scholarly journals Homebased Standing Core Exercise Training Improves Femoral Blood Flow but not Arterial Stiffness in Middle-Aged to Older Adults

2021 ◽  
Author(s):  
Hsin-Fu Lin ◽  
Soun-Cheng Wang ◽  
Hao-Min Cheng ◽  
Jun Sugawara
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 < 0.05) and 8 (P < 0.01). Plasma NOx level was gradually elevated during exercise intervention and significantly increased from baseline at weeks 6 (P < 0.05) and 8 (P < 0.01). Interestingly, plasma ADMA level was significantly decreased at 8-week intervention (P < 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 < 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 < 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 < 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.


Aging ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 1201-1212 ◽  
Author(s):  
Shumpei Fujie ◽  
Natsuki Hasegawa ◽  
Kiyoshi Sanada ◽  
Takafumi Hamaoka ◽  
Seiji Maeda ◽  
...  

Author(s):  
Nobuhiko AKAZAWA ◽  
Koichiro TANAHASHI ◽  
Keisei KOSAKI ◽  
Satoshi OIKAWA ◽  
Hiroshi KUMAGAI ◽  
...  

2007 ◽  
Vol 293 (3) ◽  
pp. H1466-H1472 ◽  
Author(s):  
Jun Sugawara ◽  
Hidehiko Komine ◽  
Koichiro Hayashi ◽  
Mutsuko Yoshizawa ◽  
Takeshi Otsuki ◽  
...  

Endurance training improves endothelium-dependent vasodilation, yet it does not increase basal blood flow in the legs. We determined the effects of a 3-mo aerobic exercise intervention on basal leg blood flow and α-adrenergic vasoconstriction and nitric oxide (NO) release in seven apparently healthy middle-aged and older adults (60 ± 3 yr). Basal femoral artery blood flow (via Doppler ultrasound) (pretraining: 354 ± 29; posttraining: 335 ± 34 ml/min) and vascular conductance did not change significantly with the exercise training. Before the exercise intervention, femoral artery blood flow increased 32 ± 16% with systemic α-adrenergic blockade (with phentolamine) ( P < 0.05), and the addition of nitric oxide synthase (NOS) inhibition using NG-monomethyl-l-arginine (l-NMMA) did not affect femoral artery blood flow. After training was completed, femoral artery blood flow increased 47 ± 7% with α-adrenergic blockade ( P < 0.01) and then decreased 18 ± 7% with the subsequent administration of l-NMMA ( P < 0.05). Leg vascular conductance showed a greater α-adrenergic blockade-induced vasodilation (+1.7 ± 0.5 to +3.0 ± 0.5 units, P < 0.05) as well as NOS inhibition-induced vasoconstriction (−0.8 ± 0.4 to −2.7 ± 0.7 units, P < 0.05) after the exercise intervention. Resting plasma norepinephrine concentration significantly increased after the training. These results suggest that regular aerobic exercise training enhances NO bioavailability in middle-aged and older adults and that basal limb blood flow does not change with exercise training because of the contrasting influences of sympathetic nervous system activity and endothelium-derived vasodilation on the vasculature.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Fujie ◽  
N Hasegawa ◽  
K Sanada ◽  
T Hamaoka ◽  
J Padilla ◽  
...  

Abstract Introduction Cardiovascular disease risk augments with advance of age. The mechanism of the increased cardiovascular disease risk by aging is related to attenuation of arterial function via endothelium-derived relaxing factor, such as nitric oxide (NO). Recently, apelin and adropin have identified as NO-upregulated hormones, whereas augmented secretion of asymmetric dimethylarginine (ADMA) have identified as NO-downregulated hormones. However, the effects of exercise training-induced changes in NO-regulated hormones on the reduction of arterial stiffness via NO productions remain unclear. Purpose This study aimed to determine the time-dependent changes in NO-regulated hormones related to exercise-training effects of arterial stiffness via NO productions 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 nitrite/nitrate (NOx), apelin, and ADMA levels, serum apelin level 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 apelin and serum adropin levels were gradually elevated during exercise intervention and significantly increased from baseline at weeks 4, 6 and 8 (each P&lt;0.01). Additionally, plasma ADMA level was significantly decreased at 8-week intervention (P&lt;0.01). Furthermore, the exercise training-induced increase in plasma NOx level was significantly correlated with the changes in circulating apelin (r=0.505, P&lt;0.05), adropin (r=0.662, P&lt;0.01), or ADMA (r=−0.483, P&lt;0.05) levels before and after the 8-week. The exercise training-induced increase in plasma NOx level was significantly correlated with training-induced changes in circulating apelin (r=0.483, P&lt;0.05) or adropin (r=0.556, P&lt;0.05) before and after the 6-week. Conclusions These results suggest that the NO-upregulated hormones (apelin and adropin) were increased at the early stage of exercise training intervention and NO-downregulated hormone (ADMA) was decreased at the late stage of exercise training intervention, and these changes in NO-regulated hormones may be contributed to the reduction of arterial stiffness in the middle-aged and older adults. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): This work was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan.


2018 ◽  
Vol 314 (1) ◽  
pp. R94-R101 ◽  
Author(s):  
Natsuki Hasegawa ◽  
Shumpei Fujie ◽  
Naoki Horii ◽  
Masataka Uchida ◽  
Toshiyuki Kurihara ◽  
...  

Adiponectin regulates endothelial nitric oxide synthase in endothelial cells, and body fat loss by aerobic exercise training promotes adiponectin secretion. Recently, C1q/tumor necrosis factor-related proteins (CTRPs) have been identified as novel adipokines and are paralogs of adiponectin, but the association between exercise training-induced reduction of arterial stiffness and circulating CTRPs levels remains unclear. This study aimed to clarify whether the reduction of arterial stiffness in middle-aged and older adults is associated with the change in serum levels of CTRPs induced by exercise training. A total of 52 middle-aged and older participants were randomly divided into two groups: a training group ( n = 26) and a sedentary control group ( n = 26). Participants in the training group completed 8 wk of aerobic exercise training (60–70% peak oxygen uptake for 45 min, 3 days/wk). The reduction of percent whole body fat, abdominal visceral fat area, and carotid-femoral pulse-wave velocity (cfPWV) was significantly greater in the training group than in the control group ( P < 0.05). Moreover, the increase in serum adiponectin, CTRP3, and CTRP5 from baseline to 8 wk was significantly higher in the training group compared with the control group ( P < 0.05). Additionally, the training-induced change in cfPWV was negatively correlated with the training-induced change in serum adiponectin, CTRP3, and CTRP5 levels ( r = −0.51, r = −0.48, r = −0.42, respectively, P < 0.05), and increased plasma nitrite/nitrate level by exercise training was correlated only with adiponectin levels ( r = 0.41, P < 0.05). These results suggest that the exercise training-induced increase in serum CTRPs levels may be associated with the reduction of arterial stiffness in middle-aged and older adults.


PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e93545 ◽  
Author(s):  
Shumpei Fujie ◽  
Koji Sato ◽  
Eri Miyamoto-Mikami ◽  
Natsuki Hasegawa ◽  
Satoshi Fujita ◽  
...  

2012 ◽  
Vol 112 (4) ◽  
pp. 560-565 ◽  
Author(s):  
John McDaniel ◽  
Stephen J. Ives ◽  
Russell S. Richardson

Although a multitude of factors that influence skeletal muscle blood flow have been extensively investigated, the influence of muscle length on limb blood flow has received little attention. Thus the purpose of this investigation was to determine if cyclic changes in muscle length influence resting blood flow. Nine healthy men (28 ± 4 yr of age) underwent a passive knee extension protocol during which the subjects' knee joint was passively extended and flexed through 100–180° knee joint angle at a rate of 1 cycle per 30 s. Femoral blood flow, cardiac output (CO), heart rate (HR), stroke volume (SV), and mean arterial pressure (MAP) were continuously recorded during the entire protocol. These measurements revealed that slow passive changes in knee joint angle did not have a significant influence on HR, SV, MAP, or CO; however, net femoral blood flow demonstrated a curvilinear increase with knee joint angle ( r2 = 0.98) such that blood flow increased by ∼90% (125 ml/min) across the 80° range of motion. This net change in blood flow was due to a constant antegrade blood flow across knee joint angle and negative relationship between retrograde blood flow and knee joint angle ( r2 = 0.98). Thus, despite the absence of central hemodynamic changes and local metabolic factors, blood flow to the leg was altered by changes in muscle length. Therefore, when designing research protocols, researchers need to be cognizant of the fact that joint angle, and ultimately muscle length, influence limb blood flow.


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