Effects of intense exercise training on endothelium‐dependent exercise‐induced vasodilatation

Franke,; Stephens,

doi:10.1046/j.1365-2281.1998.00122.x

Cited by 32 publications

(33 citation statements)

References 27 publications

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“…The time-dependent normalization of brachial artery endothelial function raises the possibility that, depending on the time of (re)assessment, previous studies that have not demonstrated an effect of prolonged exercise training on NO-mediated vasodilator function may conceivably have missed the response by measuring it at a limited number of time points. 28,30 The present finding relating to the time course of functional adaptation is also consistent with our recent report of brachial and popliteal changes in function across 8 weeks of lower-limb exercise training. 34 Further research will be required to specifically address the question of whether structural remodeling, which is NO-dependent, 35 may supersede changes in vascular function, is associated with the return of arterial function to resting values.…”

Section: Tinken Et Al Vascular Adaptation To Exercise Trainingdiscussionsupporting

confidence: 93%

Shear Stress Mediates Endothelial Adaptations to Exercise Training in Humans

et al. 2010

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Abstract-Although episodic changes in shear stress have been proposed as the mechanism responsible for the effects of exercise training on the vasculature, this hypothesis has not been directly addressed in humans. We examined brachial artery flow-mediated dilation, an index of NO-mediated endothelial function, in healthy men in response to an acute bout of handgrip exercise and across an 8-week period of bilateral handgrip training. Shear stress responses were attenuated in one arm by cuff inflation to 60 mm Hg. Similar increases were observed in grip strength and forearm volume and girth in both limbs. Acute bouts of handgrip exercise increased shear rate (PϽ0.005) and flow-mediated dilation percentage (PϽ0.05) in the uncuffed limb, whereas no changes were evident in the cuffed arm. Handgrip training increased flow-mediated dilation percentage in the noncuffed limb at weeks 2, 4, and 6 (PϽ0.001), whereas no changes were observed in the cuffed arm. Brachial artery peak reactive hyperemia, an index of resistance artery remodeling, progressively increased with training in the noncuffed limb (PϽ0.001 and 0.004); no changes were evident in the cuffed arm. Neither acute nor chronic shear manipulation during exercise influenced endothelium-independent glyceryl trinitrate responses. These results demonstrate that exercise-induced changes in shear provide the principal physiological stimulus to adaptation in flow-mediated endothelial function and vascular remodeling in response to exercise training in healthy humans. (Hypertension. 2010;55:312-318.)

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Section: Tinken Et Al Vascular Adaptation To Exercise Trainingdiscussionsupporting

confidence: 93%

Shear Stress Mediates Endothelial Adaptations to Exercise Training in Humans

et al. 2010

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“…However, we did not find a difference in eNOS-dependent reactivity of cerebral arterioles between sedentary and exercised nondiabetic rats. This finding was surprising given the fact that others have shown that ExT increases the reactivity of peripheral blood vessels (5,11,22,37). However, in a previous study (43), we found that ExT did not influence eNOS-dependent responses of the basilar artery.…”

Section: Discussioncontrasting

confidence: 92%

“…However, not all studies are in agreement. Franke et al (22) found that ExT enhanced eNOS-dependent increases in forearm vascular conductance but did not alter vascular responses to eNOS-dependent agonists. In addition, Oltman et al (47) found that ExT did not influence NOS-dependent responses of porcine coronary arteries, and Rogers et al (53) report that ExT actually decreased responsiveness of isolated canine coronary arteries to ␤-adrenergic agonists.…”

Section: Discussionmentioning

confidence: 99%

“…Although the precise cellular/molecular mechanisms accounting for the favorable effects of ExT on the cardiovascular system remain uncertain, many investigators have suggested that ExT may dramatically influence vascular endothelial function. Support for this concept can be found in studies that have examined the effects of ExT on endothelial nitric oxide synthase (eNOS)-dependent vasoreactivity in animals and human subjects (22,23,27,28,60,69). These studies have reported that ExT can enhance eNOS-dependent responses of large and small blood vessels in skeletal muscle, heart, and skin.…”

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confidence: 93%

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Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

Mayhan

Arrick

Patel

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Mayhan WG, Arrick DM, Patel KP, Sun H. Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats. Am J Physiol Heart Circ Physiol 300: H1013-H1020, 2011. First published December 17, 2010; doi:10.1152/ajpheart.00873.2010.-Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [N-methyl-D-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. In addition, we measured superoxide anion levels in brain tissue under basal conditions in sedentary and exercised nondiabetic and diabetic rats. Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. We found that ADP and NMDA produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic rats. In contrast, ADP and NMDA produced only minimal vasodilation in sedentary diabetic rats. ExT restored impaired ADP-and NMDA-induced vasodilation observed in diabetic rats to that observed in nondiabetics. Nitroglycerin produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic and diabetic rats. Superoxide levels in cortex tissue were similar in sedentary and exercised nondiabetic rats, were increased in sedentary diabetic rats, and were normalized by ExT in diabetic rats. Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. We conclude that ExT can alleviate impaired eNOS-and nNOS-dependent responses of pial arterioles during T1D. adenosine 5=-diphosphate; N-methyl-D-aspartate; nitroglycerin; pial arterioles; Western blot; superoxide; endothelial nitric oxide synthase; neuronal nitric oxide synthase EXERCISE TRAINING (ExT) has been shown to play a significant role in the prevention of cardiovascular-related diseases. Although the precise cellular/molecular mechanisms accounting for the favorable effects of ExT on the cardiovascular system remain uncertain, many investigators have suggested that ExT may dramatically influence vascular endothelial function. Support for this concept can be found in studies that have examined the effects of ExT on endothelial nitric oxide synthase (eNOS)-dependent vasoreactivity in animals and human subjects (22,23,27,28,60,69). These studies have reported that ExT can enhance eNOS-dependent responses of large and small blood vessels in skeletal muscle, heart, and skin. Mechanisms by which ExT potentiates nitric oxide synthase (NOS)-dependent relaxation/dilation of blood vessels are not entirely clear but are likely to be related to an increase in shear forces actin...

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“…Physical training appears to en-Serebruany/Davis/Meister/Atar/Whellan/ O'Connor hance endothelial function in healthy young men [157] and in patients with heart failure [158]. However, other investigators, using the same technique, failed to determine any meaningful effects of exercise training on forearm vascular conductance responses to such vasodilators as acetylcholine or sodium nitroprusside [159]. It is known that dynamic exercise leads to shedding of the cell adhesion molecule ICAM-1, but not E-selectin, via adrenergic mechanisms [160].…”

Section: Endothelial Markersmentioning

confidence: 99%

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Serebruany¹,

Davis

Meister

et al. 2001

Heart Drug

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Knowledge of the pathogenesis of congestive heart failure (CHF) has improved greatly in recent years. Nevertheless, this disease still causes high morbidity and mortality in the Western world. In particular, there have been many advancements in our understanding, treatment and prophylaxis of CHF in recent years, yet the incidence of this disease continues to rise. Due to the staggering numbers of patients afflicted, CHF is becoming the most expensive burden on the health care system. The relationship between the deterioration of cardiac function and ongoing ischemic events has not been fully investigated and could conceivably be both monitored and modulated via various biomarkers. Recent data also indicate that heart failure is associated with altered hemostasis, i.e. a prothrombotic state which can lead to complications arising from occlusive and/or thromboembolic phenomena. Although the incidence of overt and clinically apparent thrombotic events is low, it is possible that subclinical events contribute to the increasing morbidity and mortality from this disease. These subclinical events may include silent ischemic events or microinfarcts which are being recognized as contributing to the progression of heart failure. As far as nonpharmacologic approaches to heart failure are concerned, the use of uniform exercise training regimens in heart failure is still a very controversial topic. Before more definitive recommendations can be made regarding the justification of such procedures, further large-scale studies investigating the effects of physical exercise on the development and progression of heart failure are needed. Furthermore, these studies must have sufficient statistical power to detect effects on clinical outcomes, specifically mortality. The purpose of this review article is to bridge the gap between biomarkers, exercise training and heart failure by discussing our current knowledge of different markers of platelet activation, thrombin generation, inflammation, endothelial dysfunction and myocardial necrosis in CHF patients undertaking physical exercise.

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Effects of intense exercise training on endothelium‐dependent exercise‐induced vasodilatation

Cited by 32 publications

References 27 publications

Shear Stress Mediates Endothelial Adaptations to Exercise Training in Humans

Shear Stress Mediates Endothelial Adaptations to Exercise Training in Humans

Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

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