scholarly journals Prolonged sitting-induced leg endothelial dysfunction is prevented by fidgeting

2016 ◽  
Vol 311 (1) ◽  
pp. H177-H182 ◽  
Author(s):  
Takuma Morishima ◽  
Robert M. Restaino ◽  
Lauren K. Walsh ◽  
Jill A. Kanaley ◽  
Paul J. Fadel ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Shear Rate ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Popliteal Artery ◽  
Artery Blood Flow ◽  
Pronounced Increase ◽  
Prolonged Sitting ◽  
Leg Movement

Prolonged sitting impairs endothelial function in the leg vasculature, and this impairment is thought to be largely mediated by a sustained reduction in blood flow-induced shear stress. Indeed, preventing the marked reduction of shear stress during sitting with local heating abolishes the impairment in popliteal artery endothelial function. Herein, we tested the hypothesis that sitting-induced reductions in shear stress and ensuing endothelial dysfunction would be prevented by periodic leg movement, or “fidgeting.” In 11 young, healthy subjects, bilateral measurements of popliteal artery flow-mediated dilation (FMD) were performed before and after a 3-h sitting period during which one leg was subjected to intermittent fidgeting (1 min on/4 min off) while the contralateral leg remained still throughout and served as an internal control. Fidgeting produced a pronounced increase in popliteal artery blood flow and shear rate (prefidgeting, 33.7 ± 2.6 s−1 to immediately postfidgeting, 222.7 ± 28.3 s−1; mean ± SE; P < 0.001) that tapered off during the following 60 s. Fidgeting did not alter popliteal artery blood flow and shear rate of the contralateral leg, which was subjected to a reduction in blood flow and shear rate throughout the sitting period (presit, 71.7 ± 8.0 s−1 to 3-h sit, 20.2 ± 2.9 s−1; P < 0.001). Popliteal artery FMD was impaired after 3 h of sitting in the control leg (presit, 4.5 ± 0.3% to postsit: 1.6 ± 1.1%; P = 0.039) but improved in the fidgeting leg (presit, 3.7 ± 0.6% to postsit, 6.6 ± 1.2%; P = 0.014). Collectively, the present study provides evidence that prolonged sitting-induced leg endothelial dysfunction is preventable with small amounts of leg movement while sitting, likely through the intermittent increases in vascular shear stress.

scholarly journals Endothelial dysfunction following prolonged sitting is mediated by a reduction in shear stress

2016 ◽  
Vol 310 (5) ◽  
pp. H648-H653 ◽  
Author(s):  
Robert M. Restaino ◽  
Lauren K. Walsh ◽  
Takuma Morishima ◽  
Jennifer R. Vranish ◽  
Luis A. Martinez-Lemus ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Internal Control ◽  
Popliteal Artery ◽  
Local Heating ◽  
Underlying Mechanism ◽  
Flow Mediated Dilation ◽  
Prolonged Sitting ◽  
Artery Flow

We and others have recently reported that prolonged sitting impairs endothelial function in the leg vasculature; however, the mechanism(s) remain unknown. Herein, we tested the hypothesis that a sustained reduction in flow-induced shear stress is the underlying mechanism by which sitting induces leg endothelial dysfunction. Specifically, we examined whether preventing the reduction in shear stress during sitting would abolish the detrimental effects of sitting on popliteal artery endothelial function. In 10 young healthy men, bilateral measurements of popliteal artery flow-mediated dilation were performed before and after a 3-h sitting period during which one foot was submerged in 42°C water (i.e., heated) to increase blood flow and thus shear stress, whereas the contralateral leg remained dry and served as internal control (i.e., nonheated). During sitting, popliteal artery mean shear rate was reduced in the nonheated leg (pre-sit, 42.9 ± 4.5 s−1; and 3-h sit, 23.6 ± 3.3 s−1; P < 0.05) but not in the heated leg (pre-sit, 38.9 ± 3.4 s−1; and 3-h sit, 63.9 ± 16.9 s−1; P > 0.05). Popliteal artery flow-mediated dilation was impaired after 3 h of sitting in the nonheated leg (pre-sit, 7.1 ± 1.4% vs. post-sit, 2.8 ± 0.9%; P < 0.05) but not in the heated leg (pre-sit: 7.3 ± 1.5% vs. post-sit, 10.9 ± 1.8%; P > 0.05). Collectively, these data suggest that preventing the reduction of flow-induced shear stress during prolonged sitting with local heating abolishes the impairment in popliteal artery endothelial function. Thus these findings are consistent with the hypothesis that sitting-induced leg endothelial dysfunction is mediated by a reduction in shear stress.

Eight weeks of fish oil supplementation does not prevent sitting-induced leg endothelial dysfunction

2020 ◽  
Vol 45 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Takuma Morishima ◽  
Yosuke Tsuchiya ◽  
Jaume Padilla ◽  
Eisuke Ochi
Keyword(s):  
Blood Flow ◽  
Placebo Group ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Fish Oil ◽  
Popliteal Artery ◽  
Double Blind ◽  
Prolonged Sitting ◽  
Epa And Dha ◽  
Before And After

Prolonged sitting impairs leg endothelial function and this impairment is thought to be mediated by a sustained reduction in blood flow-induced shear stress. However, whether nutritional strategies can be used to prevent sitting-induced leg endothelial dysfunction remains unknown. Herein, we tested the hypothesis that 8 weeks of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation would prevent endothelial dysfunction associated with sitting. Nineteen healthy men were randomly assigned to a placebo group or EPA+DHA group in a double-blind fashion. The EPA+DHA group was administered EPA-rich fish oil, containing 600 mg EPA and 260 mg DHA per day for 8 weeks. The placebo group received matching capsules for the same duration of time. Popliteal artery flow-mediated dilation (FMD) was measured at baseline and before and after a 3-h sitting period. During sitting, blood pressure, popliteal artery diameter, and blood velocity were measured every hour. Throughout the sitting period, popliteal artery blood flow and shear rate were markedly and similarly reduced in both groups (P < 0.05). However, counter to the hypothesis, 3 h of sitting impaired popliteal artery FMD to the same extent in both groups (P < 0.05). In conclusion, daily EPA and DHA supplementation is not effective at preventing the detrimental effects of prolonged sitting on leg endothelial function. Novelty We provide evidence that sitting-induced leg endothelial dysfunction in young healthy subjects cannot be remediated by a nutritional strategy known to produce cardiovascular benefits. This could be partially due to the low total dose of EPA and DHA administered.

scholarly journals Prior exercise and standing as strategies to circumvent sitting-induced leg endothelial dysfunction

2017 ◽  
Vol 131 (11) ◽  
pp. 1045-1053 ◽  
Author(s):  
Takuma Morishima ◽  
Robert M. Restaino ◽  
Lauren K. Walsh ◽  
Jill A. Kanaley ◽  
Jaume Padilla
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Popliteal Artery ◽  
Local Heating ◽  
Standing Position ◽  
Prolonged Sitting ◽  
Prior Exercise ◽  
Significant Impairment ◽  
Experimental Trials ◽  
Artery Flow

We have previously shown that local heating or leg fidgeting can prevent prolonged sitting-induced leg endothelial dysfunction. However, whether physical activity prevents subsequent sitting-induced leg endothelial dysfunction remains unknown. Herein, we tested the hypothesis that sitting-induced leg endothelial dysfunction would be prevented by prior exercise. We also examined if, in the absence of exercise, standing is an effective alternative strategy to sitting for conserving leg endothelial function. Fifteen young healthy subjects completed three randomized experimental trials: (1) sitting without prior exercise; (2) sitting with prior exercise; and (3) standing without prior exercise. Following baseline popliteal artery flow-mediated dilation (FMD) measurements, subjects maintained a supine position for 45 min in the sitting and standing trials, without prior exercise, or performed 45 min of leg cycling before sitting (i.e. sitting with prior exercise trial). Thereafter, subjects were positioned into a seated or standing position, according to the trial, for 3 h. Popliteal artery FMD measures were then repeated. Three hours of sitting without prior exercise caused a significant impairment in popliteal artery FMD (baseline: 3.8±0.5%, post-sitting: 1.5±0.5%, P<0.05), which was prevented when sitting was preceded by a bout of cycling exercise (baseline: 3.8±0.5%, post-sitting: 3.6±0.7%, P>0.05). Three hours of standing did not significantly alter popliteal artery FMD (baseline: 4.1±0.4%, post-standing: 4.3±0.4%, P>0.05). In conclusion, prolonged sitting-induced leg endothelial dysfunction can be prevented by prior aerobic exercise. In addition, in the absence of exercise, standing represents an effective substitute to sitting for preserving leg conduit artery endothelial function.

Influence of prostaglandins and endothelial-derived hyperpolarizing factors on brachial and popliteal endothelial-dependent function in young adults

2021 ◽  
Vol 130 (1) ◽  
pp. 17-25
Author(s):  
Jennifer L. Petterson ◽  
Myles W. O’Brien ◽  
Jarrett A. Johns ◽  
Jack Chiasson ◽  
Derek S. Kimmerly
Keyword(s):  
Blood Flow ◽  
Young Adults ◽  
Shear Rate ◽  
Brachial Artery ◽  
Popliteal Artery ◽  
Lower Limb ◽  
Low Flow ◽  
Flow Mediated Dilation ◽  
Artery Blood Flow ◽  
Dependent Function

We compared changes in upper- and lower-limb artery endothelial-dependent vasodilatory and vasoconstrictor responses between control, prostaglandin inhibition, and endothelial-derived hyperpolarizing factor inhibition conditions. Neither prostaglandins nor endothelial-derived hyperpolarizing factor influenced flow-mediated dilation responses in either the brachial or popliteal artery. In contrast, endothelial-derived hyperpolarizing factor, but not prostaglandins, reduced resting brachial artery blood flow and shear rate and resting popliteal artery diameter, as well as low-flow-mediated constriction responses in both the popliteal and brachial arteries.

scholarly journals Reactive oxygen species modulate coronary wall shear stress and endothelial function during hyperglycemia

2003 ◽  
Vol 284 (5) ◽  
pp. H1552-H1559 ◽  
Author(s):  
Eric R. Gross ◽  
John F. LaDisa ◽  
Dorothee Weihrauch ◽  
Lars E. Olson ◽  
Tobias T. Kress ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Flow ◽  
Shear Stress ◽  
Endothelial Dysfunction ◽  
Wall Shear Stress ◽  
Endothelial Function ◽  
Ros Production ◽  
Oxygen Species ◽  
Wall Shear ◽  
Oscillatory Shear Stress

Hyperglycemia is associated with generation of reactive oxygen species (ROS), and this action may contribute to accelerated atherogenesis. We tested the hypothesis that hyperglycemia produces alterations in left anterior descending coronary artery (LAD) wall shear stress concomitant with endothelial dysfunction and ROS production in dogs ( n = 12) instrumented for measurement of LAD blood flow, velocity, and diameter. Dogs were randomly assigned to receive vehicle (0.9% saline) or the superoxide dismutase mimetic 4- hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (tempol) and were administered intravenous infusions of d-glucose to achieve target blood glucose concentrations of 350 and 600 mg/dl (moderate and severe hyperglycemia, respectively). Endothelial function and ROS generation were assessed by coronary blood flow responses to acetylcholine (10, 30, and 100 ng/kg) and dihydroethidium fluorescence of myocardial biopsies, respectively. Indexes of wall shear stress were calculated with conventional fluid dynamics theory. Hyperglycemia produced dose-related endothelial dysfunction, increases in ROS production, and reductions in oscillatory shear stress that were normalized by tempol. The results suggest a direct association between hyperglycemia-induced ROS production, endothelial dysfunction, and decreases in oscillatory shear stress in vivo.

scholarly journals Elevated oxidative stress and endothelial dysfunction in right coronary artery of right ventricular hypertrophy

2011 ◽  
Vol 110 (6) ◽  
pp. 1674-1681 ◽  
Author(s):  
Xiao Lu ◽  
Charles Q. Dang ◽  
Xiaomei Guo ◽  
Sabee Molloi ◽  
Cynthia D. Wassall ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Wall Shear Stress ◽  
Endothelial Function ◽  
Right Ventricular ◽  
Right Coronary Artery ◽  
Ventricular Hypertrophy ◽  
Basal Tone

Remodeling of right coronary artery (RCA) occurs during right ventricular hypertrophy (RVH) induced by banding of the pulmonary artery (PA). The effect of RVH on RCA endothelial function and reactive oxygen species (ROS) in vessel wall remains unclear. A swine RVH model ( n = 12 pigs) induced by PA banding was used to study RCA endothelial function and ROS level. To obtain longitudinal coronary hemodynamic and geometric data, digital subtraction angiography was used during the progression of RVH. Blood flow in the RCA increased by 82% and lumen diameter of RCA increased by 22% over a 4-wk period of RVH. The increase in blood flow and the commensurate increase in diameter resulted in a constant wall shear stress in RCA throughout the RVH period. ROS was elevated by ∼100% in RCA after 4 wk of PA banding. The expressions of p47phox, NADPH oxidase (NOX1, NOX2, and NOX4) were upregulated in the range of 20–300% in RCA of RVH. The endothelial function was compromised in RCA of RVH as attributed to insufficient endothelial nitric oxide synthase cofactor tetrahydrobiopterin. In vivo angiographic analysis suggests an increased basal tone in the RCA during RVH. In conclusion, stretch due to outward remodeling of RCA during RVH (at constant wall shear stress), similar to vessel stretch in hypertension, appears to induce ROS elevation, endothelial dysfunction, and an increase in basal tone.

Repeated increases in blood flow, independent of exercise, enhance conduit artery vasodilator function in humans

2011 ◽  
Vol 300 (2) ◽  
pp. H664-H669 ◽  
Author(s):  
Louise H. Naylor ◽  
Howard Carter ◽  
Matthew G. FitzSimons ◽  
N. Timothy Cable ◽  
Dick H. J. Thijssen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Complex Stimulus ◽  
Artery Blood Flow ◽  
Handgrip Exercise ◽  
Repeated Heating ◽  
Conduit Artery ◽  
Pressure Cuff ◽  
Ischemic Handgrip Exercise ◽  
Bilateral Heating

This study aimed to determine the importance of repeated increases in blood flow to conduit artery adaptation, using an exercise-independent repeated episodic stimulus. Recent studies suggest that exercise training improves vasodilator function of conduit arteries via shear stress-mediated mechanisms. However, exercise is a complex stimulus that may induce shear-independent adaptations. Nine healthy men immersed their forearms in water at 42°C for three 30-min sessions/wk across 8 wk. During each session, a pneumatic pressure cuff was inflated around one forearm to unilaterally modulate heating-induced increases in shear. Forearm heating was associated with an increase in brachial artery blood flow ( P < 0.001) and shear rate ( P < 0.001) in the uncuffed forearm; this response was attenuated in the cuffed limb ( P < 0.005). Repeated episodic exposure to bilateral heating induced an increase in endothelium-dependent vasodilation in response to 5-min ischemic ( P < 0.05) and ischemic handgrip exercise ( P < 0.005) stimuli in the uncuffed forearm, whereas the 8-wk heating intervention did not influence dilation to either stimulus in the cuffed limb. Endothelium-independent glyceryl trinitrate responses were not altered in either limb. Repeated heating increases blood flow to levels that enhance endothelium-mediated vasodilator function in humans. These findings reinforce the importance of the direct impacts of shear stress on the vascular endothelium in humans.

Influence of sex on microvascular and macrovascular responses to prolonged sitting

2017 ◽  
Vol 312 (4) ◽  
pp. H800-H805 ◽  
Author(s):  
Jennifer R. Vranish ◽  
Benjamin E. Young ◽  
Jasdeep Kaur ◽  
Jordan C. Patik ◽  
Jaume Padilla ◽  
...  
Keyword(s):  
Sex Differences ◽  
Shear Rate ◽  
Young Women ◽  
Popliteal Artery ◽  
Reactive Hyperemia ◽  
Sitting Time ◽  
Calf Circumference ◽  
Men And Women ◽  
Microvascular Reactivity ◽  
Prolonged Sitting

Increased daily sitting time is associated with greater cardiovascular risk, and, on average, women are more sedentary than men. Recent reports have demonstrated that prolonged sitting reduces lower leg microvascular (reactive hyperemia) and macrovascular [flow-mediated dilation (FMD)] vasodilator function. However, these studies have predominately included men, and the effects of sitting in young women are largely unexplored. This becomes important given known sex differences in vascular function. Thus, herein, we assessed popliteal artery reactive hyperemia and FMD before and after a 3-h sitting period in healthy young women ( n = 12) and men ( n = 8). In addition, resting popliteal artery hemodynamics (duplex Doppler ultrasound) and calf circumference were measured before, during, and after sitting. Resting popliteal artery shear rate was reduced to a similar extent in both groups during the sitting period (women: −48.5 ± 8.4 s−1 and men: −52.9 ± 12.3 s−1, P = 0.45). This was accompanied by comparable increases in calf circumference in men and women ( P = 0.37). After the sitting period, popliteal artery FMD was significantly reduced in men (PreSit: 5.5 ± 0.9% and PostSit: 1.6 ± 0.4%, P < 0.001) but not women (PreSit: 4.4 ± 0.6% and PostSit: 3.6 ± 0.6%, P = 0.29). In contrast, both groups demonstrated similar reductions in hyperemic blood flow area under the curve (women: −28,860 ± 5,742 arbitrary units and men: −28,691 ± 9,685 arbitrary units, P = 0.99), indicating impaired microvascular reactivity after sitting. These findings indicate that despite comparable reductions in shear rate during 3 h of uninterrupted sitting, macrovascular function appears protected in some young women but the response was variable, whereas men exhibited more consistent reductions in FMD. In contrast, the leg microvasculature is susceptible to similar sitting-induced impairments in men and women. NEW & NOTEWORTHY We demonstrate that leg macrovascular function was consistently reduced in young men but not young women after prolonged sitting. In contrast, both men and women exhibited similar reductions in leg microvascular reactivity after sitting. These data demonstrate, for the first time, sex differences in vascular responses to prolonged sitting.

scholarly journals Physical and Chemical Characterization of Drag Reducing Polymer Based on Polyvinylpyrrolidone (PVP) in Human Blood Flow

2021 ◽  
Vol 8 (2) ◽  
pp. 20218207
Author(s):  
Akram Jassim Jawad ◽  
Auda J. Braihi
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Shear Rate ◽  
Human Blood ◽  
Chemical Characterization ◽  
Tissue Perfusion ◽  
Moderate Intensity ◽  
Mixing Efficiency ◽  
Reduced Pressure ◽  
Drag Reducing Polymer

A new attempt to use Polyvinylpyrrolidone (PVP) as a bio-drag reducing polymer agent for human blood flow has been studied. PVP was added at 0, 500, 750 and 1000 part per million (ppm) and mixed with human blood at room temperature for 2 minutes. Then, a cone on plate rheometer was used to investigate the effectiveness of PVP agent on blood rheological properties. The results showed significant effecting of PVP on blood fluidity characteristics, where the viscosity decreased as the PVP content increased or as a shear rate increased. For a certain shear rate, the shear stress decreased as PVP content increased. These changes will lead to increased mixing efficiency within the capillaries, increased oxygen transportation, increased tissue perfusion, modified red blood cells (RBCs) distribution, reduced pressure drop gradients, enhanced turbulent flow tendency, enhanced viscoelasticity nature of the blood and its strengthened non-Newtonian pattern. Also, the results showed that the viscosity-shear stress relationships become more linear at higher PVP concentrations. PVP addition caused no shifting in UV-absorbing positions and only moderate intensity changing. Atomic force microscopy (AFM) parameters provide other indicators about the role of PVP as a drag reduction agent for blood flow, where all of the amplitude, hybrid and special parameters decreased significantly.

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