Exercise Training for the Modification of Arterial Stiffness and Wave Reflections

Author(s):  
Julian W. Sacre ◽  
Bronwyn A. Kingwell
2008 ◽  
Vol 10 (4) ◽  
pp. 295-303 ◽  
Author(s):  
Wilmer W. Nichols ◽  
Scott J. Denardo ◽  
Ian B. Wilkinson ◽  
Carmel M. McEniery ◽  
John Cockcroft ◽  
...  

2021 ◽  
Vol 39 (Supplement 1) ◽  
pp. e48
Author(s):  
Francesco Bozzao ◽  
Nina Colapietro ◽  
Carlotta Xodo ◽  
Andrea Grillo ◽  
Matteo Rovina ◽  
...  

2016 ◽  
Vol 121 (3) ◽  
pp. 771-780 ◽  
Author(s):  
Isabella Tan ◽  
Hosen Kiat ◽  
Edward Barin ◽  
Mark Butlin ◽  
Alberto P. Avolio

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.


2013 ◽  
Vol 26 (3) ◽  
pp. 416-423 ◽  
Author(s):  
A. Figueroa ◽  
F. Vicil ◽  
M. A. Sanchez-Gonzalez ◽  
A. Wong ◽  
M. J. Ormsbee ◽  
...  

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
John J. Durocher ◽  
Sarah E. LewAllen ◽  
Carley B. Maanika ◽  
Steven J. Elmer ◽  
Lavanya Rajeshkumar ◽  
...  

2019 ◽  
Vol 127 (3) ◽  
pp. 816-827 ◽  
Author(s):  
An Ouyang ◽  
T. Dylan Olver ◽  
Craig A. Emter ◽  
Bradley S. Fleenor

Heart failure (HF) is associated with increased large conduit artery stiffness and afterload resulting in stiffening of the coronary arteries. Perivascular adipose tissue (PVAT) and advanced glycation end products (AGE) both promote arterial stiffness, yet the mechanisms by which coronary PVAT promotes arterial stiffness and the efficacy of exercise to prevent coronary stiffness are unknown. We hypothesized that both chronic continuous and interval exercise training would prevent coronary PVAT-mediated AGE secretion and arterial stiffness. Yucatan miniature swine were divided into four groups: control-sedentary (CON), aortic banded sedentary-heart failure (HF), aortic banded HF-continuous exercise trained (HF+CONT), and aortic banded HF-interval exercise trained (HF+IT). The left circumflex and right coronary arteries underwent ex vivo mechanical testing, and arterial AGE, elastin, and collagen were assessed. Coronary elastin elastic modulus (EEM) and elastin protein were lower and AGE was increased with HF compared with CON, which was prevented by both HF+CONT and HF+IT. Mouse aortic segments treated with swine coronary PVAT conditioned medium had lower EEM and elastin content and greater AGE secretion and arterial AGE accumulation in HF compared with CON, which was prevented by both HF+CONT and HF+IT. Aminoguanidine (AMG), an AGE inhibitor, prevented the reduction in EEM, arterial elastin content, and AGE accumulation in mouse aortic segments treated with PVAT conditioned medium in the HF group. Our data demonstrate efficacy for chronic continuous and interval exercise to prevent coronary artery stiffness via inhibition of PVAT-derived AGE secretion in a preclinical miniswine model of pressure overload-induced HF. NEW & NOTEWORTHY Our findings show that chronic continuous and interval exercise training regimens prevent coronary artery stiffness associated with inhibition of perivascular adipose tissue-derived advanced glycation end products in a translational pressure overload-induced heart failure model potentially providing an effective therapeutic option for heart failure patients.


2020 ◽  
Vol 41 (Supplement_1) ◽  
Author(s):  
S Fujie ◽  
N Hasegawa ◽  
K Sanada ◽  
T Hamaoka ◽  
S Maeda ◽  
...  

Abstract Funding Acknowledgements Supported by Grants-in-Aid for Scientific Research (#17H02182, #16K13059, M. Iemitsu; #18J01024, S. Fujie) Introduction Aging is well known to elevate risks of cardiovascular diseases. As a mechanism of these increased risks with aging, a reduction of nitric oxide (NO) production via augmented secretion of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthesis is related. Habitual aerobic exercise has shown to improve secretory unbalance of endothelium-derived regulating factors with aging, such as increase in NO and decrease in ADMA, resulting in the reduction of arterial stiffness. However, the time course of improvement in secretory unbalance of NO and ADMA productions in response to exercise training in middle-aged and older adults remains unclear. Purpose This study aimed to determine the time course of changes in plasma nitrite/nitrate (NOx) and ADMA levels related to exercise-training effects of arterial stiffness in healthy middle-aged and older adults. Methods Thirty-two Japanese healthy middle-aged and older subjects (67 ± 1 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). We evaluated plasma NOx and ADMA concentrations and carotid-femoral pulse wave velocity (cfPWV) as an index of arterial stiffness, measured every 2 weeks for 8-week in the training group. Results cfPWV was gradually declined from baseline to 8-week and significantly decreased from baseline at weeks 6 (P &lt; 0.05) and 8 (P &lt; 0.01). Plasma NOx level was gradually elevated during exercise intervention and significantly increased from baseline at weeks 6 (P &lt; 0.05) and 8 (P &lt; 0.01). Interestingly, plasma ADMA level was significantly decreased at 8-week intervention (P &lt; 0.05). Furthermore, the exercise training-induced reduction in plasma ADMA level was negatively correlated with the change in plasma NOx level before and after the 8-week (r = -0.483, P &lt; 0.05). The exercise training-induced change in plasma ADMA concentration was positively correlated with training-induced change in cfPWV before and after the 8-week (r = 0.633, P &lt; 0.01). Additionally, there was a negative correlation between the changes in plasma NOx level and cfPWV before and after the 8-week (r = -0.642, P &lt; 0.05). Conclusions These results suggest that habitual aerobic exercise can normalize the secretory unbalance of NO and ADMA productions in 6 to 8 weeks, and these balance normalizations may be contributed to the reduction of arterial stiffness in the middle-aged and older adults.


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