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Reduction of Arterial Stiffness by Exercise Training Is Associated with Increasing Plasma Apelin Level in Middle-Aged and Older Adults  [PDF]
Shumpei Fujie, Koji Sato, Eri Miyamoto-Mikami, Natsuki Hasegawa, Satoshi Fujita, Kiyoshi Sanada, Takafumi Hamaoka, Motoyuki Iemitsu
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0093545
Abstract: Aging-induced deterioration of arterial stiffness is decreased by regular exercise, and increased nitric oxide (NO) production participates in this effect. Apelin regulates endothelial NO synthase in endothelial cells, promoting NO production. However, the effect of aerobic exercise training on circulating apelin levels in healthy middle-aged and older adults remains unknown. Accordingly, this study aimed to clarify the effects of regular aerobic exercise on apelin concentrations in middle-aged and older adults. Thirty-four healthy middle-aged and older subjects (67.0 ± 1.3 years) were randomly divided into two groups: exercise intervention and sedentary controls. Subjects in the training group completed 8-week of aerobic exercise training (60–70% peak oxygen uptake [VO2peak] for 45 min, 3 days/week). Before and after the intervention, we evaluated plasma apelin and nitrite/nitrate (NOx) concentrations, VO2peak, and arterial stiffness index. In the training group, VO2peak was significantly increased, and carotid β-stiffness was significantly decreased, after the intervention (P<0.05). Moreover, plasma apelin and NOx levels were significantly increased in the training group after the intervention (P<0.05). Additionally, there was a correlation between the training effects of plasma apelin levels and carotidβ-stiffness (r = ?0.508, P = 0.032) and plasma NOx levels (r = 0.494, P = 0.037). By contrast, none of these parameters changed significantly in the control group. These results suggest that the increased in plasma apelin levels may be associated with exercise training-induced alternation of arterial stiffness in middle-aged and older adults.
Combination Treatment of Rosuvastatin or Atorvastatin, with Regular Exercise Improves Arterial Wall Stiffness in Patients with Coronary Artery Disease  [PDF]
Kensuke Toyama, Seigo Sugiyama, Hideki Oka, Yuri Iwasaki, Hitoshi Sumida, Tomoko Tanaka, Shinji Tayama, Hideaki Jinnouchi, Hisao Ogawa
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041369
Abstract: Objective Statin- and exercise-therapy are both clinically beneficial by preventing cardiovascular events in patients with coronary artery disease (CAD). However, there is no information on the vascular effects of the combination of statins and exercise on arterial wall stiffness in CAD patients. Methods The present study is a sub-analysis of PRESET study that determined the effects of 20-week treatment with statins (rosuvastatin, n = 14, atorvastatin, n = 14) combined with regular exercise on arterial wall stiffness assessed by measurement of brachial and ankle pulse wave velocity (baPWV) in CAD patients. Results The combination of statins and regular exercise significantly improved exercise capacity, lipid profile, including low- and high-density lipoprotein cholesterol, and high-sensitivity C-reactive protein (hs-CRP), baPWV (baseline: 1747±355, at 20 weeks of treatment: 1627±271 cm/s, p = 0.008), and basophil count (baseline: 42±32, 20 weeks: 26±15 cells/μL, p = 0.007), but had no effect on blood pressure (baseline: 125±22, 20 weeks: 121±16 mmHg). Changes in baPWV correlated significantly with changes in basophil count (r = 0.488, p = 0.008), but not with age, lipids profile, exercise capacity, or hs-CRP. Conclusion In CAD patients, the combination treatment with statins and exercise resulted in significant amelioration of arterial wall stiffness, at least in part, through reduction of circulating basophils.
THE EFFECT OF REGULAR EXERCISE TRAINING DURING PREGNANCY ON POSTPARTUM BRACHIAL-ANKLE PULSE WAVE VELOCITY, A MEASURE OF ARTERIAL STIFFNESS  [cached]
Ikuno Kawabata,Akihito Nakai,Atsuko Sekiguchi,Yuko Inoue
Journal of Sports Science and Medicine , 2012,
Abstract: The aim of our study was to use brachial-ankle pulse wave velocity (baPWV) measurements to noninvasively assess the effect of exercise training on arterial stiffness in normal pregnant women. Arterial stiffness was assessed at the beginning of the early second trimester of pregnancy and 1 month after delivery in 17 women with normal singleton pregnancies who exercised regularly throughout pregnancy: 81 matched controls were used for comparison. No significant differences were observed in baPWV between the exercise and control groups at the beginning of the second trimester. BaPWV 1 month after delivery (1160.2 ± 109.1 cm·second-1) was significantly higher than that in the early second trimester (1116.7 ± 87.9 cm·second-1) in the control group (indicating increased arterial stiffness), but not in the exercise group (1145.9 ± 88.1 cm/second vs 1122.7 ± 100.2 cm·second-1, respectively: not significant). The results indicated that regular maternal exercise training decreased arterial stiffness in normal pregnant women, which suggests that regular exercise may help prevent hypertensive disorders during pregnancy
Altered Arterial Stiffness and Subendocardial Viability Ratio in Young Healthy Light Smokers after Acute Exercise  [PDF]
Robert J. Doonan, Patrick Scheffler, Alice Yu, Giordano Egiziano, Andrew Mutter, Simon Bacon, Franco Carli, Marios E. Daskalopoulos, Stella S. Daskalopoulou
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026151
Abstract: Background Studies showed that long-standing smokers have stiffer arteries at rest. However, the effect of smoking on the ability of the vascular system to respond to increased demands (physical stress) has not been studied. The purpose of this study was to estimate the effect of smoking on arterial stiffness and subendocardial viability ratio, at rest and after acute exercise in young healthy individuals. Methods/Results Healthy light smokers (n = 24, pack-years = 2.9) and non-smokers (n = 53) underwent pulse wave analysis and carotid-femoral pulse wave velocity measurements at rest, and 2, 5, 10, and 15 minutes following an exercise test to exhaustion. Smokers were tested, 1) after 12h abstinence from smoking (chronic condition) and 2) immediately after smoking one cigarette (acute condition). At rest, chronic smokers had higher augmentation index and lower aortic pulse pressure than non-smokers, while subendocardial viability ratio was not significantly different. Acute smoking increased resting augmentation index and decreased subendocardial viability ratio compared with non-smokers, and decreased subendocardial viability ratio compared with the chronic condition. After exercise, subendocardial viability ratio was lower, and augmentation index and aortic pulse pressure were higher in non-smokers than smokers in the chronic and acute conditions. cfPWV rate of recovery of was greater in non-smokers than chronic smokers after exercise. Non-smokers were also able to achieve higher workloads than smokers in both conditions. Conclusion Chronic and acute smoking appears to diminish the vascular response to physical stress. This can be seen as an impaired ‘vascular reserve’ or a blunted ability of the blood vessels to accommodate the changes required to achieve higher workloads. These changes were noted before changes in arterial stiffness or subendocardial viability ratio occurred at rest. Even light smoking in young healthy individuals appears to have harmful effects on vascular function, affecting the ability of the vascular bed to respond to increased demands.
IMMEDIATE RE-HYDRATION POST-EXERCISE IS NOT COINCIDENT WITH RAISED MEAN ARTERIAL PRESSURE OVER A 30-MINUTE OBSERVATION PERIOD  [cached]
Bartholomew Kay,Brendan J. O'Brien,Nicholas D. Gill
Journal of Sports Science and Medicine , 2005,
Abstract: This investigation assessed the effects of immediate or delayed re-hydration post-exercise, on mean arterial blood pressure (MAP) and on blood plasma volume (PV) expansion post-exercise. It was hypothesised that fluid ingestion would raise MAP and attenuate PV expansion. On two occasions separated by seven days, eight males (age 20.4 ± 1.7 years, mass 79 ± 5 kg [means ± SD]; VO2max 48 ± 11 mL·kg-1·minute-1, [mean ± SE]) cycled in the heat (35oC, 50% relative humidity) at a power output associated with 50% VO2max, until 1.0kg body mass was lost. 1L water was given either immediately thereafter, or two hours post-exercise by random assignment. On both occasions, MAP was calculated every five minutes for a period of 30-minutes post-exercise, and change in PV was calculated 24-hours post-exercise. Repeated measures ANOVA for MAP results suggested a low probability of a treatment effect (p = 0.655), a high probability of a time effect (p = 0.006), and a moderately high probability of a time x treatment interaction (p = 0.076); MAP tended to be lower when fluid had been consumed. PV expansions 24-hours post-exercise were not significant changes with respect to zero, and were not significantly different by treatment condition. In conclusion: (a) The exercise was not sufficient to elicit significant PV expansions; thus, we were unable to determine the effects of the timing of post-exercise re-hydration on PV expansion. (b) The hypothesis regarding MAP in response to drinking was not supported, rather there was a 92% probability that the inverse affect occurs
Experimental exposure to diesel exhaust increases arterial stiffness in man
Magnus Lundb?ck, Nicholas L Mills, Andrew Lucking, Stefan Barath, Ken Donaldson, David E Newby, Thomas Sandstr?m, Anders Blomberg
Particle and Fibre Toxicology , 2009, DOI: 10.1186/1743-8977-6-7
Abstract: In a double-blind randomized fashion, 12 healthy volunteers were exposed to diesel exhaust (approximately 350 μg/m3) or filtered air for one hour during moderate exercise. Arterial stiffness was measured using applanation tonometry at the radial artery for pulse wave analysis (PWA), as well as at the femoral and carotid arteries for pulse wave velocity (PWV). PWA was performed 10, 20 and 30 min, and carotid-femoral PWV 40 min, post-exposure. Augmentation pressure (AP), augmentation index (AIx) and time to wave reflection (Tr) were calculated.Blood pressure, AP and AIx were generally low reflecting compliant arteries. In comparison to filtered air, diesel exhaust exposure induced an increase in AP of 2.5 mmHg (p = 0.02) and in AIx of 7.8% (p = 0.01), along with a 16 ms reduction in Tr (p = 0.03), 10 minutes post-exposure.Acute exposure to diesel exhaust is associated with an immediate and transient increase in arterial stiffness. This may, in part, explain the increased risk for cardiovascular disease associated with air pollution exposure. If our findings are confirmed in larger cohorts of susceptible populations, this simple non-invasive method of assessing arterial stiffness may become a useful technique in measuring the impact of real world exposures to combustion derived-air pollution.The adverse health effects of air pollution have been studied intensely over the last 50 years. Epidemiological studies have identified a strong association between air pollution and increased cardiovascular and respiratory morbidity and mortality [1]. Airborne particles with a diameter of less than 2.5 μm (PM2.5) are considered the main cause of these adverse health effects [2]. In most countries, diesel exhaust (DE) is a major contributor to combustion-derived PM in urban areas [3], exposure to which appears to be an important trigger for acute myocardial infarction [4].In recent years, there has been considerable interest and scientific research into the mechanisms that underpin
Sex differences in resting hemodynamics and arterial stiffness following 4 weeks of resistance versus aerobic exercise training in individuals with pre-hypertension to stage 1 hypertension
Scott R Collier, Vincent Frechette, Kathryn Sandberg, Patrick Schafer, Hong Ji, Harold Smulyan, Bo Fernhall
Biology of Sex Differences , 2011, DOI: 10.1186/2042-6410-2-9
Abstract: In total, 40 moderately active, pre-hypertensive or stage 1 essential hypertensive male (M) and female (F) participants aged 40 to 60 years were randomly divided into four groups: M AE, M RE, F AE, and F. Each group exercised at moderate intensity, 3 days/week for 4 weeks. Hemodynamic, vascular and blood-flow data were collected before and after exercise training.Men showed a significant increase in central pulse wave velocity following RE while females showed no significant changes (12 ± to 13.9 ± vs. 9.2 ± to 9.6 ± m/s, respectively). RE showed significantly greater increases in peak blood flow when compared to AE (F RE 15 ± to 20 ± vs. F AE 17.5 ± to19.5 ±, M RE 19 ± to 24 ± vs M AE 21 ± to 25 ± ml* 100 ml*min, respectively). In addition, systolic and diastolic BP decreased greater for women following RE when compared to AE whereas men showed comparable decreases in BP following either exercise mode.Moderate-intensity RE training may be a more favorable for women as a treatment option for hypertension because of greater decreases in diastolic BP and significant increases in flow-mediated dilation without concomitant increases in arterial stiffness, compared with their male counterparts.Hypertension exhibits sexual dimorphism; women have lower systolic blood pressure (SBP) levels than men from puberty through their mid-fifties, whereas the opposite is true after the sixth decade of life [1]. Hypertension is not only more prevalent in women than in men, but also more severe and less amenable to control, especially in older women [2].Moderate-intensity aerobic exercise (AE) is recommended as a non-pharmacological therapy for the management of raised BP because it reduces both SBP and diastolic blood pressure (DBP), and improves arterial function in pre- to stage 1 essential hypertension in both sexes [3]. Our laboratory previously showed that resistance exercise (RE) also reduced BP but to a slightly lesser extent than AE in a study with a predominantly male populat
Arterial Stiffness and Dialysis Calcium Concentration  [PDF]
Fabrice Mac-Way,Amélie Leboeuf,Mohsen Agharazii
International Journal of Nephrology , 2011, DOI: 10.4061/2011/839793
Abstract: Arterial stiffness is the major determinant of isolated systolic hypertension and increased pulse pressure. Aortic stiffness is also associated with increased cardiovascular morbidity and mortality in patients with chronic kidney disease, hypertension, and general population. Hemodynamically, arterial stiffness results in earlier aortic pulse wave reflection leading to increased cardiac workload and decreased myocardial perfusion. Although the clinical consequence of aortic stiffness has been clearly established, its pathophysiology in various clinical conditions still remains poorly understood. The aim of the present paper is to review the studies that have looked at the impact of dialysis calcium concentration on arterial stiffness. Overall, the results of small short-term studies suggest that higher dialysis calcium is associated with a transient but significant increase in arterial stiffness. This calcium dependant increase in arterial stiffness is potentially explained by increased vascular smooth muscle tone of the conduit arteries and is not solely explained by changes in mean blood pressure. However, the optimal DCa remains to be determined, and long term studies are required to evaluate its impact on the progression of arterial stiffness. 1. Introduction Midsize and large-size arteries are primarily responsible for carrying blood from the heart to the tissues (conductive function) and contribute little to the total vascular resistance. However, the arterial tree must also cope with the cyclic cardiac output and assure the perfusion of organs even during diastole. In this respect, aorta, with its unique elastic capacity, plays a vital role in dampening of the peak systolic pressure and uses its elastic recoil to assure blood flow to the organs even during diastole. Consequently, aortic stiffness, a major determinant of isolated systolic hypertension and increased pulse pressure, has been associated with increased cardiovascular events and mortality [1–5]. The mechanisms of arterial stiffness in various clinical conditions still remain poorly understood. It is thought that stiffness of central elastic arteries is the result of fragmentation of elastin fibers, increased extracellular matrix production of collagen (vascular fibrosis), modification of extracellular matrix by advances glycation end-products, and medial vascular calcification (M?nckeberg sclerosis) [6–10]. 2. Arterial Stiffness and Its Hemodynamic Consequences Arterial stiffness is best evaluated by determination of pulse wave velocity (PWV) over the arterial segment of interest
Effects of safflower seed extract on arterial stiffness  [cached]
Katsuya Suzuki,Shigekazu Tsubaki,Masami Fujita,et al
Vascular Health and Risk Management , 2010,
Abstract: Katsuya Suzuki1, Shigekazu Tsubaki2, Masami Fujita3, Naoto Koyama1, Michio Takahashi1, Kenji Takazawa41Research Institute for Health Fundamentals, Ajinomoto Co., Inc., Kawasaki; 2Samoncho Clinic, Tokyo; 3Shinanozaka Clinic, Tokyo; 4Tokyo Medical University Hachioji Medical Center, Tokyo, JapanAbstract: Safflower seed extract (SSE) contains characteristic polyphenols and serotonin derivatives (N-(p-coumaroyl) serotonin and N-feruloylserotonin), which are reported to inhibit oxidation of low-density lipoprotein (LDL), formation of atherosclerotic plaques, and improve arterial stiffness as assessed by pulse wave analysis in animal models. The effects of long-term supplementation with SSE on arterial stiffness in human subjects were evaluated. This double-blind, placebo-controlled study was conducted in 77 males (35–65 years) and 15 postmenopausal females (55–65 years) with high-normal blood pressure or mild hypertension who were not undergoing treatment. Subjects received SSE (70 mg/day as serotonin derivatives) or placebo for 12 weeks, and pulse wave measurements, ie, second derivative of photoplethysmogram (SDPTG), augmentation index, and brachial-ankle pulse wave velocity (baPWV) were conducted at baseline, and at weeks 4, 8, and 12. Vascular age estimated by SDPTG aging index improved in the SSE-supplemented group when compared with the placebo group at four (P = 0.0368) and 12 weeks (P = 0.0927). The trend of augmentation index reduction (P = 0.072 versus baseline) was observed in the SSE-supplemented group, but reduction of baPWV by SSE supplementation was not observed. The SSE-supplemented group also showed a trend towards a lower malondialdehyde-modified-LDL autoantibody titer at 12 weeks from baseline. These results suggest long-term ingestion of SSE in humans could help to improve arterial stiffness.Keywords: safflower, serotonin derivatives, antioxidants, augmentation index, pulse wave velocity
Effects of safflower seed extract on arterial stiffness
Katsuya Suzuki, Shigekazu Tsubaki, Masami Fujita, et al
Vascular Health and Risk Management , 2010, DOI: http://dx.doi.org/10.2147/VHRM.S13998
Abstract: ts of safflower seed extract on arterial stiffness Original Research (3351) Total Article Views Authors: Katsuya Suzuki, Shigekazu Tsubaki, Masami Fujita, et al Published Date November 2010 Volume 2010:6 Pages 1007 - 1014 DOI: http://dx.doi.org/10.2147/VHRM.S13998 Katsuya Suzuki1, Shigekazu Tsubaki2, Masami Fujita3, Naoto Koyama1, Michio Takahashi1, Kenji Takazawa4 1Research Institute for Health Fundamentals, Ajinomoto Co., Inc., Kawasaki; 2Samoncho Clinic, Tokyo; 3Shinanozaka Clinic, Tokyo; 4Tokyo Medical University Hachioji Medical Center, Tokyo, Japan Abstract: Safflower seed extract (SSE) contains characteristic polyphenols and serotonin derivatives (N-(p-coumaroyl) serotonin and N-feruloylserotonin), which are reported to inhibit oxidation of low-density lipoprotein (LDL), formation of atherosclerotic plaques, and improve arterial stiffness as assessed by pulse wave analysis in animal models. The effects of long-term supplementation with SSE on arterial stiffness in human subjects were evaluated. This double-blind, placebo-controlled study was conducted in 77 males (35–65 years) and 15 postmenopausal females (55–65 years) with high-normal blood pressure or mild hypertension who were not undergoing treatment. Subjects received SSE (70 mg/day as serotonin derivatives) or placebo for 12 weeks, and pulse wave measurements, ie, second derivative of photoplethysmogram (SDPTG), augmentation index, and brachial-ankle pulse wave velocity (baPWV) were conducted at baseline, and at weeks 4, 8, and 12. Vascular age estimated by SDPTG aging index improved in the SSE-supplemented group when compared with the placebo group at four (P = 0.0368) and 12 weeks (P = 0.0927). The trend of augmentation index reduction (P = 0.072 versus baseline) was observed in the SSE-supplemented group, but reduction of baPWV by SSE supplementation was not observed. The SSE-supplemented group also showed a trend towards a lower malondialdehyde-modified-LDL autoantibody titer at 12 weeks from baseline. These results suggest long-term ingestion of SSE in humans could help to improve arterial stiffness.
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