Journal of Human Hypertension (2014) 28, 246–250

& 2014 Macmillan Publishers Limited All rights reserved 0950-9240/14

www.nature.com/jhh

ORIGINAL ARTICLE
Eight weeks of stretching training reduces aortic wave reflection
magnitude and blood pressure in obese postmenopausal women
A Wong and A Figueroa

The augmentation index (AIx, a marker of wave reflection) is reduced and peripheral artery vasodilation increased following acute
stretching exercise. We examined the effects of stretching training (ST) on arterial function, blood pressure (BP) and sympathetic
vasomotor modulation. Twenty-eight obese postmenopausal women (57±1 years) were randomized to a ST (n ¼ 14) or no-exercise
control (CON) group ( n ¼ 14). ST included stretching exercises 3 days week  1 for 8 weeks. Brachial (b) and aortic (a) systolic BP
(SBP), diastolic BP (DBP), mean arterial pressure (MAP), heart rate (HR), brachial-ankle pulse wave velocity (baPWV), carotid–femoral
PWV (aPWV), femoral–ankle PWV (faPWV), AIx, low-frequency component of SBP (LFSBP) and sit/reach score (SRS) were measured
before and after interventions. There were significant decreases in bSBP (Po0.05), aSBP (Po0.01), aDBP (Po0.05), aMAP (Po0.01),
aAIx (Po0.05) and LFSBP (Po0.05) after ST compared with CON. SRS significantly (Po0.01) increased after ST but not after CON.
There were no significant effects (P40.05) on HR, baPWV, aPWV and faPWV after ST or CON. Eight weeks of ST decreases BP, AIx
and LFSBP in obese postmenopausal women. Our findings show that ST reduces peripheral and central BP, wave reflection
magnitude and vascular sympathetic activity in obese postmenopausal women with prehypertension and hypertension.

Journal of Human Hypertension (2014) 28, 246–250; doi:10.1038/jhh.2013.98; published online 17 October 2013
Keywords: stretching; blood pressure; augmentation index; vascular sympathetic activity

INTRODUCTION rehabilitation via improved flexibility.11 Flexibility decreases with

Menopause and obesity are associated with impaired aortic age and obesity,12 and poor trunk flexibility has been associated
hemodynamics, increased sympathetic modulation and arterial with increased baPWV in middle-aged and older individuals.13
stiffness (pulse wave velocity (PWV)).1,2 The increases in central Although it is clear that stretching increases flexibility,11 evidence
(carotid-femoral PWV (aortic PWV))3 and systemic PWV (brachial- on the cardiovascular effects of stretching training (ST) is limited
ankle (baPWV))4 observed in early postmenopausal women and unclear. Stretching exercise has been shown to acutely
appear to be associated with Oestrogen deficiency. This decrease AIx and increase nitric oxide-dependent vasodilation.14
increased PWV may contribute to the high brachial systolic Reduced AIx following acute resistance and aerobic exercise is
blood pressure (bSBP) often observed at the prehypertension or attributed to decreased wave reflection magnitude and
stage-1-hypertension stages in early postmenopausal women.3,4 vasodilation of muscular arteries.15,16 Recently, 13 weeks of ST
Furthermore, impaired vasodilation and vascular sympathetic resulted in improved carotid artery compliance and pulse pressure
activity may negatively influence aortic hemodynamics and PWV in the absence of changes in aortic PWV (aPWV) and bBP in
by increasing the vasomotor tone.2 Increased PWV and magnitude normotensive middle-aged and older adults.17 In addition, Mueck-
of the reflected wave cause an increase in augmented pressure Weymann et al.18 found an improved sympathovagal balance,
(AP), the main determinant of increased aortic SBP (aSBP) and suggesting that reduced sympathetic outflow may occur after ST
augmentation index (AIx),5 markers of ventricular workload.6 in individuals with reduced muscular flexibility. Thus it is possible
Moreover, increased left ventricular workload reduces blood that ST may improve aortic hemodynamics parameters and
supply to the myocardium in postmenopausal women, which baPWV through reduced wave reflection and sympathetic activity.
may explain the higher risk for cardiovascular complications in The purpose of this study was to evaluate the effectiveness of
women compared with age-matched men.2,5 an 8-week ST program on arterial function in obese postmeno-
Physical activity has been shown to have an important role in pausal women. We hypothesized that ST would decrease aBP, AIx,
controlling cardiovascular disease risk factors. The positive effects AP, baPWV and sympathetic vasomotor modulation in obese
of aerobic exercise on BP and PWV have been well documented.7 postmenopausal women.
Although the effects of resistance exercise training on BP and
arterial stiffness are contradictory,7–9 it has been shown that when
combined with aerobic exercise it improves BP and baPWV.10 MATERIALS AND METHODS
However, special populations such as the elderly and obese may Subjects
have physical and/or musculoskeletal limitations, which may Thirty (age, 50–65 years) postmenopausal women volunteered to
inhibit their participation in conventional exercise modalities. participate in the present study. Menopause was defined as the absence
Stretching is a modality that is usually part of an exercise of menstruation for at least 1 year. Subjects were recruited from
program and is widely used for muscle injury prevention and Tallahassee, FL, USA and surrounding areas through flyers and word of

Department of Nutrition, Food, and Exercise Sciences, The Florida State University, Tallahassee, FL, USA. Correspondence: Dr A Figueroa, Department of Nutrition, Food and
Exercise Sciences, The Florida State University, 120 Convocation way, Tallahassee, FL 32306-1493, USA.
E-mail: afi[email protected]
Received 4 June 2013; revised 7 August 2013; accepted 3 September 2013; published online 17 October 2013
 Stretching and blood pressure
A Wong and A Figueroa
247
mouth. The inclusion criterion was postmenopausal women between the Blood pressure variability
ages of 50–65 years, a BP between 121/81 and 159/99 mm Hg, and a body Five minutes of continuous BP was obtained from the middle finger using
mass index (BMI)430 kg m  2. Exclusion criteria included smoking, a Finometer device (TNO Biomedical Instrumentation, Amsterdam, The
cardiovascular disease, diabetes, and musculoskeletal problems that would Netherlands). Blood pressure pulse intervals were automatically detected
limit stretching exercises and the use of medication or hormone using the commercially available software (WinCPRS, Turku, Finland). The
replacement therapy during the 6 months before the study. All women SBP time series was resampled at 5 Hz and the continuous data stream
were sedentary, defined as having o1 h of regular exercise per week in the passed through a low-pass impulse response filter with a cutoff frequency
previous year. All of the subjects gave written informed consent before of 0.5 Hz. Autoregressive model transformation was used to obtain power
their inclusion in the study. The study protocol was approved by The spectrums. The power was calculated by measuring the area under the
Florida State University Human Subject committee and registered in peak of the power spectra density curve. Power spectra within the 0.04–
Clinicaltrial.gov (NCT01741766). 0.15 Hz range were defined as the low-frequency component of SBP
(LFSBP) and taken as an estimate of sympathetic vasomotor modulation.23

Study design Stretching training

We used a randomized, parallel design. Subjects were randomly assigned The ST group underwent supervised sessions in 3 nonconsecutive days per
to a ST group (n ¼ 15) or a non-exercising control (CON, n ¼ 15) group. week for 8 weeks. Subjects performed 1 set of 18 active and 20 passive
Before baseline measurements, allocation was stratified for BMI (430.0– stretches with at least 2 of them for the major muscle groups (pectoralis
o35 orZ35 kg m  2), and the sequence was generated by a computer- major and minor, latissimus dorsi, bicep brachii, triceps, deltoid, trapezius,
based number. Measurements were performed at baseline and after 8 illiopsas, gluteus, quadriceps, hamstring, leg adductors and gastrocnemius)
weeks in the afternoon hours after at least 4 h postprandial and at the through the full range of motion. The 38 stretches were performed in the
same time of the day (± 1 h) to minimize potential diurnal variations and standing (20), sitting (8), and lying (10) positions. Although the sessions
the effects of food intake. Subjects refrained from caffeine and alcohol for included exercise for the whole body, subjects performed predominantly
24 h and from moderate-to-intense physical activity for at least 48 h before (70%) upper-body or lower-body stretches in alternate days. The stretched
and after ST. In the ST group, 8-week measurements were performed at muscle was held for 30 s at the point of maximal exertion (defined as
least 48 h after the last stretching session. BP, arterial tonometry, PWV and RPE418) followed by a 15-s relaxation period. In the passive stretches, the
heart rate (HR) were performed in the supine position after at least 10 min researchers pushed or pulled the specific body part until they received
of rest in a quiet temperature-controlled room (23±1 1C). Subjects were verbal acknowledgment that the stretch was felt at maximal exertion for
instructed not to do changes in their regular lifestyle habits during the 30 s. Each session lasted B50 min.
study. They provided a 3-day food and exercise log during the first and last
week of the study.
Statistical analysis
Data were examined for normality with the Shapiro–Wilk test. Student’s
Pulse wave velocity, bBP and heart rate t-test was used to detect possible difference in parameters between groups
bBP and PWV were measured using an automatic device (VP-2000; Omron at baseline. A two-way analysis of variance with repeated measures (group
Healthcare, Vernon Hills, IL, USA). Appropriate-size BP cuffs were wrapped (CON and ST)  time (before and after 8 weeks)) was used to determine the
around both arms (B2 cm above the antecubital fossa with the position effects of the intervention over time. If a significant interaction or main
mark aligned with the brachial artery) and ankles (the bottom edge of the effect was noted, a paired t-test was used for post hoc comparisons.
cuff above the maleoli with the sensor aligned with the posterior tibial Statistical significance was defined a priori as Po0.05. Statistical analyses
artery), and two tonometers were placed over the right carotid and were performed using the SPSS version 20.0 (SPSS Inc., Chicago, IL, USA).
femoral arteries to obtain PWV measurements from three arterial A power calculation done a priori determined that a population of 28
segments: baPWV, carotid–femoral PWV (aortic), and femoral–ankle PWV subjects would allow the observation of a difference of 3–5% between the
(faPWV). The carotid, femoral, brachial and ankle arterial waveforms were treatments on central BP and AIx with a power of 80%.14,17
recorded simultaneously by tonometers, and the transient time was
calculated automatically by relating the foot of each waveform to the
R-wave of the electrocardiogram. The distance from the carotid and RESULTS
femoral artery was measured with a nonelastic tape measure as a straight Data are shown as means±s.e. Two subjects dropped out of the
line, while the distance between sampling points of baPWV and faPWV was study for personal reasons unrelated to ST or CON. Data are
calculated automatically according to the height of the subjects.19 The presented for 28 subjects (14 subjects in each group). Attendance
values of baPWV, aPWV and faPWV were calculated from measurements of to the ST session was 496%.
transit time and the distance between two recording sites.19 Mean arterial
pressure (MAP) was calculated as DBP þ 0.45 (SBP  DBP). The intraclass
correlation coefficient for all measurements derived from BP and PWV, Subject characteristics
calculated on 2 separate days in a subsample, was 40.92. Age, height, weight, BMI and flexibility values at baseline and
after 8 weeks for the CON and ST groups are presented in
Table 1. Baseline parameters in the two groups were not
Pulse wave analysis
bSBP and diastolic BP (DBP) were used to calibrate radial waveforms, which
were obtained from a 10-s epoch using a high-fidelity tonometer (SPT- Table 1. Subject characteristics before and after 8 weeks of control or
301B; Millar Instruments, Houston, TX, USA). Aortic pulse waveforms were stretching training
derived using a validated generalized transfer function (SphygmoCor,
AtCor Medical, Sydney, NSW, Australia). The aortic wave is composed of a Variable Control Stretching training
forward wave, caused by stroke volume ejection, and a reflected wave that
returns to the aorta from peripheral sites.20 AP is the difference between
the second (P2) and first (P1) systolic peaks. The AIx was defined as the AP Before After Before After
expressed as a percentage of the aortic pulse pressure. AIx was normalized
to a HR of 75 beats min  1 (AIx@75), because it is influenced by HR.21 Age (years) 56±1 — 57±1 —
Transit time of the reflected wave (Tr) indicates the round-trip travel of the Height (m) 1.62±0.02 — 1.60±0.02 —
forward wave to the peripheral reflecting sites and back to the aorta.20 Body weight (kg) 89.4±4.0 89.0±4.0 87.6±4.1 87.7±4.1
Systolic tension time index (TTI) was considered as a measure of BMI (kg m  2) 34.0±1.0 33.8±1.0 34.2±1.2 34.3±1.2
myocardial oxygen demand.22 The average of two measurements of bBP Sit and reach 26±2 27±2 24±2.0 29±2**z
and high-quality (operator index X80%) aortic hemodynamics was used in score (cm)
the analysis. The intraclass correlation coefficient for all measurements Abbreviation: BMI, body mass index. **Po0.001 different from before.
derived from pulsewave analysis, calculated on 2 separate days in a zPo0.01 different from CON. Data are mean±s.e.
subsample, was 40.90.

& 2014 Macmillan Publishers Limited Journal of Human Hypertension (2014) 246 – 250
 Stretching and blood pressure
A Wong and A Figueroa
248
significantly different. There was a significant group  time Hemodynamics, arterial stiffness and sympathetic vascular activity
interaction (Po0.01) for sit/reach score as it significantly increased Hemodynamic, arterial stiffness and autonomic variables at
after ST (5±1 cm, Po0.001) but not after CON. There were baseline and after 8 weeks for the CON and ST groups are
no significant effects (P40.05) on body weight and BMI after presented in Table 2. There were significant group  time
ST or CON. interactions (Po0.05) for bSBP, aSBP, aDBP, aMAP, P2, AP, AIx,

Table 2. Hemodynamic variables before and after 8 weeks of control or stretching training

Variable Control Stretching training

Before After Before After

Brachial SBP (mm Hg) 137±4 138±4 133±3 128±3*w

Brachial DBP (mm Hg) 80±2 79±2 77±2 73±2*
Brachial MAP (mm Hg) 104±3 103±3 102±3 97±3**
Aortic SBP (mm Hg) 128±4 127±4 125±3 118±3**z
Aortic DBP (mm Hg) 84±4 84±4 78±2 74±2*w
Aortic MAP (mm Hg) 103±4 102±4 99±3 91±3**z
Aortic P1 (mm Hg) 113±4 113±4 108±3 106±3
Aortic P2 (mm Hg) 128±4 127±4 125±3 119±3**w
AP (mm Hg) 15±2 14±2 17±2 13±1**w
Aortic AIx (%) 32±2 32±3 35±3 29±3*w
Aortic AIx@75 (%) 28±2 29±3 30±3 23±2*w
Time of reflection (ms) 135±3 137±4 129±6 145±5
TTI (mm Hg s min  1) 2574±96 2542±98 2516±95 2350±99**w
Heart rate (beats min  1) 67±3 67±3 64±2 63±2
Aortic PWV (cm s  1) 1132±41 1128±48 1143±34 1121±42
faPWV (cm s  1) 979±31 972±30 947±22 917±19
baPWV (cm s  1) 1397±40 1386±47 1359±29 1319±33
LFSBP (mm Hg2) 7.05±0.83 7.00±0.78 7.24±0.84 5.62±0.53*w
Abbreviations: AIx, augmentation index; AIx@75, AIx adjusted to 75 beats min  1; AP, augmented pressure; baPWV, brachial–ankle PWV; DBP, diastolic blood
pressure; faPWV, femoral–ankle PWV; LFSBP, low-frequency component of SBP; MAP, mean arterial pressure; P1, first systolic peak; P2, second systolic peak;
PWV, pulse wave velocity; SBP, systolic blood pressure; TTI, tension time index. *Po0.05, **Po0.01 different from before. wPo0.05, zPo0.01 different from
CON. Data are mean±s.e.

Figure 1. Changes in aortic systolic blood pressure (SBP; a), second systolic peak (P2; b), augmented pressure (AP; c) and aortic augmentation
index (AIx; d) after 8 weeks of stretching training (ST) and control (CON). Values are mean±s.e. *Po0.05, **Po0.01 different from before.
wPo0.05, zPo0.01 different from CON.

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AIx@75, TTI and LFSBP. bSBP (  5±2 mm Hg), aSBP associated with AP31 and P2 but not Tr in women.25 In the present
(  7±2 mm Hg, Figure 1a), aDBP (  4±1 mm Hg), aMAP study, AP was reduced exclusively due to a decrease in P2. As no
(  8±2 mm Hg), P2 (  6±2 mm Hg, Figure 1b), AP change in P1 and Tr occurred after ST, the decrease in P2 may
(  4±1 mm Hg, Figure 1c), AIx (  6±2%, Figure 1d), AIx@75 explain the reduction in AIx. In contrast to our findings, previous
(  7±2%,), TTI (  166±42 mm Hg  s min  1) and LFSBP studies have reported no change in aortic AIx following low- and
(  1.62±0.57 mm Hg2) significantly (Po0.05) decreased following high-intensity resistance training in obese postmenopausal
ST compared with no changes after CON. bDBP (  4±1 mm Hg), women29 and older adults30 with prehypertension. Thus, due to
BMAP (  5±2 mm Hg) significantly (Po0.05) decreased after 8 the beneficial effects on AIx, ST should not be ignored in an
weeks of ST, but the reduction was no different compared with exercise program for postmenopausal women.
CON. There were no significant effects (P40.05) after ST or CON We found that ST did not change aPWV, faPWV and baPWV.
on HR, Tr, P1, aPWV, faPWV and baPWV. Our observation is consistent with a previous finding of no
change in aPWV in middle age and adults after 13 weeks of a
stretching intervention.17 In addition, resistance training alone and
DISCUSSION its combination with aerobic training did not affect aPWV.17
The novelty of this study is that 8 weeks of ST improved bBP, Decreases in aPWV have been previously reported after 4 weeks of
aortic hemodynamic parameters, sympathetic vasomotor activity aerobic training in prehypertensives and stage-1 hypertensives.7
and trunk flexibility. To the best of our knowledge, this is the first Conversely, high-intensity resistance training increases aPWV and
report of the effects of ST on aortic hemodynamics and vascular faPWV, the main components of baPWV,19 in older adult with
sympathetic control. prehypertension and stage-1 hypertension.7 Interestingly, the
There is evidence that indicates that Oestrogen deficiency may combination of resistance training and aerobic training has
contribute to the increase in BP, aPWV and baPWV in post- reduced baPWV by 0.8 m s  1 in postmenopausal women.10
menopausal women.3,4 Furthermore, wave reflection magnitude Although not significant, baPWV (B0.4 m s  1, P ¼ 0.08) and
leading to increased aSBP and AIx and consequent greater left faPWV (B0.3 m s  1, P ¼ 0.11) showed a trend to decrease after
ventricle afterload and myocardial ischemia is greater in ST. It has been previously reported that a bout of external
postmenopausal women than in age-matched men.2,24 This is mechanical muscle compressions of leg arteries acutely decreases
particularly evident in older women with prehypertension and faPWV due to local vasodilation.32 As we stretched muscle groups,
hypertension.2,25 Therefore, lifestyle interventions that improve BP we speculate that peripheral arteries are compressed, resulting in
and arterial function may reduce the risk for cardiovascular reduced peripheral PWV following ST.
complications in postmenopausal women with high BP. Increased P2 and HR are associated with decreased myocardial
We found that ST decreased bSBP (B5 mm Hg), bDBP (B4 mm perfusion in postmenopausal women through increased left
Hg) and bMAP (B5 mm Hg). Similar decreases in bSBP, bDBP and ventricular load (aSBP and pulse pressure) and oxygen demand.24
bMAP have been reported after 8 weeks of static leg exercise It has been recently reported that obesity may have a significant
training26 in healthy young males. Moreover, both aerobic and role in the greater ventricular dysfunction seen in women
resistance exercise training have reduced SBP and DBP by 4 and compared with men.2,24 We found that ST reduced TTI, a
3–4 mm Hg, respectively, in older adults with prehypertension and surrogate marker of myocardial oxygen demand. In the current
hypertension.7 Conversely, although not significant, a trend study, the reduction in P2 and aSBP may have influenced the
towards a decrease in resting bSBP (B3 mm Hg) was reported decrease in TTI after ST,33 as there was no change in HR.
after 13 weeks of ST in normotensive middle-aged and older One possible mechanism underlying the effects of ST on arterial
adults.17 It is possible that the reductions in BP following ST would function and BP may be related to the improvements in
have been influenced by a high volume of stretching exercises sympathetic control of vasomotor tone. In the current study, ST
and the BP level of our subjects. decreased the LFSBP, a marker of vascular sympathetic activity.23
In the present study, we found that ST decreased aSBP Considering that sympathetic nerve activity regulates the vascular
(B7 mm Hg) and aDBP (B4 mm Hg). There is evidence suggesting tone, our data suggest that the reduction in BP and wave
that ST has a positive effect on central (carotid) BP through an reflection magnitude could be partially attributed to a decrease in
increase in artery compliance in middle-aged and older adults.17 vascular sympathetic activity after ST. Another possible
Although not significant, similar decreases in central (carotid) SBP mechanism for the effects of ST on arterial function is an
(B7 mm Hg) were found after ST on the previously mentioned improved endothelial-mediated vasodilation. A stretching exercise
study by Cortez-Cooper et al.17 In contrast, no changes in aSBP session acutely improved nitric oxide-mediated vasodilation in
and aDBP were found after 16 weeks of ST in older individuals.27 patients with coronary artery disease.14 A recent study by Wang
The discrepancy would be related to higher session frequency (3 et al.34 showed that in vivo stretch of pig aortas increases blood
vs 2 per week) and more exercises per session (38 vs 12) in the flow, suggesting vasodilation. As in the present study we found
present study compared with the previous study.27 Notably, attenuated LFSBP, the improvements in aortic hemodynamics
reductions in aSBP of X7 mm Hg have been shown after 6 weeks after ST might be related to decreased vasomotor tone and
of aerobic exercise in overweight and obese individuals28 and improved vasodilation as a result of attenuated sympathetic
after 12 weeks of resistance exercise29 in obese postmenopausal activity.
women with mildly high BP. Similarly, Taaffe et al.30 reported Trunk flexibility was increased by B5 cm after ST. Consistent
reduced aSBP (B6 mm Hg) and DBP (3 mm Hg) following 20 with the present study, trunk flexibility improvements have been
weeks of high-intensity resistance training in older adults with reported after 16 weeks of active stretching in young women.35 In
prehypertension. However, many obese postmenopausal women the present study, the subjects had poor trunk flexibility (B24 cm),
may not be willing to perform prolonged and/or intense aerobic which has been associated with an increased aPWV and baPWV.13
or resistance exercise. After ST, even though trunk flexibility significantly increased, it
We found that ST over 8 weeks decreased AIx. A recent study was still categorized as poor trunk flexibility.13 It has been
showed that a 15-min active stretching session acutely decreased previously shown that there is a linear relationship between the
AIx during the 15-min post stretching due to improved frequency of ST with increase in flexibility.11 Therefore, we can
endothelial-mediated vasodilation.14 AIx is influenced by the speculate that a more frequent stretching intervention might be
amplitude of both incident (P1) and reflected wave (P2) and required to improve PWV.
thereby is increased by wave reflection (AP and P2), as well as the In conclusion, 8 weeks of ST was effective in decreasing bBP,
timing (Tr) of the reflected wave.6,20 Elevated aSBP and AIx are aBP and AIx through improvements in wave reflection magnitude

& 2014 Macmillan Publishers Limited Journal of Human Hypertension (2014) 246 – 250
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and vascular sympathetic activity in obese postmenopausal 12 Vaquero-Cristobal R, Martinez Gonzalez-Moro I, Alacid Carceles F, Ros Simon E.
women. Future studies should aim to evaluate the long-term Strength, flexibility, balance, resistance and flexibility assessment according to
effects of ST on arterial stiffness and the use ST as an adjunct body mass index in active older women. Rev Esp Geriatr Gerontol 2013; 48(4):
therapy to prevent the development or progression of hyperten- 171–176.
sion in obese postmenopausal women. 13 Yamamoto K, Kawano H, Gando Y, Iemitsu M, Murakami H, Sanada K et al. Poor
trunk flexibility is associated with arterial stiffening. Am J Physiol Heart Circ Physiol
2009; 297(4): H1314–H1318.
14 Hotta K. Stretching exercise improves vascular endothelial function and periph-
eral circulation in patients with ischemic heart disease. Eur Heart J 2010; 31: 382.
15 Munir S, Jiang B, Guilcher A, Brett S, Redwood S, Marber M et al. Exercise reduces
arterial pressure augmentation through vasodilation of muscular arteries in
What is known about this topic?
humans. Am J Physiol Heart Circ Physiol 2008; 294(4): H1645–H1650.
 Poor trunk flexibility is associated with increased aortic PWV and
16 Figueroa A, Vicil F. Post-exercise aortic hemodynamic responses to low-intensity
baPWV in middle-aged and older individuals.
resistance exercise with and without vascular occlusion. Scand J Med Sci Sports
 Acute stretching exercise acutely decreases AIx and increases NO
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production.
17 Cortez-Cooper MY, Anton MM, Devan AE, Neidre DB, Cook JN, Tanaka H. The
 Stretching training improves carotid artery compliance and pulse
effects of strength training on central arterial compliance in middle-aged and
pressure in middle-aged and older adults.
older adults. Eur J Cardiovasc Prev Rehabil 2008; 15(2): 149–155.
18 Mueck-Weymann M, Janshoff G, Mueck H. Stretching increases heart rate varia-
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bility in healthy athletes complaining about limited muscular flexibility. Clin Auton
 Stretching training reduces brachial and aortic BP, AIx and vascular
Res 2004; 14(1): 15–18.
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19 Yamashina A, Tomiyama H, Takeda K, Tsuda H, Arai T, Hirose K et al. Validity,
pausal women.
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20 Nichols WW, Singh BM. Augmentation index as a measure of peripheral vascular
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21 Wilkinson IB, MacCallum H, Flint L, Cockcroft JR, Newby DE, Webb DJ. The
CONFLICT OF INTEREST influence of heart rate on augmentation index and central arterial pressure in
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22 Chemla D, Nitenberg A, Teboul JL, Richard C, Monnet X, le Clesiau H et al.
Subendocardial viability ratio estimated by arterial tonometry: a critical evaluation
in elderly hypertensive patients with increased aortic stiffness. Clin Exp Pharmacol
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