Original Article
Effects of Diet and/or Low-Intensity Resistance Exercise
Training on Arterial Stiffness, Adiposity, and Lean Mass in
Obese Postmenopausal Women
Arturo Figueroa,1 Florence Vicil,1 Marcos Angel Sanchez-Gonzalez,1 Alexei Wong,1
Michael J Ormsbee,1 Shirin Hooshmand,2 and Bruce Daggy1
Background
Obesity and aging are associated with increased arterial stiffness as
indicated by an increased pulse-wave velocity (PWV). We evaluated the
independent and combined effects on PWV and body composition of
a hypocaloric diet and low-intensity resistance exercise training (LIRET)
with slow movement.
Methods
Forty-one postmenopausal women (mean age, 54 ± 6 years; body mass
index (BMI), 33.8 ± 0.5 kg/m2) were randomly assigned to LIRET (n = 14),
diet (n = 13), or diet + LIRET (n = 14) for 12 weeks. The women’s PWV,
mean arterial pressure (MAP), body composition by dual-en ergy x-ray
absorptiometry (DXA), and plasma adipokine and insulin levels were
measured before and after the interventions.
Results
Body weight (P = 0.0001), trunk-fat mass (FM, P = 0.0001), and the
serum concentration of leptin (P = 0.02 and P = 0.004) decreased simi-
larly with diet and diet + LIRET, but not with LIRET alone. Leg lean
mass (LM) decreased (P = 0.02) with diet, but did not change with
diet + LIRET or with LIRET alone. Leg muscle strength increased simi-
larly with LIRET (P = 0.001) and diet + LIRET (P = 0.0001), but did not
Obesity and hypertension are important risk factors for car-
diovascular disease (CVD), the leading cause of death in post-
menopausal women.1 Aging and obesity are associated with
increased arterial stiffness (pulse-wave velocity, PWV),2–4 an
independent predictor of systolic hypertension,5 and with
cardiovascular mortality in hypertensive adults.6 Aging and
the main components of the metabolic syndrome, abdom-
inal obesity and hypertension, increase peripheral arter-
ial stiffness, especially in women.2,7,8 In postmenopausal
women, central adiposity is associated with increased aor-
tic PWV (aPWV) and leg PWV (legPWV),8 the main com-
ponents of brachial–ankle PWV (baPWV),9 explaining the
progressive increase in baPWV after menopause.10
It is well established that interventions designed to produce
weight loss reduce blood pressure (BP) in obese adults.11–13
However, the impact of a hypocaloric diet on PWV is not
Correspondence: Arturo Figueroa (afiguero@fsu.edu).
Initially submitted July 19, 2012; date of first revision October 12, 2012;
accepted for publication October 13, 2012.
416 American Journal of Hypertension 26(3) March 2013
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change with diet alone. Brachial–ankle PWV (baPWV) decreased with
diet (P = 0.04) and diet + LIRET (P = 0.01), whereas femoral–ankle PWV
(legPWV) decreased only with diet (P = 0.01). Mean arterial pressure
(MAP) decreased after LIRET (P = 0.03), diet (P = 0.04), and diet + LIRET
(P = 0.004). Carotid–femoral PWV, serum adiponectin concentration,
and insulin were not significantly affected by the interventions exam-
ined in the study. The reductions in baPWV and legPWV were corre-
lated with one another (r = 0.73, P = 0.0001), and the reductions in
legPWV and trunk FM were also correlated with one another (r = 0.36,
P = 0.03).
Conclusions
A hypocaloric diet decreases baPWV mainly by reducing legPWV, and
this reduction is related to the loss of truncal fat. Although LIRET alone
does not affect PWV or body composition, LIRET combined with diet
improves baPWV and muscle strength while preventing loss of lean
body mass in obese postmenopausal women.
Keywords: pulse-wave velocity; fat mass; leg lean mass; diet; resistance
exercise; blood pressure; hypertension.
doi:10.1093/ajh/hps050
clear. Some studies have reported reductions in aPWV after 12
weeks of such a diet in overweight and obese adults.11,14–16 In
contrast, Samaras et al.13 reported that 12 weeks of a hypoca-
loric diet failed to decrease aPWV in obese adults. Apparently,
the increase in arterial elasticity induced by weight loss occurs
earlier in peripheral than in central arteries.12,17 Thus, it is pos-
sible that a short-term diet would decrease legPWV and hence
baPWV rather than decreasing aPWV. Because leptin deter-
mines the relationship between PWV and abdominal adipos-
ity,18 a possible mechanism responsible for the reduction in
PWV with diet could be changes in adipokines and insulin
levels.19–21 Diet-induced weight loss is accompanied by loss
of lean mass (LM),11,16,22 preferentially from the legs,23 which
may aggravate the age-related loss in muscle mass known as
sarcopenia. Although high-intensity resistance exercise train-
ing (HIRET) can attenuate the diet-induced loss of muscle
1Department of Nutrition, Food and Exercise Sciences, The Florida
State University, Tallahassee, FL; 2Department of Exercise & Nutritional
Sciences, San Diego State University, San Diego, CA
© American Journal of Hypertension, Ltd 2013. All rights reserved.
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mass19 or leg LM,23 there is evidence that HIRET may increase
aPWV, legPWV, and baPWV.24,25 However, it appears that the
adverse effect of HIRET on baPWV occurs with upper-body
but not lower-body exercises25 and with concentric rather
than eccentric contractions.26 Alternatively, low-intensity
resistance exercise training (LIRET) with slow movement can
improve muscle mass27 and baPWV in young healthy adults.28
Because a negative association exists between leg LM and
PWV in older women,29 maintaining or improving leg LM
with LIRET during diet-induced weight loss may positively
influence arterial function. Therefore, we hypothesized that
the combination of diet and LIRET would produce greater
improvements in PWV and adiposity than would either inter-
vention alone in obese postmenopausal women. We also
hypothesized that LIRET would improve muscle strength and
attenuate the loss of LM induced by diet.
Methods
Subjects
Forty-five women volunteered for a randomized, parallel-
design study to evaluate the independent and combined effects
on PWV and body composition of a hypocaloric diet and
LIRET with slow movement. The subjects were overweight or
obese (body mass index (BMI) ≥ 25 kg/m2), postmeno­pausal
(≥ 1 year without menstruation), sedentary (< 60 minutes of
aerobic exercise/week and no resistance training during the
past 6 months), and nonsmokers. They were screened for
chronic diseases with a medical-history questionnaire and were
excluded if they had diabetes or cardiovascular disease or both.
All of the subjects gave written informed consent to participat-
ing in the study. The study protocol was approved by The Florida
State University Human Subject Committee (2011.5485) and
registered in Clinicaltrial.gov (NCT01371370).
Study design
Women were randomly assigned to diet or LIRET alone
or to diet + LIRET for 12 weeks. The subjects had their BP,
PWV, muscle strength, and body composition measured and
had blood samples drawn at baseline and at the end of the
study for measurement of leptin, adiponectin, and insulin.
Specimens for cardiovascular and blood measurements were
collected after an overnight fast and between 48 and 72 hours
after a lack of moderate or intense physical activity.
Subjects were asked to refrain from caffeine, alcohol,
or prescribed medication for 24 hours before each visit.
Measurements at each visit were made in the morning at the
same time of day in a quiet, temperature-controlled room
(23 ± 1 °C). Subjects rested in the supine position for at least
10 minutes before data collection. Subjects were instructed
not to make changes in their medications, diet, or exercise
habits during the study, other than those required by the
assigned intervention.
Interventions
Subjects in the LIRET group underwent 3 supervised
exercise sessions per week on nonconsecutive days. Four
Diet and Resistance Exercise on Arterial Stiffness
exercises (leg press, leg extension, leg flexion, and calf raise)
were performed on variable-resistance machines (MedX,
Ocala, FL). Women performed 2 sets of exercises involving
18–22 repetitions of each exercise, to the point of volitional
fatigue, during the first 2 weeks of the study, and 3 sets of
such exercises thereafter. Resistance was increased to main-
tain a protocol of ~20 repetitions/set as a bout of resistance
exercise because this range of repetitions has been found to
acutely decrease legPWV30and BP.31 The speed of contrac-
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tion was controlled with a metronome and concentric and
eccentric contractions were performed in phases lasting 2
seconds and 3 seconds each, respectively. Compliance was
assessed by attendance at supervised exercise sessions.
Subjects in the diet group were enrolled in a commercial
weight-loss program (Nutrisystem, Fort Washington, PA) at
no cost to themselves. The program includes portion-con-
trolled foods, which are supplemented with recommended
conventional foods (e.g. fruits, vegetables, dairy items) to
complete a structured meal plan that provides ~1,250 kcal/
day. The subjects’ diet included breakfast, lunch, and dinner
entrees plus 1 snack per day. Participants purchased their
daily choice of 4 vegetable, 3 lean protein or low-fat dairy, 3
fruit, and 1 fat servings. Beyond being given an initial brief-
ing on the diet, participants received no individual or group
counseling sessions. The meal plans were structured to pro-
vide energy from carbohydrate (55%–60%), fat (20%–25%),
and protein (20%–25%). Participants completed a 3-day
food record during the last week of the study. Subjects in
the diet + LIRET group participated in the diet and LIRET
programs described for the other two groups.
Arterial function
Pulse-wave velocity, brachial systolic BP (SBP), and dias-
tolic BP (DBP) were measured with an an automated device
for measuring PWV and ABI (VP-2000, Omron Healthcare,
Vernon Hills, IL). Blood pressure cuffs were wrapped around
both the subject’s arms and ankles while tonometers were
positioned over the right carotid and the femoral arteries to
obtain measurements of the carotid–femoral PWV (aPWV),
femoral–ankle PWV (legPWV), and baPWV. Transit time
was automatically determined from the time delay between
the feet of the pulse waves and the R-wave of an electrocra-
diogram. The distance between the common carotid and
femoral arteries was measured with a nonelastic tape meas-
ure and the brachial–ankle and femoral–ankle distances
were calculated automatically by the device used for measur-
ing PWV on the basis of the subject’s height.32 The values of
aPWV, legPWV, and baPWV were calculated from measure-
ments of transit time and the distance between 2 recording
sites.32 Mean arterial pressure (MAP) was calculated as DBP
+ 0.45 (SBP–DBP).
Body composition
Height and body weight were measured to the nearest
0.5 cm and 0.1 kg, respectively, with a stadiometer and beam
scale, respectively. Body mass index was calculated as weight
in kg/height in meters squared. Total body fat mass (FM),
trunk FM, total LM, arm LM, and leg LM were measured
American Journal of Hypertension 26(3) March 2013 417
Figueroa et al.
from whole-body dual-energy X-ray absorptiometry (DXA)
scans (GE Lunar DPX-IQ, Madison, WI).
Muscle strength
Muscle strength was assessed with the eight-repetition
maximum (8RM) test, defined as the maximum weight that
can be moved eight times through a full range of motion, for
the leg press exercise. Relative strength was calculated as leg
strength divided by leg LM.
Biomarkers
Blood samples (~10 ml) were obtained by venipunc-
ture to determine leptin, adiponectin, and insulin levels
with commercially available enzyme-linked immunosorb-
ent assay kits for leptin and adiponectin (R&D Systems,
Minneapolis, MN) and for insulin (IBL International,
Hamburg, Germany)). The sensitivities of the assays were 7.8
pg/ml, 0.246 ng/ml, and 1.76 μIU/ml for leptin, adiponectin,
and insulin, respectively. Intra- and interassay coefficients of
variation were 1.2% and 8.4%, 3.2% and 8.8%, and 2.3% and
5.4% for leptin, adiponectin, and insulin, respectively.
Statistical analysis
Data were examined for normality with the Shapiro–Wilk
test. On the basis of prior data,14,28 it was calculated that 14
subjects per group would provide 80% power (two-sided
alpha = 0.05) to detect an 8% reduction in baPWV. One-way
analysis of variance (ANOVA) was used to examine possible
group differences at baseline. The effect of the interventions
over time was evaluated with a 3 × 2 ANOVA with repeated
measures (group (diet × LIRET × diet + LIRET) × time
(before × after 12 weeks)). When a significant group × time
interaction and/or time effect was identified, between-group
and within-group differences were examined with Tukey’s
test and paired t-tests, respectively. Pearson’s correlations
were calculated to evaluate the relationship between changes
in body composition and changes in PWV and biomark-
ers. A value of P < 0.05 was considered statistically signifi-
cant. Data analysis was done with SPSS version 18.0 (SPSS,
Chicago, IL). Data are presented as mean ± SE.
Results
Four subjects dropped out the study for personal reasons
unrelated to diet or LIRET. Data are presented for 14, 13,
and 14 subjects in the LIRET, diet, and diet + LIRET groups,
respectively. Women taking prescribed medications had stable
doses of these medications for at least 1 year (Table 1), and no
changes in this were reported during the study. Attendance at
the exercise sessions in the study was greater than 86% and
89% in the LIRET and diet + LIRET groups, respectively.
Anthropometry and body composition
Subjects were overweight (n = 3) or had class I (n = 22),
II (n = 13), or III (n = 3) obesity as defined by BMI
418 American Journal of Hypertension 26(3) March 2013
Table 1. Medication use at baseline in the three study-
intervention groups
Medication LIRET Diet Diet + LIRET
HRT 1 1 1
ACE inhibitors 2 2 1
Cholesterol-lowering drugs 1 2 2
Values for medication use are number of participants.
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Abbreviations: ACE, angiotensin converting enzyme; HRT,
transdermal hormone replacement therapy; LIRET, low-intensity
resistance exercise training.
(33.8 ± 0.5 kg/m2). There were no group differences in any
variable at baseline (Tables 2 and 3). Table 2 shows body
composition and leg muscle strength. There were group ×
time interactions for weight (P = 0.04), total FM (P = 0.04),
and trunk FM (P = 0.01), for which there were decreases
after both of the study diet interventions as compared with
a lack of change after LIRET. Body weight was reduced
after the diet (5.5 ± 1.0 kg, P = 0.0001) and diet + LIRET
(4.9 ± 1.0 kg, P = 0.0001) interventions. Total FM and trunk
FM were reduced after the diet (P = 0.001 and P = 0.0001)
and diet + LIRET (P = 0.0001 and P = 0.0001) interven-
tions. The decrease in total LM after the diet (P = 0.03)
intervention did not differ from that with LIRET and diet +
LIRET. There were significant group × time interactions for
leg LM (P =0.04), absolute strength (P = 0.0001), and rela-
tive strength (P = 0.001), with leg LM decreasing after diet
(P = 0.02) as compared with LIRET (P = 0.04), and abso-
lute and relative leg muscle strength increasing after LIRET
(P = 0.001 and P = 0.008) and diet + LIRET (P = 0.0001 and
P = 0.0001) as compared with the lack of a change after the
diet intervention alone.
Arterial function
Pulse-wave velocity and BP before and after the three
interventions are shown in Table 3. No statistically signifi-
cant decrease in aPWV occurred after any of the interven-
tions (Figure 1a). There were group × time interactions
for legPWV (P = 0.004) and baPWV (P = 0.04). LegPWV
decreased after diet (P = 0.01), but not after LIRET and
diet + LIRET. The change in legPWV after diet was signifi-
cant as compared with the change after LIRET (P = 0.0001)
and diet + LIRET (P = 0.04) (Figure 1b). Although there
was a decrease in baPWV after diet (P = 0.048) and diet +
LIRET P = 0.009), only the change after diet was significant
as compared with LIRET (P = 0.04) (Figure 1c). There was
no significant group × time interaction for BP. Systolic BP
and MAP decreased after LIRET (P = 0.03 for both), diet
(P = 0.02 and P = 0.04), and diet + LIRET (P = 0.004 for
both). Brachial DBP decreased after diet+LIRET (P = 0.008),
but not after LIRET (P = 0.06) and diet (P = 0.21).
Blood biochemistry
There was a group × time interaction for leptin (P = 0.03),
where leptin decreased after both diet (P = 0.02) and diet
+ LIRET (P = 0.004) as compared with LIRET (Table 3).
 Diet and Resistance Exercise on Arterial Stiffness

Table 2. Baseline characteristics, body composition, and muscle strength before and after study interventions

LIRET Diet Diet + LIRET

Variable Before After P* Before After P* Before After P* P** Pη2

Age, years 54 ± 1 - - 54 ± 1 - - 54 ± 1 - - - -
Height, m 1.66 ± 0.02 - - 1.62 ± 0.02 - - 1.63 ± 0.02 - - - -
BMI, kg/m2 32.6 ± 1.0 - - 34.8 ± 1.2 - - 32.7 ± 1.1 - - - -

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Body weight, kg 88.4 ± 4.6 86.9 ± 4.3 0.08 89.0 ± 4.4 83.4 ± 4.6a 0.0001 86.7 ± 2.7 81.9 ± 2.5a 0.0001 0.04 0.22
Total fat mass, kg 41.8 ± 3.2 40.2 ± 2.7 0.12 44.1 ± 2.9 39.7 ± 3.1a 0.001 41.9 ± 2.0 37.5 ± 2.0a 0.0001 0.04 0.19
Trunk fat mass, kg 20.2 ± 1.8 20.0 ± 1.6 0.06 23.5 ± 1.7 20.8 ± 1.5a 0.0001 22.1 ± 1.1 19.6 ± 1.2a 0.0001 0.01 0.23
Total lean mass, kg 44.0 ± 2.1 44.2 ± 2.3 0.71 43.6 ± 1.6 42.3 ± 1.8 0.03 42.4 ± 1.3 41.6 ± 1.2 0.12 0.19 0.09
Arm lean mass, kg 4.6 ± 0.2 4.7 ± 0.3 0.70 4.8 ± 0.3 4.7 ± 0.3 0.22 4.6 ± 0.2 4.5 ± 0.2 0.32 0.19 0.09
Leg lean mass, kg 15.8 ± 0.9 16.1 ± 1.1 0.40 15.6 ± 0.8 14.6 ± 0.9a 0.02 14.9 ± 0.6 14.6 ± 0.5 0.14 0.04 0.20
Absolute strength, kg 113 ± 3 141 ± 8c 0.001 118 ± 8 111 ± 8 0.12 104 ± 5 129 ± 5c 0.0001 0.0001 0.47
Relative strength, r 7.3 ± 0.4 8.8 ± 0.8b 0.008 7.6 ± 0.6 7.3 ±.6 0.47 7.1 ± 0.4 8.8 ± 0.3b 0.0001 0.001 0.37
Values are mean ± SE.
Abbreviations: FM, fat mass; LIRET, low-intensity resistance exercise training; LM, lean mass; Pη2, partial eta-squared (size effect); r, ratio
between leg strength and leg LM.
*Within-group difference by paired t-test. **Analysis of variance group × time interaction.
aP < 0.05 different from LIRET, bP<0.01, cP<0.001, different from diet (between-group differences by Tukey’s post hoc test).

Table 3. Arterial stiffness, blood pressure, adiponectin concentrations, and insulin levels before and after study interventions

LIRET Diet Diet + LIRET

Variable Before After P* Before After P* Before After P* P** Pη2

aPWV, cm/s 1,187 ± 67 1,146 ± 48 0.55 1,175 ± 94 1,125 ± 66 0.29 1,181 ± 42 1,130 ± 30 0.26 0.99 0.001
legPWV, cm/s 1,002 ± 24 1,032 ± 18 0.06 1,017 ± 33 941 ± 19bc 0.01 1,032 ± 18 1,017 ± 19 0.17 0.004 0.35
baPWV, cm/s 1,355 ± 48 1,368 ± 29 0.73 1,388 ± 96 1,261 ± 50a 0.04 1,395 ± 35 1,335 ± 27 0.01 0.04 0.15
SBP, mm Hg 132 ± 4 125 ± 2 0.03 128 ± 3 121 ± 2 0.02 133 ± 3 124 ± 3 .004 0.68 0.02
DBP, mm Hg 82 ± 3 77 ± 2 0.06 77 ± 2 72 ± 2 0.21 79 ± 2 74 ± 2 0.01 0.65 0.02
MAP, mm Hg 105 ± 3 99 ± 2 0.03 99 ± 2 94 ± 2 0.04 104 ± 2 96 ± 3 .004 0.65 0.02
Leptin, ng/ml 43.6 ± 5.2 46.2 ± 6.6 0.58 54.4 ± 5.7 41.1 ± 5.7a 0.02 50.3 ± 8.2 38.7 ± 6.5a .004 0.03 0.22
Adipo, μg/ml 11.4 ± 1.4 10.2 ± 1.3 0.11 10.7 ± 1.6 10.6 ± 1.4 0.68 8.9 ± 1.4 9.4 ± 1.5 0.73 0.52 0.04
Insulin, mU/l 12.8 ± 2.0 12.5 ± 1.4 0.84 18.2 ± 1.7 18.6 ± 2.9 0.85 18.4 ± 2.8 17.8 ± 1.7 0.84 0.95 0.003
Values are mean ± SE.
Abbreviations: Adipo, adiponectin; aPWV, aortic pulse wave velocity; baPWV, brachial–anklePWV; DBP, diastolic blood pressure; LIRET,
low-intensity resistance exercise training; MAP, mean arterial pressure; Pη2, partial eta-squared (size effect); SBP, systolic blood pressure
*Within-group difference by paired t-test. **ANOVA group × time interaction.
aP < 0.05 and bP < 0.01 different from LIRET; cP < 0.05 different from diet + LIRET (between-group difference by Tukey’s post hoc test).

Adiponectin and insulin levels did not change significantly in leptin levels was correlated with decreases in body weight
in any group (Table 3). (r = 0.55, P = 0.002) and total FM (r = 0.35, P = 0.05).

Correlations Discussion

The change in baPWV was correlated with changes in leg-
PWV (r = 0.73, P = 0.0001) and aPWV (r = 0.64, P = 0.0001).
The decrease in legPWV was correlated with the decrease in
trunk FM (r = 0.36, P = 0.03). There was no significant corre-
lation between changes in legPWV and leg LM. The decrease
We examined two interventions that individually and
combined with one another would potentially reduce
arterial stiffness and improve body composition. We used
a prepackaged structured meal program and an exercise
program consisting of four leg exercises at low-intensity

American Journal of Hypertension 26(3) March 2013 419

Figueroa et al.

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Figure 1. Changes in aortic (a), leg (b), and brachial–ankle (c) arterial stiffness after 12 weeks of low-intensity resistance exercise training (LIRET), diet,
and diet + LIRET.Abbreviations are: PWV, pulse wave velocity; aPWV, aortic PWV; legPWV, leg PWV; baPWV, brachial–ankle PWV. Values are mean ± SE.
*P = 0.04, †P = 0.01different from before intervention (paired t-test). aP = 0.04 and bP = 0.0001 different from LIRET; cP = 0.04 different from diet + LIRET
(Tukey’s post hoc test).
420 American Journal of Hypertension 26(3) March 2013

that requires approximately 30 minutes per session. The
major findings of our study indicate that 12 weeks of diet or
LIRET or both have no adverse effect on aPWV. However,
diet alone or combined with LIRET can decrease body
weight, total FM, and trunk FM concurrently with improve-
ments in baPWV. We also show that LIRET does not affect
adiposity and PWV, but that it decreases BP and prevents
the loss of total LM and leg LM induced by diet in obese
postmenopausal women.
Both of the diet interventions examined in our study
caused a modest weight loss of ~5.1 kg (5.8%), which was
due primarily to a reduction in body FM in the trunk. Our
data show that despite a reduction in adiposity after diet and
diet + LIRET, the ~51 cm/s reduction in aPWV with these
interventions was not statistically significant. In accord with
our findings, Samaras et al.13 observed similar nonsignifi-
cant reductions in aPWV (50 cm/s) and body weight (~6 kg)
after 12 weeks of a hypocaloric diet in obese adults. In con-
trast, previous studies have reported a decrease in aPWV of
from 61 cm/sec to 187 cm/s after 12 weeks of diet-induced
weight loss (~6 to 8 kg) in adults who were overweight or
had class I obesity.11,14,15 Dengo et al.11 demonstrated that
the reduction in aPWV was associated with the magnitude
of weight loss in middle-aged and older adults. Because a
difference in aPWV of 40–70 cm/s exists in obese as com-
pared with nonobese individuals,4,33 the reduction in aPWV
observed after diet and diet + LIRET in our study may have
a positive influence on cardiovascular function in obese
postmenopausal women.
Although baPWV includes aPWV and legPWV, it has
been considered a measure of central arterial stiffness
because it is highly correlated with aPWV, and both baPWV
and aPWV have similar associations with cardiovascular risk
factors.9,32,34 We showed that legPWV decreased significantly
with diet alone (~72 cm/s), whereas the reduction in leg-
PWV with diet + LIRET was minimal (~15 cm/s). Previous
studies have reported improvements in peripheral arterial
elasticity after body-weight reduction,12.22 but to the best of
our knowledge, the effect of diet on legPWV and baPWV
has not been reported. Since legPWV is a main determinant
of baPWV,9 there was a significant decrease in baPWV with
diet (~126 cm/s). In addition, there was a small but signifi-
cant decrease in baPWV after diet + LIRET (~60 cm/s). It is
possible that the concurrent decreases in aPWV and legPWV
may have contributed to reducing baPWV in the interven-
tion consisting of diet + LIRET. Our findings indicate that
there is an early effect of diet on legPWV that influences
baPWV, a marker of central arterial stiffness.9 Therefore, diet
with and without LIRET may be recommended to attenu-
ate the progressive increase in baPWV observed following
menopause.10
Our data show that neither adiposity nor PWV were
affected by LIRET in obese postmenopausal women. In
accord with our findings, previous studies have shown that
neither whole-body nor leg HIRET affects either aPWV in
elderly normotensive adults35.36 or baPWV in young adults.25
On the other hand, a recent study found that whole-body
HIRET increased aPWV and legPWV in middle-aged adults
with prehypertension or hypertension.24 It is important to
note that our subjects had similar risk factors to those in the
Diet and Resistance Exercise on Arterial Stiffness
study conducted by Collier et al.24 However, our leg LIRET
intervention, which was of longer duration and lower inten-
sity than in the previous study, did not have a deleterious
effect on aPWV, legPWV, or baPWV.24 Although the small
increase in legPWV after LIRET alone was not statistically
significant, LIRET may have attenuated the diet-induced
decrease in legPWV in the diet + LIRET intervention. We
found no correlation between reductions in baPWV and BP
(SBP and MAP), as previously shown in middle-aged and
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older adults after 12 weeks of a hypocaloric diet.11 Thus, the
present findings may indicate that the decreases in baPWV
with diet and diet + LIRET are not determined by the dis-
tending effect of BP on the arterial wall.
A main concern associated with a hypocaloric diet is the
loss of DXA-measured LM.11 occurs in the legs.23 Our data
show that 12 weeks of diet reduced total LM (~1.2 kg) and
leg LM (~0.7 kg) in obese women. Straznicky et al.37 reported
a similar loss of total LM after 12 weeks of diet alone and
diet + aerobic exercise training in obese adults. In agree-
ment with the findings in the present study, Anton et al.38
found no increase in leg LM after 13-weeks of HIRET alone
in middle-aged adults. In a previous study,23 HIRET attenu-
ated the significant loss of leg LM (~0.9 kg) observed in obese
older adults. We demonstrated for the first time that LIRET
is an effective countermeasure for the negative effects of a
hypocaloric diet on leg LM. Importantly, leg muscle strength
increased similarly in both the LIRET-only and diet + LIRET
interventions in our study. Because sarcopenia, specifically as
a reduction in leg LM,2 and muscle strength are negatively
associated with baPWV,39 our findings may support the use of
LIRET to prevent loss of LM and improve leg muscle strength
and baPWV in obese postmenopausal women undertaking a
dietary weight-loss intervention. The decrease in leptin in our
study was similar with both the diet and diet + LIRET inter-
ventions. Reductions in body weight and total FM were posi-
tively correlated with changes in leptin. In accord with our
data, past studies have reported decreases in leptin levels4,20,21
without an effect on adiponectin13,20 or insulin levels follow-
ing weight loss.13,17 Indeed, leptin but not insulin,4 adiponec-
tin, or C-reactive protein are related to aPWV, legPWV,8 and
baPWV.40 Increased abdominal adiposity has been positively
associated with baPWV,40 and with legPWV8 in women. It is
likely that in our study a reduced concentration of leptin may
have influenced the decrease in legPWV through reductions
in FM, which occurred primarily in the trunk.
The present study has several limitations. It included
obese postmenopausal women with prehypertension or
stage 1 hypertension. Whether our findings remain true for
men, nonobese, or normotensive individuals is unknown.
The duration of LIRET in the study was 12 weeks, and a
longer intervention may be needed to elicit increases in LM
detectable by DXA in postmenopausal women.41 Another
limitation of our study is that it did not have a nonexercise
control group. However, because LIRET did not affect PWV
or body composition, it provided a control group for the
study. Additionally, a relatively small sample size may have
limited the effect of weight loss on aPWV and correlations
between body composition and PWV.
In conclusion, our study demonstrates that a hypocaloric
diet with and without LIRET results in similar decreases in
American Journal of Hypertension 26(3) March 2013 421
Figueroa et al.
FM and baPWV. Although LIRET does not improve LM or
reduce PWV, the addition of LIRET to diet prevents the loss
of LM and improves muscle strength in obese postmeno-
pausal women. Our data demonstrate the benefits of adding
LIRET to a weight-loss intervention in obese postmenopau-
sal women.
Acknowledgments
We extend our gratitude to David Thomas for his techni-
cal expertise. This study was supported by Nutrisystem Inc.
Clinicaltrial.gov register, NCT01371370.
Disclosure
Dr. Daggy works for Nutrisystem, Inc., in addition to being
an adjunct faculty member at The Florida State University.
The other authors declare no conflict of interest.
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