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.

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 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.

Abstract 530: Impact of a Single Mixed Mediterranean-Type Meal Compared with a High-Saturated Fat Meal on Postprandial Endothelial Function and Metabolic Markers

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Sebastien Lacroix ◽  
Christine Des Rosiers ◽  
Mathieu Gayda ◽  
Anil Nigam
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Saturated Fat ◽  
Random Order ◽  
Flow Mediated Dilation ◽  
Omega 3 ◽  
Metabolic Markers ◽  
Endothelial Impairment ◽  
Artery Flow ◽  
Fat Meal

Background: Endothelial dysfunction is considered a precursor of atherosclerosis and is an independent predictor of cardiovascular events. A high-saturated fat meal (HFM) has been shown to induce postprandial endothelial dysfunction. However, no studies have evaluated the acute endothelial effect of a single mixed Mediterranean-type meal (MMM). Our objective was to evaluate postprandial endothelial and metabolic function in response to a MMM in comparison to an isocaloric HFM. Methods: In this ongoing crossover study, 26 of 28 healthy non-smoking males have completed the research protocol. In random order on two separate days during a 1-week interval, subjects were fed two isocaloric meals after an overnight fast. The MMM (885 kcal) consisted of fresh salmon, almonds and vegetables baked in olive oil providing 51% of total calories from fat (7.87g SFA and 2.29g of omega-3, 2:1 DHA:EPA). The HFM consisted of a McDonald’s sausage, egg and cheese McMuffin and three hashbrowns (858 kcal) providing 58% of total energy from fat (14.78g SFA and no omega-3). Endothelial function was evaluated by measuring brachial artery flow-mediated dilation (%FMD) at baseline and at two (T2) and four (T4) hours postprandial. Results: Mean postprandial %FMD tends to be less impaired following the MMM than the HFM (variation at T4 -0.15±3.6% vs -2.83±3.3% respectively, p<0.1). Postprandial variations of TG and TG/HDL at T4 were also less severe with the MMM than the HFM (p≤0.05) and did not correlate to %FMD variations. When subdividing the population on the basis of the median fasting TG levels (0.90 mmol/L), the HFM led to significant endothelial impairment in the subjects with higher-TG while it had no effect in the low-TG group. Conclusion: Our data suggest that a single MMM exerts less of a deleterious effect on postprandial endothelial function and metabolic markers than does a HFM. A single MMM could thus be less atherogenic than a HFM. Moreover, subjects with higher fasting TG levels (avg. 1.54±0.59 mmol/L, well bellow hypertriglyceridemia threshold) could be at higher risk of endothelial injury following a single HFM. Data on all 28 subjects will be available in April 2012.

Popliteal flow-mediated dilatory responses to an acute bout of prolonged sitting between earlier and later phases of natural menstrual and oral contraceptive pill cycles

2020 ◽  
Vol 129 (4) ◽  
pp. 637-645 ◽  
Author(s):  
Myles W. O’Brien ◽  
Jarrett A. Johns ◽  
Amera Al-Hinnawi ◽  
Derek S. Kimmerly
Keyword(s):  
Oral Contraceptive ◽  
Endothelial Function ◽  
Popliteal Artery ◽  
Oral Contraceptive Pill ◽  
Acute Bout ◽  
Acute Period ◽  
Contraceptive Pill ◽  
Young Females ◽  
Conduit Artery ◽  
Prolonged Sitting

We compared changes in popliteal artery endothelial function to a 3-h bout of sitting in females across their natural menstrual or oral contraceptive pill cycles. Pre-sitting endothelial-dependent vasodilation was greater in females who naturally menstruate during the later versus earlier phase but unchanged among contraceptive pill phases. Neither menstrual nor oral contraceptive pill phases attenuated the robust decline in conduit artery health following an acute period of uninterrupted sitting in young females.

Interictal cerebral and systemic endothelial dysfunction in patients with migraine: a case–control study

2014 ◽  
Vol 86 (11) ◽  
pp. 1253-1257 ◽  
Author(s):  
Roopa Rajan ◽  
Dheeraj Khurana ◽  
Vivek Lal
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Cerebral Artery ◽  
Breath Holding ◽  
Flow Mediated Dilation ◽  
Function Impairment ◽  
The Right ◽  
A Prospective Study ◽  
Artery Flow ◽  
Breath Holding Index

BackgroundAlthough systemic endothelial function is unimpaired in migraine, it is unknown whether cerebral endothelial function impairment exists in migraineurs.Materials and methodsWe conducted a prospective study to assess endothelial function in migraineurs (n=45) and healthy volunteers (n=44). Cerebral endothelial function was assessed by Breath Holding Index (BHI) on transcranial Doppler in bilateral middle cerebral artery (MCA at 30–60 mm), posterior cerebral artery (PCA at 60–80 mm) and basilar artery (BA at 80–120 mm) using bilateral monitoring probes fixed on headband. Brachial artery flow-mediated dilation (FMD) was used as measure of systemic endothelial function.ResultsThere was no difference in baseline mean velocities of MCA, PCA, BA among migraineurs and controls. Mean BHI was significantly lower in PCA (p<0.001) and BA (p<0.001) in patients with migraine with no difference in MCA (p=0.909, 0.450). Cerebral endothelial dysfunction (BHI<1.15) was present in 62.2% of migraineurs in the right PCA (p<0.001), 57.8% in left PCA (p<0.001) and 77.8% in BA (BHI <0.83, p<0.001). There was no difference in BHI among migraineurs without and with aura (n=15). Cerebral and systemic endothelial function had no correlation in migraineurs. Increasing BMI was identified as a predictor of impaired BHI in the BA in migraineurs (p=0.020). Age, sex, presence of aura, lateralisation of headache, headache frequency, time to last attack and impaired FMD were not associated with impaired PCA and BA BHI in migraineurs.ConclusionsMigraineurs may have isolated cerebral endothelial dysfunction restricted to the posterior circulation in the absence of systemic endothelial dysfunction.

scholarly journals Endothelial Dysfunction in Cystic Fibrosis: Role of Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Matthew A. Tucker ◽  
Brandon M. Fox ◽  
Nichole Seigler ◽  
Paula Rodriguez-Miguelez ◽  
Jacob Looney ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cystic Fibrosis ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Vascular Dysfunction ◽  
Lipid Hydroperoxide ◽  
Vascular Endothelial ◽  
Vascular Endothelial Dysfunction ◽  
Vascular Endothelial Function ◽  
Artery Flow

Oxidative stress and vascular endothelial dysfunction are established characteristics of cystic fibrosis (CF). Oxidative stress may contribute to vascular dysfunction via inhibition of nitric oxide (NO) bioavailability. Purpose. To determine if ingestion of a single antioxidant cocktail (AOC) improves vascular endothelial function in patients with CF. Methods. In 18 patients with CF (age 8-39 y), brachial artery flow-mediated dilation (FMD) was assessed using a Doppler ultrasound prior to and two hours following either an AOC (n=18; 1,000 mg vitamin C, 600 IU vitamin E, and 600 mg α-lipoic acid) or a placebo (n=9). In a subgroup of patients (n=9), changes in serum concentrations of α-tocopherol and lipid hydroperoxide (LOOH) were assessed following AOC and placebo. Results. A significant (p=0.032) increase in FMD was observed following AOC (Δ1.9±3.3%), compared to no change following placebo (Δ−0.8±1.9%). Moreover, compared with placebo, AOC prevented the decrease in α-tocopherol (Δ0.48±2.91 vs. −1.98±2.32 μM, p=0.024) and tended to decrease LOOH (Δ−0.2±0.1 vs. 0.1±0.1 μM, p=0.063). Conclusions. These data demonstrate that ingestion of an antioxidant cocktail can improve vascular endothelial function and improve oxidative stress in patients with CF, providing evidence that oxidative stress is a key contributor to vascular endothelial dysfunction in CF.

scholarly journals Endothelial Dysfunction and Impaired Neurovascular Coupling Responses Precede Cognitive Impairment in a Mouse Model of Geriatric Sepsis

2021 ◽  
Vol 13 ◽  
Author(s):  
Tamas Csipo ◽  
Benjamin R. Cassidy ◽  
Priya Balasubramanian ◽  
Douglas A. Drevets ◽  
Zoltan I. Ungvari ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Cognitive Performance ◽  
Bacterial Pathogen ◽  
Neurovascular Coupling ◽  
Brain Regions ◽  
Normal Brain ◽  
Experimental Animals ◽  
Significant Impairment

Sepsis is a life-threatening condition, the incidence of which is significantly increased in elderly patients. One of the long-lasting effects of sepsis is cognitive impairment defined as a new deficit or exacerbation of preexisting deficits in global cognition or executive function. Normal brain function is dependent on moment-to-moment adjustment of cerebral blood flow to match the increased demands of active brain regions. This homeostatic mechanism, termed neurovascular coupling (NVC, also known as functional hyperemia), is critically dependent on the production of vasodilator NO by microvascular endothelial cells in response to mediators released from activated astrocytes. The goal of this study was to test the hypothesis that sepsis in aging leads to impairment of NVC responses early after treatment and that this neurovascular dysfunction associates with impairments in cognitive performance and vascular endothelial dysfunction. To test this hypothesis, we used a commonly studied bacterial pathogen, Listeria monocytogenes, to induce sepsis in experimental animals (males, 24 months of age) and subjected experimental animals to a standard clinical protocol of 3 doses of ampicillin i.p. and 14 days of amoxicillin added to the drinking water. NVC responses, endothelial function and cognitive performance were measured in septic and age-matched control groups within 14 days after the final antibiotic treatment. Our data demonstrate that sepsis in aging significantly impairs NVC responses measured in somatosensory cortex during whisker stimulation, significantly impairs endothelial function in isolated and pressure cannulated aorta rings in response to acetylcholine stimulation. No significant impairment of cognitive function in post-sepsis aged animals has been observed when measured using the PhenoTyper homecage based system. Our findings suggest that sepsis-associated endothelial dysfunction and impairment of NVC responses may contribute to long-term cognitive deficits in older sepsis survivors.

Abstract P332: Effects of Intravenous Infusion of Polyunsaturated Fatty Acids and Dextrose on Blood Pressure and Endothelial Function in Obese Subjects

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Aidar R Gosmanov ◽  
Dawn Smiley ◽  
Joselita Siquiera ◽  
Gonzalo Robalino ◽  
Limin Peng ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Polyunsaturated Fatty Acids ◽  
Healthy Subjects ◽  
Flow Mediated Dilatation ◽  
Obese Subjects ◽  
Artery Flow ◽  
Dextrose Infusion

Hyperglycemia and elevated free fatty acids (FFAs) are implicated in the development of hypertension and endothelial dysfunction. We recently reported that 8-hour infusion of soy-bean oil containing polyunsaturated fatty acids (Intralipid) results in the elevation of blood pressure (BP) and endothelial dysfunction in obese healthy subjects. However, the effects of dextrose infusion or combination of dextrose and Intralipid on BP, endothelial function and insulin action are not known. Accordingly, we compared the effects of 8-hour infusion of normal saline at 40 ml/hr, Intralipid 20% at 40 mL/hr, dextrose 10% at 40 ml/hr and combination of Intralipid and dextrose on BP, endothelial function in 12 obese healthy subjects [ages:41±7 yrs, BMI:32±2 kg/m 2 , BP:113/65 mmHg, HOMA-IR: 2.0±1.0]. Blood pressure, brachial artery flow-mediated dilatation (FMD), and levels of FFAs, glucose, and insulin were measured at 0, 4 and 8 h of infusion. Intralipid infusion significantly increased BP, decreased FMD, and increased plasma FFAs (Table). Unlike Intralipid alone, the combination of Intralipid and dextrose did not increase BP but resulted in FMD changes similar to Intralipid alone. Levels of plasma glucose and insulin increased over time after dextrose infusion alone or in combination with Intralipid but not with lipid infusion alone. Compared with Intralipid, the addition of dextrose to Intralipid led to restoration of FFAs to normal level. In summary, Intralipid but not dextrose infusion alone or in combination with Intralipid results in significant elevation in blood pressure in obese healthy subjects. In contrast, dextrose administration had no effect on Intralipid-induced endothelial dysfunction. The mechanisms underlying differences in vascular response after addition of dextrose to Intralipid are not known, but these results indicate that dextrose-induced mild hyperinsulinemia may regulate adverse hemodynamic effects of fat administration in obese subjects.

scholarly journals Sex does not influence impairments in popliteal endothelial-dependent vasodilator or vasoconstrictor responses following prolonged sitting

2019 ◽  
Vol 127 (3) ◽  
pp. 679-687 ◽  
Author(s):  
Myles W. O’Brien ◽  
Jarrett A. Johns ◽  
Tanner D. Williams ◽  
Derek S. Kimmerly
Keyword(s):  
Endothelial Function ◽  
Popliteal Artery ◽  
Young Men ◽  
Low Flow ◽  
Flow Mediated Dilation ◽  
Vascular Effects ◽  
Acute Bout ◽  
Men And Women ◽  
Prolonged Sitting ◽  
Before And After

An acute bout of prolonged sitting (PS) impairs the popliteal artery flow-mediated dilation (FMD) response. Despite equivocal reductions in mean shear rate, young women demonstrate an attenuated decline in popliteal FMD versus young men. However, it is uncertain whether popliteal endothelial-dependent vasoconstrictor responses [low-flow-mediated constriction (L-FMC)] are similarly affected by PS and/or whether sex differences exist. We tested the hypothesis that women would have attenuated reductions in both popliteal FMD and L-FMC responses following an acute bout of PS. Popliteal FMD and L-FMC responses were assessed via duplex ultrasonography before and after a 3-h bout of PS. These responses were then compared between 10 men (24 ± 2 yr) and 10 women (23 ± 2 yr) with similar ( P > 0.13) levels of objectively measured habitual physical activity (via PiezoRx) and sedentary time (via activPAL). At baseline, men and women exhibited similar ( P > 0.46) popliteal FMD (4.8 ± 1.2 vs. 4.5 ± 0.6%) and L-FMC (–1.7 ± 1.0 vs. –1.9 ± 0.9%) responses. Both sexes experienced identical (group: P > 0.76; time: P < 0.001) PS-induced impairments in popliteal FMD (–2.8 ± 1.4 vs. –2.6 ± 0.9%) and L-FMC (1.3 ± 0.7% vs. 1.4 ± 0.7%). In young adults, sex did not influence the negative PS-induced FMD, L-FMC, or microvascular responses in the lower limb. As such, our findings suggest that young men and women are similarly susceptible to the acute negative vascular effects of PS. Future studies should extend these findings to older, less physically active adults and/or patients with vascular disease. NEW & NOTEWORTHY We compared changes in popliteal artery endothelial function to a single 3-h bout of sitting between young men and women. Both groups exhibited similar endothelial-dependent vasodilation (i.e., flow-mediated dilation) and endothelial-dependent vasoconstrictor responses (i.e., low-flow-mediated constriction) at baseline and equivocal impairments in these measures of endothelial function following prolonged sitting. These findings demonstrate that acute impairments in conduit artery endothelial health associated with uninterrupted sitting are not influenced by sex in young, healthy adults.

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