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Oct 17, 2013 - magnitude and blood pressure in obese postmenopausal women ... (SBP), diastolic BP (DBP), mean arterial pressure (MAP), heart rate (HR), ...
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 Menopause and obesity are associated with impaired aortic hemodynamics, increased sympathetic modulation and arterial stiffness (pulse wave velocity (PWV)).1,2 The increases in central (carotid-femoral PWV (aortic PWV))3 and systemic PWV (brachialankle (baPWV))4 observed in early postmenopausal women appear to be associated with Oestrogen deficiency. This increased PWV may contribute to the high brachial systolic blood pressure (bSBP) often observed at the prehypertension or stage-1-hypertension stages in early postmenopausal women.3,4 Furthermore, impaired vasodilation and vascular sympathetic activity may negatively influence aortic hemodynamics and PWV by increasing the vasomotor tone.2 Increased PWV and magnitude of the reflected wave cause an increase in augmented pressure (AP), the main determinant of increased aortic SBP (aSBP) and augmentation index (AIx),5 markers of ventricular workload.6 Moreover, increased left ventricular workload reduces blood supply to the myocardium in postmenopausal women, which may explain the higher risk for cardiovascular complications in women compared with age-matched men.2,5 Physical activity has been shown to have an important role in controlling cardiovascular disease risk factors. The positive effects of aerobic exercise on BP and PWV have been well documented.7 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 However, special populations such as the elderly and obese may have physical and/or musculoskeletal limitations, which may inhibit their participation in conventional exercise modalities. Stretching is a modality that is usually part of an exercise program and is widely used for muscle injury prevention and

rehabilitation via improved flexibility.11 Flexibility decreases with age and obesity,12 and poor trunk flexibility has been associated with increased baPWV in middle-aged and older individuals.13 Although it is clear that stretching increases flexibility,11 evidence on the cardiovascular effects of stretching training (ST) is limited and unclear. Stretching exercise has been shown to acutely decrease AIx and increase nitric oxide-dependent vasodilation.14 Reduced AIx following acute resistance and aerobic exercise is attributed to decreased wave reflection magnitude and vasodilation of muscular arteries.15,16 Recently, 13 weeks of ST resulted in improved carotid artery compliance and pulse pressure in the absence of changes in aortic PWV (aPWV) and bBP in normotensive middle-aged and older adults.17 In addition, MueckWeymann et al.18 found an improved sympathovagal balance, suggesting that reduced sympathetic outflow may occur after ST in individuals with reduced muscular flexibility. Thus it is possible that ST may improve aortic hemodynamics parameters and baPWV through reduced wave reflection and sympathetic activity. The purpose of this study was to evaluate the effectiveness of an 8-week ST program on arterial function in obese postmenopausal women. We hypothesized that ST would decrease aBP, AIx, AP, baPWV and sympathetic vasomotor modulation in obese postmenopausal women.

MATERIALS AND METHODS Subjects Thirty (age, 50–65 years) postmenopausal women volunteered to participate in the present study. Menopause was defined as the absence of menstruation for at least 1 year. Subjects were recruited from 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 ages of 50–65 years, a BP between 121/81 and 159/99 mm Hg, and a body mass index (BMI)430 kg m  2. Exclusion criteria included smoking, cardiovascular disease, diabetes, and musculoskeletal problems that would limit stretching exercises and the use of medication or hormone replacement therapy during the 6 months before the study. All women were sedentary, defined as having o1 h of regular exercise per week in the previous year. All of the subjects gave written informed consent before their inclusion in the study. The study protocol was approved by The Florida State University Human Subject committee and registered in Clinicaltrial.gov (NCT01741766).

Blood pressure variability

Study design

Stretching training

We used a randomized, parallel design. Subjects were randomly assigned to a ST group (n ¼ 15) or a non-exercising control (CON, n ¼ 15) group. Before baseline measurements, allocation was stratified for BMI (430.0– o35 orZ35 kg m  2), and the sequence was generated by a computerbased number. Measurements were performed at baseline and after 8 weeks in the afternoon hours after at least 4 h postprandial and at the same time of the day (± 1 h) to minimize potential diurnal variations and the effects of food intake. Subjects refrained from caffeine and alcohol for 24 h and from moderate-to-intense physical activity for at least 48 h before and after ST. In the ST group, 8-week measurements were performed at least 48 h after the last stretching session. BP, arterial tonometry, PWV and heart rate (HR) were performed in the supine position after at least 10 min of rest in a quiet temperature-controlled room (23±1 1C). Subjects were instructed not to do changes in their regular lifestyle habits during the study. They provided a 3-day food and exercise log during the first and last week of the study.

Five minutes of continuous BP was obtained from the middle finger using a Finometer device (TNO Biomedical Instrumentation, Amsterdam, The Netherlands). Blood pressure pulse intervals were automatically detected using the commercially available software (WinCPRS, Turku, Finland). The SBP time series was resampled at 5 Hz and the continuous data stream passed through a low-pass impulse response filter with a cutoff frequency of 0.5 Hz. Autoregressive model transformation was used to obtain power spectrums. The power was calculated by measuring the area under the peak of the power spectra density curve. Power spectra within the 0.04– 0.15 Hz range were defined as the low-frequency component of SBP (LFSBP) and taken as an estimate of sympathetic vasomotor modulation.23

The ST group underwent supervised sessions in 3 nonconsecutive days per week for 8 weeks. Subjects performed 1 set of 18 active and 20 passive stretches with at least 2 of them for the major muscle groups (pectoralis major and minor, latissimus dorsi, bicep brachii, triceps, deltoid, trapezius, illiopsas, gluteus, quadriceps, hamstring, leg adductors and gastrocnemius) through the full range of motion. The 38 stretches were performed in the standing (20), sitting (8), and lying (10) positions. Although the sessions included exercise for the whole body, subjects performed predominantly (70%) upper-body or lower-body stretches in alternate days. The stretched muscle was held for 30 s at the point of maximal exertion (defined as RPE418) followed by a 15-s relaxation period. In the passive stretches, the researchers pushed or pulled the specific body part until they received verbal acknowledgment that the stretch was felt at maximal exertion for 30 s. Each session lasted B50 min.

Statistical analysis Pulse wave velocity, bBP and heart rate bBP and PWV were measured using an automatic device (VP-2000; Omron Healthcare, Vernon Hills, IL, USA). Appropriate-size BP cuffs were wrapped around both arms (B2 cm above the antecubital fossa with the position mark aligned with the brachial artery) and ankles (the bottom edge of the cuff above the maleoli with the sensor aligned with the posterior tibial artery), and two tonometers were placed over the right carotid and femoral arteries to obtain PWV measurements from three arterial segments: baPWV, carotid–femoral PWV (aortic), and femoral–ankle PWV (faPWV). The carotid, femoral, brachial and ankle arterial waveforms were 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 femoral artery was measured with a nonelastic tape measure as a straight line, while the distance between sampling points of baPWV and faPWV was calculated automatically according to the height of the subjects.19 The values of baPWV, aPWV and faPWV were calculated from measurements of 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, calculated on 2 separate days in a subsample, was 40.92.

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 (SPT301B; Millar Instruments, Houston, TX, USA). Aortic pulse waveforms were derived using a validated generalized transfer function (SphygmoCor, AtCor Medical, Sydney, NSW, Australia). The aortic wave is composed of a 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 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 Transit time of the reflected wave (Tr) indicates the round-trip travel of the forward wave to the peripheral reflecting sites and back to the aorta.20 Systolic tension time index (TTI) was considered as a measure of myocardial oxygen demand.22 The average of two measurements of bBP and high-quality (operator index X80%) aortic hemodynamics was used in the analysis. The intraclass correlation coefficient for all measurements derived from pulsewave analysis, calculated on 2 separate days in a subsample, was 40.90. & 2014 Macmillan Publishers Limited

Data were examined for normality with the Shapiro–Wilk test. Student’s t-test was used to detect possible difference in parameters between groups at baseline. A two-way analysis of variance with repeated measures (group (CON and ST)  time (before and after 8 weeks)) was used to determine the effects of the intervention over time. If a significant interaction or main effect was noted, a paired t-test was used for post hoc comparisons. Statistical significance was defined a priori as Po0.05. Statistical analyses were performed using the SPSS version 20.0 (SPSS Inc., Chicago, IL, USA). A power calculation done a priori determined that a population of 28 subjects would allow the observation of a difference of 3–5% between the treatments on central BP and AIx with a power of 80%.14,17

RESULTS Data are shown as means±s.e. Two subjects dropped out of the study for personal reasons unrelated to ST or CON. Data are presented for 28 subjects (14 subjects in each group). Attendance to the ST session was 496%. Subject characteristics 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 Table 1.

Subject characteristics before and after 8 weeks of control or stretching training Variable

Age (years) Height (m) Body weight (kg) BMI (kg m  2) Sit and reach score (cm)

Control

Stretching training

Before

After

56±1 1.62±0.02 89.4±4.0 34.0±1.0 26±2

— — 89.0±4.0 33.8±1.0 27±2

Before

After

57±1 — 1.60±0.02 — 87.6±4.1 87.7±4.1 34.2±1.2 34.3±1.2 24±2.0 29±2**z

Abbreviation: BMI, body mass index. **Po0.001 different from before. zPo0.01 different from CON. Data are mean±s.e.

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 interaction (Po0.01) for sit/reach score as it significantly increased after ST (5±1 cm, Po0.001) but not after CON. There were no significant effects (P40.05) on body weight and BMI after ST or CON.

Table 2.

Hemodynamics, arterial stiffness and sympathetic vascular activity Hemodynamic, arterial stiffness and autonomic variables at baseline and after 8 weeks for the CON and ST groups are presented in Table 2. There were significant group  time interactions (Po0.05) for bSBP, aSBP, aDBP, aMAP, P2, AP, AIx,

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

Variable

Brachial SBP (mm Hg) Brachial DBP (mm Hg) Brachial MAP (mm Hg) Aortic SBP (mm Hg) Aortic DBP (mm Hg) Aortic MAP (mm Hg) Aortic P1 (mm Hg) Aortic P2 (mm Hg) AP (mm Hg) Aortic AIx (%) Aortic AIx@75 (%) Time of reflection (ms) TTI (mm Hg s min  1) Heart rate (beats min  1) Aortic PWV (cm s  1) faPWV (cm s  1) baPWV (cm s  1) LFSBP (mm Hg2)

Control

Stretching training

Before

After

Before

After

137±4 80±2 104±3 128±4 84±4 103±4 113±4 128±4 15±2 32±2 28±2 135±3 2574±96 67±3 1132±41 979±31 1397±40 7.05±0.83

138±4 79±2 103±3 127±4 84±4 102±4 113±4 127±4 14±2 32±3 29±3 137±4 2542±98 67±3 1128±48 972±30 1386±47 7.00±0.78

133±3 77±2 102±3 125±3 78±2 99±3 108±3 125±3 17±2 35±3 30±3 129±6 2516±95 64±2 1143±34 947±22 1359±29 7.24±0.84

128±3*w 73±2* 97±3** 118±3**z 74±2*w 91±3**z 106±3 119±3**w 13±1**w 29±3*w 23±2*w 145±5 2350±99**w 63±2 1121±42 917±19 1319±33 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. Journal of Human Hypertension (2014) 246 – 250

& 2014 Macmillan Publishers Limited

Stretching and blood pressure A Wong and A Figueroa

249 AIx@75, TTI and LFSBP. bSBP (  5±2 mm Hg), aSBP (  7±2 mm Hg, Figure 1a), aDBP (  4±1 mm Hg), aMAP (  8±2 mm Hg), P2 (  6±2 mm Hg, Figure 1b), AP (  4±1 mm Hg, Figure 1c), AIx (  6±2%, Figure 1d), AIx@75 (  7±2%,), TTI (  166±42 mm Hg  s min  1) and LFSBP (  1.62±0.57 mm Hg2) significantly (Po0.05) decreased following ST compared with no changes after CON. bDBP (  4±1 mm Hg), BMAP (  5±2 mm Hg) significantly (Po0.05) decreased after 8 weeks of ST, but the reduction was no different compared with CON. There were no significant effects (P40.05) after ST or CON on HR, Tr, P1, aPWV, faPWV and baPWV. DISCUSSION The novelty of this study is that 8 weeks of ST improved bBP, aortic hemodynamic parameters, sympathetic vasomotor activity and trunk flexibility. To the best of our knowledge, this is the first report of the effects of ST on aortic hemodynamics and vascular sympathetic control. There is evidence that indicates that Oestrogen deficiency may contribute to the increase in BP, aPWV and baPWV in postmenopausal women.3,4 Furthermore, wave reflection magnitude leading to increased aSBP and AIx and consequent greater left ventricle afterload and myocardial ischemia is greater in postmenopausal women than in age-matched men.2,24 This is particularly evident in older women with prehypertension and hypertension.2,25 Therefore, lifestyle interventions that improve BP and arterial function may reduce the risk for cardiovascular complications in postmenopausal women with high BP. We found that ST decreased bSBP (B5 mm Hg), bDBP (B4 mm Hg) and bMAP (B5 mm Hg). Similar decreases in bSBP, bDBP and bMAP have been reported after 8 weeks of static leg exercise training26 in healthy young males. Moreover, both aerobic and resistance exercise training have reduced SBP and DBP by 4 and 3–4 mm Hg, respectively, in older adults with prehypertension and hypertension.7 Conversely, although not significant, a trend towards a decrease in resting bSBP (B3 mm Hg) was reported after 13 weeks of ST in normotensive middle-aged and older adults.17 It is possible that the reductions in BP following ST would have been influenced by a high volume of stretching exercises and the BP level of our subjects. In the present study, we found that ST decreased aSBP (B7 mm Hg) and aDBP (B4 mm Hg). There is evidence suggesting that ST has a positive effect on central (carotid) BP through an increase in artery compliance in middle-aged and older adults.17 Although not significant, similar decreases in central (carotid) SBP (B7 mm Hg) were found after ST on the previously mentioned study by Cortez-Cooper et al.17 In contrast, no changes in aSBP and aDBP were found after 16 weeks of ST in older individuals.27 The discrepancy would be related to higher session frequency (3 vs 2 per week) and more exercises per session (38 vs 12) in the present study compared with the previous study.27 Notably, reductions in aSBP of X7 mm Hg have been shown after 6 weeks of aerobic exercise in overweight and obese individuals28 and after 12 weeks of resistance exercise29 in obese postmenopausal women with mildly high BP. Similarly, Taaffe et al.30 reported reduced aSBP (B6 mm Hg) and DBP (3 mm Hg) following 20 weeks of high-intensity resistance training in older adults with prehypertension. However, many obese postmenopausal women may not be willing to perform prolonged and/or intense aerobic or resistance exercise. We found that ST over 8 weeks decreased AIx. A recent study showed that a 15-min active stretching session acutely decreased AIx during the 15-min post stretching due to improved endothelial-mediated vasodilation.14 AIx is influenced by the amplitude of both incident (P1) and reflected wave (P2) and thereby is increased by wave reflection (AP and P2), as well as the timing (Tr) of the reflected wave.6,20 Elevated aSBP and AIx are & 2014 Macmillan Publishers Limited

associated with AP31 and P2 but not Tr in women.25 In the present study, AP was reduced exclusively due to a decrease in P2. As no change in P1 and Tr occurred after ST, the decrease in P2 may explain the reduction in AIx. In contrast to our findings, previous studies have reported no change in aortic AIx following low- and high-intensity resistance training in obese postmenopausal women29 and older adults30 with prehypertension. Thus, due to the beneficial effects on AIx, ST should not be ignored in an exercise program for postmenopausal women. We found that ST did not change 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 its combination with aerobic training did not affect aPWV.17 Decreases in aPWV have been previously reported after 4 weeks of aerobic training in prehypertensives and stage-1 hypertensives.7 Conversely, high-intensity resistance training increases aPWV and faPWV, the main components of baPWV,19 in older adult with prehypertension and stage-1 hypertension.7 Interestingly, the combination of resistance training and aerobic training has reduced baPWV by 0.8 m s  1 in postmenopausal women.10 Although not significant, baPWV (B0.4 m s  1, P ¼ 0.08) and faPWV (B0.3 m s  1, P ¼ 0.11) showed a trend to decrease after ST. It has been previously reported that a bout of external mechanical muscle compressions of leg arteries acutely decreases faPWV due to local vasodilation.32 As we stretched muscle groups, we speculate that peripheral arteries are compressed, resulting in reduced peripheral PWV following ST. Increased P2 and HR are associated with decreased myocardial perfusion in postmenopausal women through increased left ventricular load (aSBP and pulse pressure) and oxygen demand.24 It has been recently reported that obesity may have a significant role in the greater ventricular dysfunction seen in women compared with men.2,24 We found that ST reduced TTI, a surrogate marker of myocardial oxygen demand. In the current study, the reduction in P2 and aSBP may have influenced the decrease in TTI after ST,33 as there was no change in HR. One possible mechanism underlying the effects of ST on arterial function and BP may be related to the improvements in sympathetic control of vasomotor tone. In the current study, ST decreased the LFSBP, a marker of vascular sympathetic activity.23 Considering that sympathetic nerve activity regulates the vascular tone, our data suggest that the reduction in BP and wave reflection magnitude could be partially attributed to a decrease in vascular sympathetic activity after ST. Another possible mechanism for the effects of ST on arterial function is an improved endothelial-mediated vasodilation. A stretching exercise session acutely improved nitric oxide-mediated vasodilation in patients with coronary artery disease.14 A recent study by Wang et al.34 showed that in vivo stretch of pig aortas increases blood flow, suggesting vasodilation. As in the present study we found attenuated LFSBP, the improvements in aortic hemodynamics after ST might be related to decreased vasomotor tone and improved vasodilation as a result of attenuated sympathetic activity. Trunk flexibility was increased by B5 cm after ST. Consistent with the present study, trunk flexibility improvements have been reported after 16 weeks of active stretching in young women.35 In the present study, the subjects had poor trunk flexibility (B24 cm), which has been associated with an increased aPWV and baPWV.13 After ST, even though trunk flexibility significantly increased, it was still categorized as poor trunk flexibility.13 It has been previously shown that there is a linear relationship between the frequency of ST with increase in flexibility.11 Therefore, we can speculate that a more frequent stretching intervention might be required to improve PWV. In conclusion, 8 weeks of ST was effective in decreasing bBP, aBP and AIx through improvements in wave reflection magnitude Journal of Human Hypertension (2014) 246 – 250

Stretching and blood pressure A Wong and A Figueroa

250 and vascular sympathetic activity in obese postmenopausal women. Future studies should aim to evaluate the long-term effects of ST on arterial stiffness and the use ST as an adjunct therapy to prevent the development or progression of hypertension in obese postmenopausal women.

What is known about this topic?  Poor trunk flexibility is associated with increased aortic PWV and baPWV in middle-aged and older individuals.  Acute stretching exercise acutely decreases AIx and increases NO production.  Stretching training improves carotid artery compliance and pulse pressure in middle-aged and older adults. What this study adds?  Stretching training reduces brachial and aortic BP, AIx and vascular sympathetic activity but does not affect PWV in obese postmenopausal women.

CONFLICT OF INTEREST The authors declare no conflict of interest.

ACKNOWLEDGEMENTS We thank Orly Reznik, Carter Egly, Chelsea Ready, Lincoln Little, Travis Lewek, John Kim, Ilisa Lee and Nina Stark for their assistance with training.

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