 of 8
were performed under cardiologist’s supervision. The
study was approved by the local ethical committee (process nº CEP/UCB 63/2008).
General Procedures
All 268 women had a blood collection for the determination of their I/D polymorphism of ACE gene. After
that, 30 volunteers were selected according to their
availability to underwent to testing protocol, their ACE
genotype (individuals with and without the I allele of
ACE) as well as considering the exclusion criteria (e.g.
use of medicines that would interfere on RAS). Before
each experimental session, all volunteers remained on
resting for 20 minutes, and blood pressure (BP) was
measured every five minutes, being the average considered the resting BP. Experimental design consisted in an
incremental test session, one session at 90% of anaerobic
threshold and another session without exercise (control
session). After all sessions, the volunteers remained in
the laboratory for recovery during one hour. In this
time span, the post-exercise BP was measured every 15
min, and the mean of these measures was considered.
NO was inferred from the measurement of nitrite (NO2) in saliva [31-34]. For this analysis, saliva was collected
during resting before exercise (or control) in all testing
days (PRE), immediately after exercise (IAE) and concomitantly to BP measurements throughout the recovery
period. The saliva was collected through a cotton swab.
Methods
Participants
ACE Genotyping
In the initial phase of this study 268 elderly women (≤ 60
years-old) clinically diagnosed with hypertension were
genotyped for the I/D polymorphism of ACE gene. The
diagnosis of hypertension in this sample was performed
in 2005 and confirmed in 2006/2007 at the medical
department of the University according to IV Brazilian
Hypertension Guidelines (2006) [29] following procedures previously described by Moraes et al. (2008) [30].
From these initial volunteers, thirty elderly women (70.5
± 6.0 years, 60.4 ± 8.5 kg, 153.3 ± 6.3 cm and 25.7 ± 3.0
kg/m 2 ) diagnosed with mild hypertension and whose
pharmacotherapy consisted only on diuretics as hydrochlorothiazide and indapamide (not interfering with the
RAS) were selected to enrolled in a local program for
SAH treatment which included regular physical activity
and recommendation of a balanced food intake.
After recruitment, participants were allocated into two
different groups according to the presence (II and ID)
or absence (DD) of 287 pairs of base. Participants of
both groups (II/ID and DD) randomly underwent to
three experimental test sessions on non-consecutive
days, inter a spread with at least 48-hours apart. After
giving a written consent, each volunteer was first submitted to a resting electrocardiogram, and exercise tests
Total DNA was isolated from peripheral blood according to standard procedures. The insertion(I)/deletion(D)
polymorphism in the human ACE gene (rs4646994) was
determined by inspection of the electrophoretic profile
of polymerase chain-reaction (PCR) products, and performed as described by Marre et al. with modifications
[34]. Either the 490 bp (I allele) or the 190 bp (D allele)
products were amplified using primers: 5′-CTGCAGACCACTCCCATCCTTTCT-3′ and 5′-GATGTGGCCATCACATTCGTCAGAT-3′, which flank the polymorphic
site. Reaction tubes contained 100 ng DNA, 10 mmol/L
Tris-HClpH8.3,75 mmol/L KCl, 3.5 mmol/L MgCl2, 0,2
mmol/L dNTP, 20 pmol of each primer, 0.5 μg of purified chicken albumin and 1 U of Taq DNA polymerase
(Phoneutria®, Minas Gerais, Brazil) in a final volume of
25 μL. After 1 min of hot start at 80 °C and an initial
denaturation for 2 min at 94 °C, the amplifications were
done for 30 cycles of 40 s at 94 °C, 45 s at 64 °C and 50
s at 72 °C followed by a final 5 min extension at 72 °C.
Inspection of DD subjects was carried out using oligonucleotides (5′-TGGGACCACAGCGCCCGCCACTAC3′ and 5′-TCGCCAGCCCTCCCATGCCCATAA-3′)
specific to amplify a 335 bp fragment of the insertion
sequence. In brief, DNA was amplified for 30 cycles
Santana et al. BMC Cardiovascular Disorders 2011, 11:71
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with denaturation at 92 °C for 40 s, annealing at 63 °C
for 40 s, and extension at 72 °C for 40 s. All PCR products were separated by electrophoresis on 2% agarose
gels containing ethidium bromide at 50 μg/ml, visualized by using CCD camera (Vilber Lourmat®, Eberhardzell, Deutschland), examined using the gel analysis
software enclosed (Photo Capt 1D), and confirmed by
visual inspection.
Incremental Test and Anaerobic Threshold (AT)
determination
The volunteers performed a maximal incremental test
(IT) in cycle ergometer (Lode Excalibur, Netherlands)
that consisted in 1-min warm-up at 0 watts followed by
a pace of linear, incremental gradient in 15 watts every
3 minutes stage. The test was terminated due volitional
exhaustion, incapacity of maintaining 60 rpm or if any
cardiovascular-related risk was detected by cardiologist.
In each stage of IT, a blood sample was withdrawn from
earlobe to assess blood lactate concentration [Lac]. Measures of rate of perceived exertion (RPE) as well as ventilation (VE), oxygen uptake (VO2) and carbon dioxide
production (VCO 2 ) (Cortex Metamax, Leipzig, Germany) were performed at the end of each stage.
The AT intensity was determined by assessing the
ventilatory threshold (disproportional increase in the
ventilatory equivalent for oxygen (VE/VO2) in relation
to ventilatory equivalent for dioxide carbon (VE/VCO2)
and the [Lac] turnpoint (workload corresponding to
deflection point where the concentration of blood lactate increased disproportionally). The AT was considered the mean workload (watts) between ventilatory and
lactate thresholds.
Sub-maximal constant load exercise test
Participants underwent to a constant load exercise test
at intensity corresponding to 90% AT. During the 20
min exercise at 90% AT, expired gases were measured
continuously and the RPE were asked at the 10th and at
the end of exercise. This intensity was chosen due to
benefits on blood pressure and cognitive performance
observed in other studies in elderly individuals [11,35].
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The blood was collected in microcapillary heparinized
tubes and deposited in microtubes containing 50 μL
of sodium fluoride (1%) for [Lac] measurements
through an electrochemical analyzer (YSI 2700, YSI,
Inc., Yellow Springs, OH, USA). Expired gases were
collected breath by breath (Cortex Metamax, Leipzig,
Germany). For the 90% AT and CONT groups, blood
collection occurred at the 10th and 20th minutes; however gas measurement occurred during the whole 20
min span.
Heart Rate, Rate of Perceived Exertion and Blood Pressure
During the all sessions, the heart rate (HR) (Polar
s810i ®, Kempelle, Finland), a 15 point RPE scale [36]
and blood pressure (BP) (Microlife BP3AC1-1, Berneck,
Switzerland) were determined. All resting and post-exercise BP measurements were made according to the procedures of JNC 7 [2] on the participant’s left arm while
they were seated with their feet on the ground and arm
resting comfortably at the level of the heart.
NO Metabolic Measurement in saliva
Saliva was collected with a cotton swab (Salivette Sarstedt ® , Nümbrecht, Germany) which was chewed for
one minute. Then it was centrifuged according to the
manufacture instructions and stored in -20°C for latter
analysis. Dosage of nitrite (NO 2 - ) a NO metabolite
[31-33] was done through the Griess’ colorimetric
method 22 . Briefly, N-(1-naphthyl)-ethylenediamine
(NED) (Sigma®- Aldrich, St. Louis, USA) was prepared
at 0.1%, whereas sulfanilamide (Sigma ® ) at 1%, both
with phosphoric acid at 2.5% as diluent. Saliva (50 μL)
and the Griess’ reagent (50 μL) were mixed and placed
in microplates. Absorbance was measured at 450 nm, in
Versamax tunable® (Molecular Devices, Sunnyvale, California, USA), and sodium nitrite (NaNO2-) was used as
a standard. The data were analyzed in the Microplate®
software. Saliva samples of only 28 (II/ID - n = 18, DD n = 10) elderly women were processed due technical
problem in collecting procedures of two volunteers that
unable to run the analyses.
Statistical Analyses
Control Session
During control session the volunteers remained in resting for 20 min instead of exercising. However, all measurements were the same as those performed during a
constant load exercise session.
Measurements
Blood Lactate and Gases Analyses
In the incremental test on cycle ergometer, blood
samples were drawn and expired gases were collected
during the last 20 seconds of each incremental stage.
An exploratory analysis was used to verify data normality and then descriptive statistics were performed. Data
are presented as means (± standard deviation) for BP
and means (± standard error of mean) for NO 2 - . In
addition, the delta variations (absolute variation from
rest to post-exercise values) were calculated for comparison. Student’s t-test and One-Way ANOVA for
repeated measures were used to compare experimental
sessions. The Tukey test was adopted as a post hoc to
identify differences. The level of significance was set at
p ≤ 0.05.
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Results
The general characteristics of the volunteers and power
output, aerobic fitness, heart rate, metabolic variables
and RPE results of IT and 90%AT according to the genotypes of the investigated groups are presented on table 1.
The systolic blood pressure (SBP), diastolic blood
pressure (DBP) and mean arterial pressure (MAP) are
presented on table 2 as related to the studied ACE genotype groups. Since the data did not present any significant differences for the resting values (P > 0.05), the
delta variation results (post-exercise values minus resting values) was also used to analyze variation among
sessions.
During the post-exercise recovery from IT the SBP
values (table 2) were significantly lower than pre-
Table 1 General characteristics and descriptive data of
the studied groups of carriers or non-carriers of “I” allele
of ACE gene (n = 30).
N
I/D-I/I
D/D
p
10/10
10
-
Age (years)
70.4 ± 6.2
70.6 ± 5.8
0.93
Weight (kg)
60.6 ± 8.4
60.0 ± 9.1
0.86
Height (cm)
BMI (kg·m-2)
153.1 ± 7.1
25.9 ± 3.0
153.7 ± 4.7 0.82
25.4 ± 3.2 0.70
86.9 ± 13.1
79.6 ± 17.1 0.21
Metabolic and Hemodynamic
Variables
Glycaemia (mg·dL-1)
SBP IT rest (mm·Hg-1)
129.0 ±
17.0
125.0 ±
14.0
DBP IT rest (mm·Hg-1)
77.0 ± 8.0
77.0 ± 7.0
0.87
294.4 ±
176.5
278.2 ±
159.0
0.81
NO2- rest (μM)
0.47
Performance data of IT and 90%AT
Watts peak IT (Watts)
62.3 ± 21.4
Watts at AT (Watts)
38.4 ± 14.4
57.0 ± 19.7 0.52
39.6 ± 14.8 0.83
Watts at 90%AT (Watts)
34.5 ± 13.0
35.6 ± 13.3 0.83
VO2peak IT (mL·kg-1·min-1)
20.5 ± 4.3
20.1 ± 3.0
0.78
VO2 at 90%AT(mL·kg-1·min-1)
HRpeak IT (bpm)
15.8 ± 3.3
142.7 ±
19.6
116.8 ±
17.6
4.4 ± 1.4
0.37
0.51
[Lac] peak (mM)
14.8 ± 2.3
148.0 ±
21.0
119.5 ±
15.8
4.8 ± 1.9
[Lac] 90%AT (mM)
3.0 ± 1.1
3.3 ± 1.2
0.42
RPE peak IT (Borg)
17.6 ± 1.5
18.1 ± 1.6
0.41
RPE at 90%LA (Borg)
13.2 ± 2.0
13.8 ± 1.2
0.42
20.0
20.0
-
HR at 90%AT (bpm)
Diuretics Medication (% of
volunteers)
0.68
0.54
I/D-I/I and D/D - angiotensin converting enzyme (ACE) genotype; BMI - body
mass index, SBP - systolic blood pressure, DBP - diastolic blood pressure, NO2- nitrite concentration, VO2peak: peak oxygen consumption reached in IT;
VO2: oxygen consumption; HRpeak: peak heart rate reached in IT; HR: heart
rate; [Lac] peak: peak lactate concentration reached in IT; [Lac]: lactate
concentration; RPE peak: peak rate of perceived exertion reached in IT; RPE:
rate of perceived exertion.
exercise resting for the II/ID group both for the IT and
90%AT sessions. These variations when analyzed in
delta were significantly lower (p < 0.05) to control session and to D/D groups in the same circumstances. The
DBP and MAP on the control sessions present differences (p < 0.05) or at least a trend to it (p = 0.06) for
the D/D group for DBP, from the rest to 1 h Mean
recovery time. The delta variation of MAP presented
significant negative values for the IT and 90%AT sessions being significant different (p < 0.05) to the control
delta variation.
The NO2- (table 3) presented a significantly higher (P
< 0.01) values immediately after experimental session at
IT (IAE) and a trend to be higher (P = 0.08) at the 90%
AT session too (Figure 1) in comparison to resting on
the group that presented the I allele of ACE gene.
The delta variation of NO2- presented significant differences (p < 0.05) with a higher NO2- release after IT
for the II/ID group when compared to DD group as
shown in Figure 1.
Discussion
This study analyzed the BP responses after different
exercise intensities and the NO2- release as related to
ACE genotypes in elderly women. The main findings
were that both the exercise intensity and the presence
of I allele of ACE gene may interfere on NO2- liberation
and post-exercise hypotension (PEH) occurrence in
hypertensive elderly women. PEH occurred for the SBP
among carriers of the I allele only. Also, those I carriers
presented lowered post-exercise blood pressure levels in
relation to the DD group. Despite the intensity of the
exercise sessions, both intensities were effective for lowering the resting values of BP whereas these values
increased in the control session, without exercise.
The fact that only elderly women that had the I allele
presented PEH of SBP after both exercise sessions (table
2) is probably due to the fact that D/D homozygote presents almost twice as higher the angiotensin converting
enzyme activity when compared to the insertion homozygote [24,25]. The role of ACE is mainly to convert
angiotensin I to angiotensin II. This last action are
related to an increased sympathetic tone induced arteriolar constriction and release of aldosterone from suprarenal cortex [22,37,38] which, in turn acts in kidneys,
leading to potassium excretion, salt reabsorption and
water retention. All those effects may elevate the BP,
and in theory would interfere in the post-exercise BP
achievement.
Additionally, the fact that DD individuals present a
higher circulating level of ACE [25] may lead to a higher
activity of ANG II that may further blind the vasodilation induced by bradykinin [37] and thus influence the
BP values [22]. This mechanism causes a negative
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Table 2 Blood Pressure results at pre and post-sessions as well as the post-exercise delta variation in relation to preexercise resting for the ID/II and DD groups.
IT
Rest
SBP
(mmHg)
90%AT
Mean
1h
∆ variation
ID/II 129.1 ± 16.9 121.7 ± 14.7*
DD
DBP
ID/II
(mmHg) DD
Rest
Mean
1h
-7.4 ± 8.4‡#
123.3 ± 12.8 119.1 ± 12.8*
CONT
∆ variation
Rest
-4.2 ± 6.0‡#
Mean
1h
∆ variation
122.0 ± 17.6 125.1 ± 16.3†
3.1 ± 7.1
124.5 ± 13.9
122.5 ± 13.7
- 2.0 ± 3.6
117.7 ± 11.4
119.7 ± 14.8
2.0 ± 8.7
118.4 ± 7.4
121.7 ± 8.3
3.3 ± 5.7
77.0 ± 8.4
76.5 ± 7.1
77.3 ± 8.6
77.8 ± 7.8
0.3 ± 6.8
1.3 ± 6.3
75.3 ± 7.1
71.9 ± 4.1
75.7 ± 5.6
74.6 ± 6.9
0.4 ± 3.7
2.7 ± 5.2
73.8 ± 7.8
73.0 ± 6.7
76.6 ± 7.4*
76.0 ± 7.3†
2.8 ± 2.4
3.0 ± 4.4
MAP
ID/II
94.3 ± 10.3
92.1 ± 9.9
-2.2 ± 5.9‡
91.3 ± 8.5
90.2 ± 7.2
-1.1 ± 3.9‡
89.9 ± 10.2
92.8 ± 9.8*
2.9 ± 3.1
(mmHg)
DD
92.5 ± 8.9
92.7 ± 9.1
0.2 ± 4.7
87.2 ± 6.3
89.6 ± 9.2
2.4 ± 6.1
88.1 ± 6.6
91.2 ± 7.3*
3.1 ± 4.4
IT - Incremental Test session, 90%AT - 90% of anaerobic threshold session, CONT - control session. *p < 0.05 to rest in the same session; †p = 0.06 to rest in the same
session; ‡p < 0.05 to Cont in the same group, #p < 0.05 to D/D in the situation.
impairment on the endothelial dependent dilation, once
it reduces the bioavailability of NO [16] what, in turn,
would be the reason of non significant post-exercise
blood pressure reduction for the D/D group in any
experimental session of the present study.
The findings of PEH of SBP in present study, for the
group that presented the I allele, were similar to others
studies. Pescatello et al. (2007) [10] analyzed the BP
response after high and low calcium ingestion and after
two sessions of low and moderate exercise intensity, and
verified in the intensity corresponding to 60% VO2 max,
the I allele carriers that had low calcium ingestion presented PEH of higher magnitude for the SBP. However,
for the DBP no ACE genotypes interactions were found.
For the present study, besides the main effect on SBP,
the exercise also presented a protective effect on postexercise DBP and MAP despite the genetic profile compared to control (table 2).
Blanchard et al. (2006) [39] verified for 14 h the
ambulatory BP in adult men at the same intensities studied by Pescatello et al. (2007) [10] and the results were
contradictory to ours, presenting increases in the mean
of 14 h in the SBP and DBP for all experimental sessions (60% VO 2 max, 40% do VO 2 max and control)
despite the genetic combinations of RAS, however the
exercise sessions had benefits when compared to control. Moreover, they found benefits of post exercise SBP
14 h after light exercise session (40% VO 2 max) with
lower values for the DD homozygote but not for the I
allele group. These distinct results may be either related
to gender differences, because some studies suggest that
associations between BP and genotype DD of ACE gene
are only significant in men showing some effect on the
BP [40,41], or to age differences, because in present
study the sample was composed by elderly people, that
presents different endothelial responses when compared
to youngsters [42].
The BP increase in the control session can be partly
explained from the waiting time (60 minutes) until the
end of data collection procedures, that may have produced some degree of distress that may have contributed to the augmentation observed. Zimmerman &
Frohlich [43] related that acutely, stress episodes have
been shown to increase blood pressure by increasing
cardiac output and heart rate but without affecting peripheral resistance. In addition, even moderate stress has
been found to increase levels of catecholamines, cortisol,
vasopressin, endorphins and aldosterone, which may in
part explain the increase in blood pressure. This may
not have occurred in the experimental session (90% AT)
due to the protective effect of exercise in situations of
acute stress, as observed by MacDonald et al. [44].
Furthermore, the increase in BP even with the nonsignificant of NO2- (p > 0.05) augmentation in the DD
group may be due to overlap of complementary input
signals, with a probable prevalence of humoral and
neural mechanisms in blood pressure control. Studies
[45-47] have reported that individuals carrying the DD
genotype have higher levels and activity of the angiotensin converting enzyme (ACE), which therefore could
result in a greater increase in blood pressure by increasing the conversion of angiotensin I to II, causing
Table 3 Nitrite (NO2-) concentrations in rest and immediately after experimental session in groups separated by ACE
genotypes (ID/II - n = 18; DD - n = 10).
TI
Rest
NO2-(μM)
90%AT
IAE
Rest
CONT
IAE
Rest
†
IAE
ID/II
286.6 ± 29.4
401.3 ± 52.8*
239.8 ± 34.6
337.5 ± 63.8
295.5 ± 39.4
292.9 ± 44.9
DD
264.9 ± 70.5
282.9 ± 63.8
318.5 ± 65.0
341.2 ± 93.6
251.1 ± 44.8
293.0 ± 94.2
IT - incremental test session, 90% AT - session at 90% of anaerobic threshold, CONT - control session, NO2- - nitrite, IAE - immediately after experimental session.
*p < 0.01 in relation to rest in the same session; †p = 0.08 in relation to rest in the same session.
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Figure 1 Mean (± SEM) delta variation of NO2- (nitrite) for IT (Incremental test), 90% AT (90% of anaerobic threshold) and CONT
(control) sessions performed by ID/II (n = 18) and DD (n = 10) genotypes of ACE gene. * p < 0.05 in relation to D/D group on IT session.
vasoconstriction and also enhancing water and sodium
reabsorption by the kidneys, increasing blood volume
and blood pressure.
The trends of a higher exercise intensity to be more
effective on inducing PEH (table 2) are in accordance to
former results in our laboratory, but on individuals with
type-2 diabetes [11]. The possible role of exercise intensity
on the present study was demonstrated for the results of
NO release as well (table 3). The NO2- results of this study
reinforce the important role of the NO on reducing BP, as
already demonstrated by other authors [2,42,48].
Nevertheless, Lauer et al. (2008) [42] showed that
elderly, when compared to youngsters, has endothelial
dysfunction being harder in increase plasmatic NO2- in
response to exercise. However, it was interesting to
demonstrate in our research that in elderly population
the ability to increase NO2- may be intensity-dependent,
and may be associated to genetic characteristics with the
DD group not presenting significant changes in NO2 and these findings together are the main contribution of
the present study.
Tanriverdi et al. (2005) [49] verified that flux mediated
dilation response in athletes presenting that II, was
higher than ID and DD genotypes, being the homozygote D with the worst response to flux mediated
dilation, what corroborates with our results (no PEH
and lower NO2- release for the DD group).
The increased liberation of the NO 2 - after exercise
sessions may occurs due to shear stress in the blood
vessels what stimulates the endothelial NO formation
[50,51]. The fact that NO 2 - being significantly higher
only after the IT session, on the I/D - I/I group, may
also be due to exercise at higher intensity to promote a
more significant shear stress [52], even for elderly that
may be predispose to endothelial dysfunction and low
NO release [42,53,54].
The study limitations were not measuring the endothelial nitric oxide synthase (eNOS) what could represent the
endothelial dependent activity and, consequently, a possible PEH. However, some authors [31-33] verified that the
NO2- in saliva predicts the plasmatic NO2- concentration
that is one of better eNOS activity indexes [55]. Another
limitation of this study was the lack of ACE measurement
in the elderly participants; however some authors [24,25]
observed higher values of this activity with homozygote D
when compared to other ACE genotypes.
Conclusion
The II/ID individuals, but not the DD group, presented
PEH for SBP in both experimental exercise sessions.
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However, both groups had a protective effect of aerobic
exercise on preventing the increase of DBP and MAP
during post-exercise period. The endothelial responses
of NO to exercise were only presented by the ID/II ACE
genotype group and, similarly to PEH, seemed to be
influenced by exercise intensity.
Therefore, the ACE genotype seems exert a role in the
NO release and BP response during post-exercise recovery in elderly women. Any extrapolation of these results
to other gender or age strata requires caution.
Page 7 of 8
6.
7.
8.
9.
10.
11.
List of Abbreviations
Angiotensin converting enzyme (ACE), nitric oxide (NO), blood pressure (BP),
systemic arterial hypertension (SAH), post-exercise hypotension (PEH),
insertion/deletion (I/D), angiotensin II (ANG II), renin-angiotensin system
(RAS), nitrite (NO2-), resting before exercise (or control) in all testing days
(PRE), immediately after exercise (IAE), blood lactate concentration ([Lac]),
maximal incremental test (IT), rate of perceived exertion (RPE), ventilation
(VE), oxygen uptake (VO2), carbon dioxide production (VCO2), ventilatory
equivalent for oxygen (VE/VO2), dioxide carbon (VE/VCO2).
Acknowledgements
Conselho Nacional de Desenvolvimento Cientifico (CNPq) and Coordenação
de Aperfeiçoamento de Pessoal de Nível Superior (CAPES).
Author details
Programa de Pós-graduação em Educação Física e Saúde, Universidade
Católica de Brasília - UCB, Brasília-DF, Brazil. 2Centro Universitário do Planalto
de Araxá - UNIARAXÀ; Araxá-MG, Brazil. 3Universidade Federal do Vale do
São Francisco -UNIVASF- Petrolina-PE, Brazil. 4Faculdade de Educação Física
do Centro Anhanguera Educacional, Taguatinga-DF, Brazil. 5Faculdade de
Educação Física do Centro Universitário - UNIRG -, Gurupi-TO, Brazil.
6
Instituto de Genética e Bioquímica da Universidade Federal de Uberlândia UFU, Uberlândia-MG, Brazil. 7Programa de Pós-Graduação em Ciências
Médicas e Programa de Pós -graduação em Ciências da Saúde, Universidade
de Brasília - UnB, Brasília-DF, Brazil.
12.
13.
14.
15.
1
Authors’ contributions
HAPS, SRM, CBS, CSGC and HGS participated in the design of the study.
HAPS, SRM, CBS, WBN and VNO performed the data collection. HAPS, SRM
performed the statistical analysis. HAPS, SRM, MMS, RYA, FSE, OTN and HGS
wrote the manuscript. All authors read and approved the final manuscript.
Competing interests
The authors declare that they have no competing interests.
Received: 19 May 2011 Accepted: 2 December 2011
Published: 2 December 2011
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Pre-publication history
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doi:10.1186/1471-2261-11-71
Cite this article as: Santana et al.: The higher exercise intensity and the
presence of allele I of ACE gene elicit a higher post-exercise blood
pressure reduction and nitric oxide release in elderly women: an
experimental study. BMC Cardiovascular Disorders 2011 11:71.
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