Augmented leg vasoconstriction in dynamically exercising older men during acute sympathetic stimulation

Koch, Dennis W.; Leuenberger, Urs A.; Proctor, David N.

doi:10.1111/j.1469-7793.2003.00337.x

Cited by 49 publications

(72 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This conclusion is also supported by observations that sympathetic control of exercise hyperemia is relatively preserved in aging where it might be critical to restrain vasodilation more compared with young subjects during heavy exercise when maximum cardiac output is limited (130,259,349).…”

Section: B Contraction Blunts Sympathetic Vasoconstrictionsupporting

confidence: 73%

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

Joyner

Casey

2015

Physiological Reviews

582

513

View full text Add to dashboard Cite

LJoyner MJ, Casey DP. Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs. Physiol Rev 95: 549 -601, 2015; doi:10.1152/physrev.00035.2013.-This review focuses on how blood flow to contracting skeletal muscles is regulated during exercise in humans. The idea is that blood flow to the contracting muscles links oxygen in the atmosphere with the contracting muscles where it is consumed. In this context, we take a top down approach and review the basics of oxygen consumption at rest and during exercise in humans, how these values change with training, and the systemic hemodynamic adaptations that support them. We highlight the very high muscle blood flow responses to exercise discovered in the 1980s. We also discuss the vasodilating factors in the contracting muscles responsible for these very high flows. Finally, the competition between demand for blood flow by contracting muscles and maximum systemic cardiac output is discussed as a potential challenge to blood pressure regulation during heavy large muscle mass or whole body exercise in humans. At this time, no one dominant dilator mechanism accounts for exercise hyperemia. Additionally, complex interactions between the sympathetic nervous system and the microcirculation facilitate high levels of systemic oxygen extraction and permit just enough sympathetic control of blood flow to contracting muscles to regulate blood pressure during large muscle mass exercise in humans.

show abstract

Section: B Contraction Blunts Sympathetic Vasoconstrictionsupporting

confidence: 73%

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

Joyner

Casey

2015

Physiological Reviews

582

513

View full text Add to dashboard Cite

show abstract

“…Elderly hypertensive patients have elevated sympathetic tone at rest, and there is some evidence there is an enhanced response to further augmentation of sympathetic outflow during exercise (25). Muscle blood flow can only increase if sympatho-excitatory transmission is overridden by locally produced factors within the exercising muscle: functional sympatholysis.…”

Section: Discussionmentioning

confidence: 99%

Arterial vasodilatory and ventricular diastolic reserves determine the stroke volume response to exercise in elderly female hypertensive patients

Sahlén

Abdula

Norman

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…33,34 Similar to our findings in hypertensive rats, sympathetic vasoconstriction is enhanced in the exercising muscles of older humans and of heart failure rats. 29,35,36 We speculate that a ROS/NO disequilibrium may be a common factor underlying the increased sympathetic vasoconstrictor responsiveness in these conditions, resulting in reduced muscle perfusion during exercise. Excessive sympathetic vasoconstriction also may cause an exaggerated rise in blood pressure during exercise, which is often seen with aging and in hypertension and heart failure and is predictive of future cardiovascular risk.…”

Section: Perspectivesmentioning

confidence: 99%

Reactive Oxygen Species Impair Sympathetic Vasoregulation in Skeletal Muscle in Angiotensin II–Dependent Hypertension

Zhao

Swanson

et al. 2006

Hypertension

View full text Add to dashboard Cite

Abstract-Sympathetic vasoconstriction is attenuated in exercising muscle by locally generated vasodilators, including NO. Skeletal muscle also produces reactive oxygen species (ROS), such as superoxide (O 2 Ϫ ), which inactivates NO. We, therefore, hypothesized that excessive ROS production would result in enhanced sympathetic vasoconstriction in exercising muscle. To increase O 2 Ϫ by activating NADPH oxidase, rats underwent chronic infusion of angiotensin II (Ang II) or unilateral renal artery stenosis (2K1C) to increase endogenous Ang II. At rest, sympathetic nerve stimulation (range: 1 to 5 Hz) evoked similar graded decreases in femoral vascular conductance (range, Ϫ34% to Ϫ66%) in rats infused with vehicle, Ang II, or norepinephrine and in 2K1C or sham-operated rats. These sympathetically mediated decreases in femoral vascular conductance were markedly attenuated during hindlimb contraction in the vehicle, norepinephrine, and sham rats (range, Ϫ3% to Ϫ26%) and to a lesser degree in the Ang II (range, Ϫ16% to Ϫ47%) and 2K1C (range, Ϫ16% to Ϫ45%) rats. In muscles from Ang II and 2K1C rats, ROS were elevated and the NADPH oxidase subunit gp91 phox was upregulated. The O 2 Ϫ scavenger tempol restored the normal attenuation of sympathetic vasoconstriction in the contracting hindlimbs of the Ang II and 2K1C rats, but this effect was prevented by pretreatment with an NO synthase inhibitor. Taken together, these data indicate that chronically elevated Ang II increases muscle ROS, which disrupts the normal NO-dependent attenuation of sympathetic vasoconstriction. These findings may have implications for muscle oxidative stress and sympathetic vasoregulation when the renin-angiotensin system is chronically activated. Key Words: angiotensin Ⅲ free radicals Ⅲ sympathetic nervous system Ⅲ vasoconstriction Ⅲ muscles T he sympathetic nervous system plays an essential role in the cardiovascular response to exercise by increasing cardiac contractility and rate, augmenting venous return, and increasing vascular resistances in the viscera and inactive muscles. These adjustments increase cardiac output and redirect it to the active muscles. At the same time, the vasoconstrictor response to sympathetic nerve discharge in the active muscles is attenuated in part by the metabolic consequences of contraction. 1-9 Such attenuation, termed functional sympatholysis, 5 is more pronounced in the distal than in the proximal segments of the microcirculation, 1,9 which may help to optimize intramuscular blood flow distribution while preserving sympathetic control of systemic vascular resistance and blood pressure.NO is proposed to be one of the factors mediating functional sympatholysis, 2,3,8,10,11 although it may not always play an essential role. 2,4 Skeletal muscle, which expresses high levels of the neuronal isoform of NO synthase (NOS; nNOS) and lower levels of endothelial NOS, 12 produces NO at a low basal rate that increases during contraction. [13][14][15] We and others have shown that ␣-adrenergic vasoconstriction is enhanced in...

show abstract

Augmented leg vasoconstriction in dynamically exercising older men during acute sympathetic stimulation

Cited by 49 publications

References 38 publications

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

Arterial vasodilatory and ventricular diastolic reserves determine the stroke volume response to exercise in elderly female hypertensive patients

Reactive Oxygen Species Impair Sympathetic Vasoregulation in Skeletal Muscle in Angiotensin II–Dependent Hypertension

Contact Info

Product

Resources

About