Divergent endothelial function but similar platelet microvesicle responses following eccentric and concentric cycling at a similar aerobic power output

2017 ◽  
Vol 122 (4) ◽  
pp. 1031-1039 ◽  
Author(s):  
Mark Rakobowchuk ◽  
Ophélie Ritter ◽  
Eurico Nestor Wilhelm ◽  
Laurie Isacco ◽  
Malika Bouhaddi ◽  
...  

Endothelial function and microvesicle concentration changes after acute bouts of continuous eccentric exercise have not been assessed previously nor compared with concentric exercise at similar aerobic power outputs. This method of training may be useful among some clinical populations, but acute responses are not well described. As such, 12 healthy males completed 2 experimental sessions of either 45 min of eccentric or concentric cycling at a matched aerobic power output below the ventilatory threshold. Brachial artery vascular function was assessed throughout 5 min of forearm ischemia and 3 min thereafter, before and at 5 and 40 min of recovery following each exercise session [flow-mediated dilation (FMD)]. Venous blood samples were acquired before each vascular function assessment. FMD significantly decreased after eccentric cycling by 40 min of recovery ( P < 0.05), but was unaltered after concentric exercise. No differences in peak hyperemic blood flow velocity occurred neither between modalities nor at any time point ( P > 0.05). Platelet-derived microvesicles increased by ~20% after both exercise modalities ( P < 0.05) while endothelial-derived microvesicles were unchanged ( P > 0.05). Moderate relationships with cardiac output, a surrogate for shear stress, and norepinephrine were apparent ( P < 0.05), but there were no relationships with inflammatory or acute phase proteins. In summary, eccentric endurance exercise induced macrovascular endothelial dysfunction; however, endothelial activation determined by endothelial microvesicles did not occur suggesting that this modality may induce oxidative stress but no significant endothelial damage. In addition, the increase in platelet microvesicle concentrations may induce beneficial microvascular adaptations as suggested by previous research. NEW & NOTEWORTHY Continuous eccentric cycling exercise induces substantial skeletal muscle, tendon, and bone strain providing a potentially beneficial stimulus among clinical populations. This modality also induces temporary endothelial dysfunction but no apparent damage or activation of the endothelium indicated by microvesicle production, whereas proangiogenic platelet microvesicles are released similarly following both concentric and eccentric cycling and may relate to the shear stress and catecholamine response to exercise.

2018 ◽  
Vol 19 (12) ◽  
pp. 3942 ◽  
Author(s):  
Ali Mahdi ◽  
Tong Jiao ◽  
Yahor Tratsiakovich ◽  
Jiangning Yang ◽  
Claes-Göran Östenson ◽  
...  

Purinergic signaling may be altered in diabetes accounting for endothelial dysfunction. Uridine adenosine tetraphosphate (Up4A), a novel dinucleotide substance, regulates vascular function via both purinergic P1 and P2 receptors (PR). Up4A enhances vascular contraction in isolated arteries of diabetic rats likely through P2R. However, the precise involvement of PRs in endothelial dysfunction and the vasoconstrictor response to Up4A in diabetes has not been fully elucidated. We tested whether inhibition of PRs improved endothelial function and attenuated Up4A-mediated vascular contraction using both aortas and mesenteric arteries of type 2 diabetic (T2D) Goto Kakizaki (GK) rats vs. control Wistar (WT) rats. Endothelium-dependent (EDR) but not endothelium-independent relaxation was significantly impaired in both aortas and mesenteric arteries from GK vs. WT rats. Non-selective inhibition of P1R or P2R significantly improved EDR in aortas but not mesenteric arteries from GK rats. Inhibition of A1R, P2X7R, or P2Y6R significantly improved EDR in aortas. Vasoconstrictor response to Up4A was enhanced in aortas but not mesenteric arteries of GK vs. WT rats via involvement of A1R and P2X7R but not P2Y6R. Depletion of major endothelial component nitric oxide enhanced Up4A-induced aortic contraction to a similar extent between WT and GK rats. No significant differences in protein levels of A1R, P2X7R, and P2Y6R in aortas from GK and WT rats were observed. These data suggest that altered PR sensitivity accounts for endothelial dysfunction in aortas in diabetes. Modulating PRs may represent a potential therapy for improving endothelial function.


2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 82
Author(s):  
Andrew W. Subudhi ◽  
J Tod Olin ◽  
Andrew C. Dimmen ◽  
Bengt Kayser ◽  
Robert C. Roach

2021 ◽  
Vol 320 (1) ◽  
pp. H29-H35
Author(s):  
Joshua M. Cherubini ◽  
Jem L. Cheng ◽  
Jennifer S. Williams ◽  
Maureen J. MacDonald

Sleep is critical for the maintenance of physiological homeostasis and, as such, inadequate sleep beckons a myriad of pathologies. Sleep deprivation is a growing health concern in contemporary society since short sleep durations are associated with increased cardiovascular disease risk and atherosclerotic plaque development. Vascular endothelial dysfunction is an antecedent to atherosclerosis and cardiovascular disease. Herein, we review seminal literature indicating that short sleep durations attenuate endothelial function and explore more recent evidence indicating that sleep deprivation perturbs autonomic balance and the circadian rhythmicity of peripheral vascular clock components. We further examine literature that indicates a mechanistic link between short sleep duration and endothelial dysfunction and subsequent morbidity. Understanding the mechanisms that regulate endothelial function in the context of sleep deprivation facilitates the development and optimization of interventions, such as exercise, that mitigate the ramifications of inadequate sleep on vascular function and cardiovascular health. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/sleep-deprivation-and-endothelial-function/


2016 ◽  
Vol 310 (5) ◽  
pp. H648-H653 ◽  
Author(s):  
Robert M. Restaino ◽  
Lauren K. Walsh ◽  
Takuma Morishima ◽  
Jennifer R. Vranish ◽  
Luis A. Martinez-Lemus ◽  
...  

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.


2012 ◽  
Vol 7 (4) ◽  
pp. 397-400 ◽  
Author(s):  
Iñigo Mujika

Age-related fitness declines in athletes can be due to both aging and detraining. Very little is known about the physiological and performance decline of professional cyclists after retirement from competition. To gain some insight into the aging and detraining process of elite cyclists, 5-time Tour de France winner and Olympic Champion Miguel Indurain performed a progressive cycle-ergometer test to exhaustion 14 y after retirement from professional cycling (age 46 y, body mass 92.2 kg). His maximal values were oxygen uptake 5.29 L/min (57.4 mL · kg−1 · min−1), aerobic power output 450 W (4.88 W/kg), heart rate 191 beats/min, blood lactate 11.2 mM. Values at the individual lactate threshold (ILT): 4.28 L/min (46.4 mL · kg−1 · min−1), 329 W (3.57 W/kg), 159 beats/min, 2.4 mM. Values at the 4-mM onset of blood lactate accumulation (OBLA): 4.68 L/min (50.8 mL · kg−1 · min−1), 369 W (4.00 W/kg), 170 beats/min. Average cycling gross efficiency between 100 and 350 W was 20.1%, with a peak value of 22.3% at 350 W. Delta efficiency was 27.04%. Absolute maximal oxygen uptake and aerobic power output declined by 12.4% and 15.2% per decade, whereas power output at ILT and OBLA declined by 19.8% and 19.2%. Larger declines in maximal and submaximal values relative to body mass (19.4–26.1%) indicate that body composition changed more than aerobic characteristics. Nevertheless, Indurain’s absolute maximal and submaximal oxygen uptake and power output still compare favorably with those exhibited by active professional cyclists.


2010 ◽  
Vol 298 (5) ◽  
pp. H1600-H1607 ◽  
Author(s):  
Jordan D. Miller ◽  
Veronica A. Peotta ◽  
Yi Chu ◽  
Robert M. Weiss ◽  
Kathy Zimmerman ◽  
...  

Endothelial function is impaired by oxidative stress in chronic heart failure (HF). Mechanisms that protect against increases in oxidative stress in HF are not clear. The goal of this study was to determine whether manganese superoxide dismutase (MnSOD) plays a key role in protecting against endothelial dysfunction in HF. Endothelial function and gene expression were examined in aorta from wild-type mice (MnSOD+/+) and mice deficient in MnSOD (MnSOD+/−) 12 wk after ligation of the left coronary artery (LCA). LCA ligation produced similar size myocardial infarctions in MnSOD+/+ and MnSOD+/− mice and reduced ejection fraction to ∼20% in both groups. Maximal relaxation in response to acetylcholine was 78 ± 3% (mean ± SE) and 66 ± 8% in sham-operated MnSOD+/+ and MnSOD+/− mice, respectively. Expression of antioxidant enzymes increased in MnSOD+/+ mice with HF, and maximal relaxation to acetylcholine was slightly impaired (68 ± 4%). Greater endothelial dysfunction was observed in MnSOD+/− mice with HF (46 ± 5%, P < 0.05), which was significantly improved by polyethylene glycol-catalase but not Tempol. Incubation with the nonspecific cyclooxygenase (COX) inhibitor indomethacin or the COX1 inhibitor valeryl salicylate, but not the COX-2 inhibitor NS-398, significantly improved relaxation to acetylcholine in HF mice (maximum relaxation = 74 ± 5, 91 ± 1, and 58 ± 5%). These data suggest that MnSOD plays a key role in protecting against endothelial dysfunction in HF. A novel mechanism was identified whereby chronic increases in oxidative stress, produced by mitochondrial SOD deficiency, impair vascular function via a hydrogen peroxide-dependent, COX1-dependent, endothelium-derived contracting factor.


Author(s):  
Arnaud Hays ◽  
Caroline Nicol ◽  
Denis Bertin ◽  
Romain Hardouin ◽  
Jeanick Brisswalter

Objectives: To identify relevant physiological, mechanical, and strength indices to improve the evaluation of elite mountain bike riders competing in the current Cross-Country Olympic (XCO) format. Methods: Considering the evolution of the XCO race format over the last decade, the present testing protocol adopted a battery of complementary laboratory cycling tests: a maximal aerobic consumption, a force–velocity test, and a multi-short-sprint test. A group of 33 elite-level XCO riders completed the entire testing protocol and at least 5 international competitions. Results: Very large correlations were found between the XCO performance and maximal aerobic power output (r = .78; P < .05), power at the second ventilation threshold (r = .83; P < .05), maximal pedaling force (r = .77; P < .05), and maximum power in the sixth sprint (r = .87; P < .05) of the multi-short-sprint test. A multiple regression model revealed that the normalized XCO performance was predicted at 89.2% (F3,29 = 89.507; r = .95; P < .001) by maximum power in the sixth sprint (β = 0.602; P < .001), maximal pedaling rate (β = 0.309; P < .001), and relative maximal aerobic power output (β = 0.329; P < .001). Discussion: Confirming our expectations, the current XCO performance was highly correlated with a series of physiological and mechanical parameters reflecting the high level of acyclic and intermittent solicitation of both aerobic and anaerobic metabolic pathways and the required qualities of maximal force and velocity. Conclusion: The combination of physiological, mechanical, and strength characteristics may thus improve the prediction of elite XCO cyclists’ performance. It seems of interest to evaluate the ability to repeatedly produce brief intensive efforts with short active recovery periods.


2007 ◽  
Vol 293 (4) ◽  
pp. H2320-H2327 ◽  
Author(s):  
Joon-Young Park ◽  
Iain K. G. Farrance ◽  
Nicola M. Fenty ◽  
James M. Hagberg ◽  
Stephen M. Roth ◽  
...  

In endothelial cells, NF-κB is an important intracellular signaling molecule by which changes in wall shear stress are transduced into the nucleus to initiate downstream endothelial nitric oxide synthase ( NOS3) gene expression. We investigated whether NF-κ light-chain gene enhancer in B cells 1 (NFKB1) promoter polymorphism (−94 NFKB1 I/D, where I is the insertion allele and D is the deletion allele) was associated with 1) NOS3 gene expression in endothelial cells under physiological levels of unidirectional laminar shear stress (LSS) and 2) endothelial function in prehypertensive and stage I hypertensive individuals before and after a 6-mo supervised endurance exercise intervention. Competitive EMSAs revealed that proteins present in the nuclei of endothelial cells preferentially bound to the I allele NFKB1 promoter compared with the D allele. Reporter gene assays showed that the I allele promoter had significantly higher activity than the D allele. In agreement with these observations, homozygous II genotype cells had higher p50 expression levels than homozygous DD genotype cells. Cells with the homozygous II genotype showed a greater increase in NOS3 protein expression than did homozygous DD genotype cells under LSS. Functional experiments on volunteers confirmed higher baseline reactive hyperemic forearm blood flow, and, furthermore, the subgroup analysis revealed that DD homozygotes were significantly less prevalent in the exercise responder group compared with II and ID genotypes. We conclude that the −94 NFKB1 I/D promoter variation contributes to the modulation of vascular function and adaptability to exercise-induced flow shear stress, most likely due to differences in NFKB1 gene transactivity.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Haruki Hashimoto ◽  
Tatsuya Maruhashi ◽  
Takayuki Yamaji ◽  
Takahiro Harada ◽  
Yiming Han ◽  
...  

AbstractIt is established that smoking is a major risk factor of atherosclerosis. Endothelial dysfunction occurs in the initial step in the pathogenesis of atherosclerosis and plays a critical role in the development of atherosclerosis. The purpose of this study was to evaluate the association between smoking status and endothelial function in detail in men. We measured flow-mediated vasodilation (FMD) in 2209 Japanese men including 1181 men who had never smoked and 1028 current smokers. All of the participants were divided into five groups by smoking pack-years: never smoker group (= 0), light smoker group (> 0 to 10), moderate smoker group (> 10 to 20), heavy smoker group (> 20 to 30) and excessive smoker group (> 30). FMD significantly decreased in relation to pack-years (6.6 ± 3.4% in the never smoker group, 6.8 ± 3.0% in the light smoker group, 6.5 ± 2.9% in the moderate smoker group, 5.9 ± 2.9% in the heavy smoker group, and 4.9 ± 2.7% in the excessive smoker group; P < 0.001). After adjustment for age (≥ 65 years), body mass index, systolic blood pressure, low-density lipoprotein cholesterol, glucose, and year of recruitment, FMD was significantly smaller in the excessive smoker group than in the never smoker group as a reference group (OR 1.95, 95% CI 1.42 to 2.67; P < 0.001). These findings suggest that FMD decreases with an increase in the number of cigarettes smoked and that excessive smoking is associated with endothelial dysfunction. Cigarette smoking is harmful to vascular function in men who are heavy smokers.


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