Progressive Resistance Training Without Volume Increases Does Not Alter Arterial Stiffness and Aortic Wave Reflection

2007 ◽  
Vol 232 (9) ◽  
pp. 1228-1235 ◽  
Author(s):  
Darren P. Casey ◽  
Darren T. Beck ◽  
Randy W. Braith
Keyword(s):  
Resistance Training ◽  
Arterial Stiffness ◽  
Pressure Wave ◽  
Wave Reflection ◽  
Augmentation Index ◽  
Aortic Pressure ◽  
Control Group ◽  
Training Volume ◽  
Leg Extension ◽  
Peripheral Arterial

Endurance exercise is efficacious in reducing arterial stiffness. However, the effect of resistance training (RT) on arterial stiffening is controversial. High-intensity, high-volume RT has been shown to increase arterial stiffness in young adults. We tested the hypothesis that an RT protocol consisting of progressively higher intensity without concurrent increases in training volume would not elicit increases in either central or peripheral arterial stiffness or alter aortic pressure wave reflection in young men and women. The RT group ( n = 24; 21 ± 1 years) performed two sets of 8–12 repetitions to volitional fatigue on seven exercise machines on 3 days/week for 12 weeks, whereas the control group ( n = 18; 22 ± 1 years) did not perform RT. Central and peripheral arterial pulse wave velocity (PWV), aortic pressure wave reflection (augmentation index; AIx), brachial flow–mediated dilation (FMD), and plasma levels of nitrate/nitrite (NOx) and norepinephrine (NE) were measured before and after RT. RT increased the one-repetition maximum for the chest press and the leg extension ( P < 0.001). RT also increased lean body mass ( P < 0.01) and reduced body fat (%; P < 0.01). However, RT did not affect carotid-radial, carotid-femoral, and femoral-distal PWV (8.4 ± 0.2 vs. 8.0 ± 0.2 m/sec; 6.5 ± 0.1 vs. 6.3 ± 0.2 m/sec; 9.5 ± 0.3 vs. 9.5 ± 0.3 m/sec, respectively) or AIx (2.5% ± 2.3% vs. 4.8% ± 1.8 %, respectively). Additionally, no changes were observed in brachial FMD, NOx, NE, or blood pressures. These results suggest that an RT protocol consisting of progressively higher intensity without concurrent increases in training volume does not increase central or peripheral arterial stiffness or alter aortic pressure wave characteristics in young subjects.

Abstract P057: Arterial Stiffness And Pressure Wave Reflection In The Development Of Isolated Diastolic Hypertension

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Hirofumi Tomiyama ◽  
Kazuki N Shiina ◽  
Taishiro Chikamori ◽  
Akira Yamashina
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Pressure Wave ◽  
Wave Reflection ◽  
Augmentation Index ◽  
Care Center ◽  
Estimating Equation ◽  
Health Care Center ◽  
Diastolic Hypertension ◽  
New Onset

Importance: While increased arterial stiffness and augmented pressure wave reflection are thought to be key factors in the development of systolic/diastolic hypertension (SDHT) or isolated systolic hypertension (ISHT) via the elevation of systolic blood pressure, their associations with the development of isolated diastolic hypertension (IDHT) have not been clarified. Objective: To examine the significance of augmented pressure wave reflection in the absence of accompanying increase of the arterial stiffness in the development of IDHT. Design and Setting: The prospective observational study conducted in the employees of a Japanese construction company at its health care center from year 2007 through year 2015 with a mean follow-up of 6.4 years, respectively. Participants: A total of 3022 Japanese male employees without hypertension at the start of this study. Main Outcomes and Measures: The annual assessment of prevalence of any phenotypes of hypertension. The blood pressure, brachial-ankle pulse wave velocity (baPWV), and radial augmentation index (rAI) were measured annually during the study period. Results: At the end of the study period, 129 subjects were diagnosed as having SDHT, 112 as having ISHT, and 74 as having IDHT. Both the baPWV and rAI showed significant individual odds ratios for new onset of SDHT and new onset of ISHT. However, only rAI, but not the brachial-ankle PWV, showed a significant odds ratio (1.44, P<0.01) for new onset of IDHT. This association was significant in subjects without elevated baPWV values at the start of the study (i.e., baPWV < 1224 cm/sec), but not in those with elevated brachial-ankle PWV at the start of the study. Generalized estimating equation analyses demonstrated a significant longitudinal association of the rAI, but not baPWV, with the prevalence of IDHT (estimate = 0.02, P=0.02). Conclusions: While increased arterial stiffness and augmented pressure wave reflection present concomitantly may be associated with the development of SDHT and ISHT, augmented pressure wave reflection alone, which may be related to isolated peripheral vascular damage, in the absence of accompanying increase of the arterial stiffness, may be a significant factor in the development of IDHT.

Waveform dispersion, not reflection, may be the major determinant of aortic pressure wave morphology

2005 ◽  
Vol 289 (6) ◽  
pp. H2497-H2502 ◽  
Author(s):  
Sarah A. Hope ◽  
David B. Tay ◽  
Ian T. Meredith ◽  
James D. Cameron
Keyword(s):  
Aortic Root ◽  
Pressure Wave ◽  
Wave Reflection ◽  
Augmentation Index ◽  
Frequency Dispersion ◽  
Aortic Pressure ◽  
Specific Reference ◽  
Thoracoabdominal Aorta ◽  
Time To Peak ◽  
Transverse Arch

The objective of this study was to investigate the determinants of aortic pressure waveform morphology in the thoracoabdominal aorta with specific reference to features of potential prognostic value for cardiovascular disease. In particular, we aimed to determine the location of major pressure wave reflection sites within the aorta. Aortic pressure waveforms were acquired with 2-Fr Millar Mikro-tip catheter transducers in 40 subjects (26 men, 14 women), and repeated in 10 subjects, at five predetermined points within the aorta: aortic root, transverse arch, and at the levels of the diaphragm, renal arteries, and aortic bifurcation. Waveforms were analyzed for augmentation index (AI), time to inflection point ( Ti), and pressure parameters. AI decreased progressively between the aortic root and bifurcation ( P < 0.001), and Ti increased ( P < 0.01). There was the expected progressive peripheral amplification of systolic and pulse pressures and fall in time to peak pressure (all P < 0.001). There was no difference on repeat pullback or between sexes. These data are at variance with the concept that central AI results solely from pressure wave reflection, when Ti would be expected to decrease and AI increase with distal progression. Pressure wave propagation phenomena may contribute, and the potential role of frequency dispersion merits investigation.

Maternal arterial stiffness in pregnancies affected by preeclampsia

2009 ◽  
Vol 297 (2) ◽  
pp. H759-H764 ◽  
Author(s):  
Christina Kaihura ◽  
Makrina D. Savvidou ◽  
James M. Anderson ◽  
Carmel M. McEniery ◽  
Kypros H. Nicolaides
Keyword(s):  
Arterial Stiffness ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Wave Reflection ◽  
Pulse Wave ◽  
Augmentation Index ◽  
Applanation Tonometry ◽  
Control Group ◽  
Arterial Tree ◽  
Cross Sectional

Preeclampsia (PE) is characterized by an aberrant maternal cardiovascular adaptation to pregnancy and increased cardiovascular risk later on in life. The aim of this study was to compare the maternal wave reflections and arterial stiffness in women with established PE and those with normotensive pregnancies, after systematic adjustment for known confounders. This was a cross-sectional study involving 69 normotensive, pregnant women and 54 women with established PE. Maternal wave reflection (augmentation index) and pulse wave velocity of the carotid-radial and carotid-femoral parts of the arterial tree were assessed noninvasively using applanation tonometry. The measurements were adjusted for maternal age, heart rate, mean arterial pressure, and aortic time to wave reflection and expressed as multiples of the median (MoM) of the control group. In the PE group, compared with controls, there was an increase in the median pulse wave velocity of both the carotid to femoral [1.1, interquartile rage (IQR) 1.0–1.3 MoM vs. 0.9, IQR 0.9–1.0 MoM; P < 0.0001] and carotid to radial (1.0, IQR 0.9–1.1 MoM vs. 0.9, IQR 0.9–1.0 MoM; P = 0.01) parts of the arterial tree. In contrast, there were no significant differences between the two groups in the median augmentation index (0.9, IQR 0.7–1.1 MoM vs. 1.0, IQR 0.5–1.8 MoM; P = 0.46). In conclusion, we found that established PE is characterized by increased maternal arterial stiffness but not altered maternal wave reflection.

Markers of arterial stiffness in peripheral arterial disease

VASA ◽  
2015 ◽  
Vol 44 (5) ◽  
pp. 341-348 ◽  
Author(s):  
Marc Husmann ◽  
Vincenzo Jacomella ◽  
Christoph Thalhammer ◽  
Beatrice R. Amann-Vesti
Keyword(s):  
Arterial Stiffness ◽  
Peripheral Arterial Disease ◽  
Pulse Wave ◽  
Augmentation Index ◽  
Arterial Disease ◽  
Care Physician ◽  
Additional Information ◽  
Non Invasive ◽  
Assessment Techniques ◽  
Peripheral Arterial

Abstract. Increased arterial stiffness results from reduced elasticity of the arterial wall and is an independent predictor for cardiovascular risk. The gold standard for assessment of arterial stiffness is the carotid-femoral pulse wave velocity. Other parameters such as central aortic pulse pressure and aortic augmentation index are indirect, surrogate markers of arterial stiffness, but provide additional information on the characteristics of wave reflection. Peripheral arterial disease (PAD) is characterised by its association with systolic hypertension, increased arterial stiffness, disturbed wave reflexion and prognosis depending on ankle-brachial pressure index. This review summarises the physiology of pulse wave propagation and reflection and its changes due to aging and atherosclerosis. We discuss different non-invasive assessment techniques and highlight the importance of the understanding of arterial pulse wave analysis for each vascular specialist and primary care physician alike in the context of PAD.

Wave reflection augments central systolic and pulse pressures during facial cooling

2008 ◽  
Vol 294 (6) ◽  
pp. H2535-H2539 ◽  
Author(s):  
David G. Edwards ◽  
Matthew S. Roy ◽  
Raju Y. Prasad
Keyword(s):  
Cardiovascular Events ◽  
Wave Reflection ◽  
Augmentation Index ◽  
Systolic Pressure ◽  
Aortic Pressure ◽  
Applanation Tonometry ◽  
Pressure Waveform ◽  
Central Aortic Pressure ◽  
Facial Cooling ◽  
Change In Mean

Cardiovascular events are more common in the winter months, possibly because of hemodynamic alterations in response to cold exposure. The purpose of this study was to determine the effect of acute facial cooling on central aortic pressure, arterial stiffness, and wave reflection. Twelve healthy subjects (age 23 ± 3 yr; 6 men, 6 women) underwent supine measurements of carotid-femoral pulse wave velocity (PWV), brachial artery blood pressure, and central aortic pressure (via the synthesis of a central aortic pressure waveform by radial artery applanation tonometry and generalized transfer function) during a control trial (supine rest) and a facial cooling trial (0°C gel pack). Aortic augmentation index (AI), an index of wave reflection, was calculated from the aortic pressure waveform. Measurements were made at baseline, 2 min, and 7 min during each trial. Facial cooling increased ( P < 0.05) peripheral and central diastolic and systolic pressures. Central systolic pressure increased more than peripheral systolic pressure (22 ± 3 vs. 15 ± 2 mmHg; P < 0.05), resulting in decreased pulse pressure amplification ratio. Facial cooling resulted in a robust increase in AI and a modest increase in PWV (AI: −1.4 ± 3.8 vs. 21.2 ± 3.0 and 19.9 ± 3.6%; PWV: 5.6 ± 0.2 vs. 6.5 ± 0.3 and 6.2 ± 0.2 m/s; P < 0.05). Change in mean arterial pressure but not PWV predicted the change in AI, suggesting that facial cooling may increase AI independent of aortic PWV. Facial cooling and the resulting peripheral vasoconstriction are associated with an increase in wave reflection and augmentation of central systolic pressure, potentially explaining ischemia and cardiovascular events in the cold.

scholarly journals Effects of aerobic, resistance and concurrent exercise on pulse wave reflection and autonomic modulation in men with elevated blood pressure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Paulo Farinatti ◽  
Alex da Silva Itaborahy ◽  
Tainah de Paula ◽  
Walace David Monteiro ◽  
Mário F. Neves
Keyword(s):  
Blood Pressure ◽  
Wave Reflection ◽  
Pulse Wave ◽  
Augmentation Index ◽  
Aortic Pressure ◽  
Elevated Blood Pressure ◽  
Autonomic Modulation ◽  
Elevated Blood ◽  
Pulse Wave Reflection ◽  
Concurrent Exercise

AbstractThe acute effects of exercise modes on pulse wave reflection (PWR) and their relationship with autonomic control remain undefined, particularly in individuals with elevated blood pressure (BP). We compared PWR and autonomic modulation after acute aerobic (AE), resistance (RE), and concurrent exercise (CE) in 15 men with stage-1 hypertension (mean ± SE: 34.7 ± 2.5 years, 28.4 ± 0.6 kg/m2, 133 ± 1/82 ± 2 mmHg). Participants underwent AE, RE, and CE on different days in counterbalanced order. Applanation tonometry and heart rate variability assessments were performed before and 30-min postexercise. Aortic pressure decreased after AE (− 2.4 ± 0.7 mmHg; P = 0.01), RE (− 2.2 ± 0.6 mmHg; P = 0.03), and CE (− 3.1 ± 0.5 mmHg; P = 0.003). Augmentation index remained stable after RE, but lowered after AE (− 5.1 ± 1.7%; P = 0.03) and CE (− 7.6 ± 2.4% P = 0.002). Systolic BP reduction occurred after CE (− 5.3 ± 1.9 mmHg). RR-intervals and parasympathetic modulation lowered after all conditions (~ 30–40%; P < 0.05), while the sympathovagal balance increased after RE (1.2 ± 0.3–1.3 ± 0.3 n.u., P < 0.05). Changes in PWR correlated inversely with sympathetic and directly with vagal modulation in CE. In conclusion, AE, RE, and CE lowered central aortic pressure, but only AE and CE reduced PWR. Overall, those reductions related to decreased parasympathetic and increased sympathetic outflows. Autonomic fluctuations seemed to represent more a consequence than a cause of reduced PWR.

scholarly journals What Is the Optimal Strength Training Load to Improve Swimming Performance? A Randomized Trial of Male Competitive Swimmers

2021 ◽  
Vol 18 (22) ◽  
pp. 11770
Author(s):  
Sofiene Amara ◽  
Emmet Crowley ◽  
Senda Sammoud ◽  
Yassine Negra ◽  
Raouf Hammami ◽  
...  
Keyword(s):  
Resistance Training ◽  
Strength Training ◽  
Bench Press ◽  
Swimming Performance ◽  
Training Volume ◽  
Front Crawl ◽  
Leg Extension ◽  
Low Resistance ◽  
Volume Load ◽  
Competitive Swimmers

This study aimed to compare the effectiveness of high, moderate, and low resistance training volume-load of maximum strength training on muscle strength and swimming performance in competitive swimmers. Thirty-three male swimmers were randomly allocated to high (age = 16.5 ± 0.30 years), moderate (age = 16.1 ± 0.32 years) and a low resistance training volume-load group (age = 15.9 ± 0.31). This study was carried out in mid-season (January to March). Pre and post strength (e.g., repetition maximum [1RM] leg extension and bench press tests), swimming (25, 50 m front-crawl), start (speed, time, distance) and turn (time of turn) performance tests were conducted. Our findings revealed a large main effect of time for 1RM bench press: d = 1.38; 1RM leg extension: d = 1.55, and for 25 (d = 1.12), and 50 m (d = 1.97) front-crawl, similarly for start and turn performance (d = 1.28–1.46). However, no significant Group × Time interactions were shown in all strength swimming performances, start and turn tests (p > 0.05). In conclusion, low training loads have been shown to elicit the same results as moderate, and high training loads protocol. Therefore, this study shows evidence that the addition of low training volume-loads as a regular part of a maximal strength training regime will elicit improvements in strength and swimming performance.

scholarly journals Endothelial Function and Arterial Stiffness Should Be Measured to Comprehensively Assess Obstructive Sleep Apnea in Clinical Practice

2021 ◽  
Vol 8 ◽  
Author(s):  
Jinmei Luo ◽  
Xiaona Wang ◽  
Zijian Guo ◽  
Yi Xiao ◽  
Wenhao Cao ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Arterial Stiffness ◽  
Endothelial Function ◽  
Augmentation Index ◽  
Reactive Hyperemia ◽  
Control Group ◽  
Apnea Hypopnea Index ◽  
Obstructive Sleep ◽  
Tnf Α

Objective: An effective clinical tool to assess endothelial function and arterial stiffness in patients with obstructive sleep apnea (OSA) is lacking. This study evaluated the clinical significance of subclinical markers for OSA management in males without serious complications.Patients/Methods: Males without serious complications were consecutively recruited. Clinical data, biomarker tests, reactive hyperemia index (RHI), and augmentation index at 75 beats/min (AIx75) measured by peripheral arterial tonometry were collected. An apnea hypopnea index (AHI) cutoff of ≥15 events/h divided the patients into two groups.Results: Of the 75 subjects, 42 had an AHI ≥15 events/h. Patients with an AHI ≥15 events/h had higher high-sensitivity C-reactive protein, tumor necrosis factor-alpha (TNF-α), vascular endothelial growth factor, and AIx75 values than the control group but no statistical difference in RHI was observed. After controlling for confounders, TNF-α was negatively correlated with the average oxygen saturation (r = −0.258, P = 0.043). RHI was correlated with the rapid eye movement (REM) stage percentage (r = 0.306, P = 0.016) but not with AHI (P &gt; 0.05). AIx75 was positively correlated with the arousal index (r = 0.289, P = 0.023) but not with AHI (r = 0.248, P = 0.052).Conclusions: In males with OSA without severe complications, TNF-α and AIx75 are independently related to OSA. The role of RHI in OSA management requires further elucidation. These markers combined can comprehensively evaluate OSA patients to provide more evidence for the primary prevention of coronary heart disease and treatment response assessment.

scholarly journals Effects of pacing modality on noninvasive assessment of heart rate dependency of indices of large artery function

2016 ◽  
Vol 121 (3) ◽  
pp. 771-780 ◽  
Author(s):  
Isabella Tan ◽  
Hosen Kiat ◽  
Edward Barin ◽  
Mark Butlin ◽  
Alberto P. Avolio
Keyword(s):  
Heart Rate ◽  
Arterial Stiffness ◽  
Pulse Pressure ◽  
Wave Reflection ◽  
Pulse Wave ◽  
Augmentation Index ◽  
Large Artery ◽  
Rate Dependency ◽  
Wave Reflections

Studies investigating the relationship between heart rate (HR) and arterial stiffness or wave reflections have commonly induced HR changes through in situ cardiac pacing. Although pacing produces consistent HR changes, hemodynamics can be different with different pacing modalities. Whether the differences affect the HR relationship with arterial stiffness or wave reflections is unknown. In the present study, 48 subjects [mean age, 78 ± 10 (SD), 9 women] with in situ cardiac pacemakers were paced at 60, 70, 80, 90, and 100 beats per min under atrial, atrioventricular, or ventricular pacing. At each paced HR, brachial cuff-based pulse wave analysis was used to determine central hemodynamic parameters, including ejection duration (ED) and augmentation index (AIx). Wave separation analysis was used to determine wave reflection magnitude (RM) and reflection index (RI). Arterial stiffness was assessed by carotid-femoral pulse wave velocity (cfPWV). Pacing modality was found to have significant effects on the HR relationship with ED ( P = 0.01), central aortic pulse pressure ( P = 0.01), augmentation pressure ( P < 0.0001), and magnitudes of both forward and reflected waves ( P = 0.05 and P = 0.003, respectively), but not cfPWV ( P = 0.57) or AIx ( P = 0.38). However, at a fixed HR, significant differences in pulse pressure amplification ( P < 0.001), AIx ( P < 0.0001), RM ( P = 0.03), and RI ( P = 0.03) were observed with different pacing modalities. These results demonstrate that although the HR relationships with arterial stiffness and systolic loading as measured by cfPWV and AIx were unaffected by pacing modality, it should still be taken into account for studies in which mixed pacing modalities are present, in particular, for wave reflection studies.

Empirical estimates of mean aortic pressure: advantages, drawbacks and implications for pressure redundancy

2002 ◽  
Vol 103 (1) ◽  
pp. 7-13 ◽  
Author(s):  
Denis CHEMLA ◽  
Jean-Louis HÉBERT ◽  
Eduardo APTECAR ◽  
Jean-Xavier MAZOIT ◽  
Karen ZAMANI ◽  
...  
Keyword(s):  
Form Factor ◽  
Pulse Pressure ◽  
Wave Reflection ◽  
Diastolic Pressure ◽  
Augmentation Index ◽  
Aortic Pressure ◽  
Arterial System ◽  
Wave Amplification ◽  
Empirical Estimates ◽  
Alternative Formula

Mean arterial pressure (MAP) is estimated at the brachial artery level by adding a fraction of pulse pressure (form factor; = 0.33) to diastolic pressure. We tested the hypothesis that a fixed form factor can also be used at the aortic root level. We recorded systolic aortic pressure (SAP) and diastolic aortic pressure (DAP), and we calculated aortic pulse pressure (PP) and the time-averaged MAP in the aorta of resting adults (n = 73; age 43±14 years). Wave reflection was quantified using the augmentation index. The aortic form factor (range 0.35-0.53) decreased with age, MAP, PP and augmentation index (each P<0.001). The mean form factor value (0.45) gave a reasonable estimation of MAP (MAP = DAP+0.45PP; bias = 0±2mmHg), and the bias increased with MAP (P<0.001). An alternative formula (MAP = DAP+PP/3+5mmHg) gave a more precise estimation (bias = 0±1mmHg), and the bias was not related to MAP. This latter formula was consistent with the previously reported mean pulse wave amplification of 15mmHg, and with unchanged MAP and diastolic pressure from aorta to periphery. Multiple linear regression showed that 99% of the variability of MAP was explained by the combined influence of DAP and SAP, thus confirming major pressure redundancy. Results were obtained irrespective of whether the marked differences in heart period and extent of wave reflection between subjects were taken into account. In conclusion, the aortic form factor was strongly influenced by age, aortic pressure and wave reflection. An empirical formula (MAP = DAP+PP/3+5mmHg) that is consistent with mechanical principles in the arterial system gave a more precise estimate of MAP in the aorta of resting humans. Only two distinct pressure-powered functions were carried out in the (SAP, DAP, MAP, PP) four-pressure set.

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