Functional Sympatholysis During Muscular Activity

Remensnyder, John P.; Mitchell, Jere H.; Sarnoff, Stanley J.

doi:10.1161/01.res.11.3.370

Cited by 369 publications

(171 citation statements)

References 24 publications

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“…48 In contrast, during dynamic exercise, sympathetic stimulation evokes an increase in cardiac output, but the BP is only moderately elevated due to the fall in peripheral resistance as a result of local muscle vasodilatation (described in the literature as 'functional sympatholysis'). 49 In this study, during the FHG the decrease in the T i was accompanied by a decrease in the PPP/CPP, Table 4 Haemodynamic parameters during dynamic KE exercise (n ¼ 14) Central stiffness during mental stress and exercise C Lydakis et al indicating that the augmentation in the CPP was greater than that observed in the periphery. In the dynamic protocol the T i was also decreased (indicating increased central AS), but the PPP/CPP ratio did not decrease but rather showed a small (but not significant) rise towards the end of exercise.…”

Section: Lydakis Et Almentioning

confidence: 48%

Changes of central haemodynamic parameters during mental stress and acute bouts of static and dynamic exercise

et al. 2008

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Chronic dynamic (aerobic) exercise decreases central arterial stiffness, whereas chronic resistance exercise evokes the opposite effect. Nevertheless, there is little information available on the effects of acute bouts of exercise. Also, there is limited data showing an increase of central arterial stiffness during acute mental stress. This study aimed to determine the effect of acute mental and physical (static and dynamic exercise) stress on indices of central arterial stiffness. Fifteen young healthy volunteers were studied. The following paradigms were performed: (1) 2 min of mental arithmetic, (2) short bouts (20 s) of static handgrip at 20 and 70% of maximal voluntary contraction (MVC), (3) fatiguing handgrip at 40% MVC and (4) incremental dynamic knee extensor exercise. Central aortic waveforms were assessed using SphygmoCor software. As compared to baseline, pulse wave transit time decreased significantly for all four interventions indicating that central arterial stiffness increased. During fatiguing handgrip there was a fall in the ratio of peripheral to central pulse pressure from 1.69 ± 0.02 at baseline to 1.56±0.05 (Po0.05). In the knee extensor protocol a nonsignificant trend for the opposite effect was noted. The augmentation index increased significantly during the arithmetic, short static and fatiguing handgrip protocols, whereas there was no change in the knee extensor protocol. We conclude that (1) during all types of acute stress tested in this study (including dynamic exercise) estimated central stiffness increased, (2) during static exercise the workload posed on the left ventricle (expressed as change in central pulse pressure) is relatively higher than that posed during dynamic exercise (given the same pulse pressure change in the periphery).

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Section: Lydakis Et Almentioning

confidence: 48%

Changes of central haemodynamic parameters during mental stress and acute bouts of static and dynamic exercise

et al. 2008

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“…During exercise, sympathetic vasoconstriction is diminished in the active muscles but preserved in the inactive muscles (65,87). This regional selectivity indicates that, akin to the intrinsic coupling between muscle fiber recruitment and blood flow described in the introduction, functional sympatholysis is mediated by local events that are confined to the active muscles and not by humoral factors carried in the systemic circulation (Fig.…”

Section: Mechanisms Underlying Functional Sympatholysismentioning

confidence: 81%

“…As early as 1930, Rein (64) reported that reflex activation of sympathetic nerves decreased blood flow to a greater extent in resting vs. exercising dog hindlimb. In 1962, Remensnyder et al (65) coined the term "functional sympatholysis" to describe the markedly reduced vasoconstrictor responses that they observed in exercising muscle in response to activation of sympathetic nerves or local intra-arterial infusion of norepinephrine. However, perusal of the literature indicates that functional sympatholysis has not been a consistent finding.…”

Section: Is Sympathetic Vasoconstriction Modulated In Exercising Muscle?mentioning

confidence: 99%

Neural control of muscle blood flow during exercise

Thomas¹,

Segal

2004

Journal of Applied Physiology

220

174

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.-Activation of skeletal muscle fibers by somatic nerves results in vasodilation and functional hyperemia. Sympathetic nerve activity is integral to vasoconstriction and the maintenance of arterial blood pressure. Thus the interaction between somatic and sympathetic neuroeffector pathways underlies blood flow control to skeletal muscle during exercise. Muscle blood flow increases in proportion to the intensity of activity despite concomitant increases in sympathetic neural discharge to the active muscles, indicating a reduced responsiveness to sympathetic activation. However, increased sympathetic nerve activity can restrict blood flow to active muscles to maintain arterial blood pressure. In this brief review, we highlight recent advances in our understanding of the neural control of the circulation in exercising muscle by focusing on two main topics: 1) the role of motor unit recruitment and muscle fiber activation in generating vasodilator signals and 2) the nature of interaction between sympathetic vasoconstriction and functional vasodilation that occurs throughout the resistance network. Understanding how these control systems interact to govern muscle blood flow during exercise leads to a clear set of specific aims for future research.

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“…An attenuation of vasoconstriction in the arterial vasculature of skeletal muscle during muscle contraction has been reported by a number of investigators (8,22,23,36,37,42). This diminished vascular responsiveness to sympathetic stimulation during muscular contraction was termed "functional sympatholysis" by Remensnyder et al (36). Recently, studies by Thomas and colleagues (12,38,40,41) have provided evidence that the mechanism by which sympatholysis occurs is related to the production of nitric oxide.…”

mentioning

confidence: 93%

“…Indeed, it has been argued that, as exercise intensity increases, sympathetic vasoconstriction in active skeletal muscle also increases (34). An attenuation of vasoconstriction in the arterial vasculature of skeletal muscle during muscle contraction has been reported by a number of investigators (8,22,23,36,37,42). This diminished vascular responsiveness to sympathetic stimulation during muscular contraction was termed "functional sympatholysis" by Remensnyder et al (36).…”

mentioning

confidence: 98%

Vasoconstriction in active skeletal muscles: a potential role for P2X purinergic receptors?

Buckwalter

Hamann

Clifford

2003

Journal of Applied Physiology

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Vasoconstriction in active skeletal muscles: a potential role for P2X purinergic receptors? J Appl Physiol 95: 953-959, 2003. First published May 23, 2003 10.1152/ japplphysiol.00173.2003.-There is evidence that ATP acts as a neurotransmitter in vascular smooth muscle and is coreleased with norepinephrine from sympathetic nerves. We hypothesized that P2X-receptor stimulation with the selective P2X-receptor agonist ␣,␤-methylene ATP would produce vasoconstriction in resting and exercising skeletal muscle. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective P2X agonist ␣,␤-methylene ATP was infused as a bolus into the femoral artery catheter at rest and during mild, moderate, and heavy exercise. Intra-arterial infusions of ␣,␤-methylene ATP elicited reductions in vascular conductance of 54 Ϯ 5, 49 Ϯ 8, 39 Ϯ 8, and 30 Ϯ 6% at rest, 3 miles/h, 6 miles/h, and 6 miles/h at a 10% grade, respectively. The agonist infusions did not affect blood flow in the contralateral iliac artery. To examine whether nitric oxide is responsible for the attenuated vasoconstrictor response to P2X stimulation, the infusions were repeated in the presence of N G -nitro-L-arginine methyl ester. After nitric oxide synthase blockade, intraarterial infusions of ␣,␤-methylene ATP elicited reductions in vascular conductance of 56 Ϯ 7, 61 Ϯ 8, 52 Ϯ 9, and 40 Ϯ 7% at rest, 3 miles/h, 6 miles/h, and 6 miles/h at a 10% grade, respectively. P2X-receptor responsiveness was attenuated during exercise compared with rest. Blockade of nitric oxide production did not affect the attenuation of P2X-receptor responsiveness during exercise. These data support the hypothesis that P2X purinergic receptors can produce vasoconstriction in exercising skeletal muscle. blood flow; sympatholysis; autonomic nervous system; dogs FOR YEARS, SYMPATHETIC VASOCONSTRICTION has been thought to be mediated entirely by norepinephrine released from sympathetic nerve terminals. However, there is strong evidence that ATP acts as a neurotransmitter in vascular smooth muscle and is coreleased with norepinephrine from sympathetic nerves (9,18,21,29). The release of ATP is thought to stimulate a purinergic receptor (P2). P2X purinergic receptors, which mediate vasoconstriction, are found predominantly in vascular smooth muscle, whereas P2Y purinergic receptors, which mediate vasodilation, are primarily located on endothelial cells (11). P2X receptors on vascular smooth muscle cells are preferentially stimulated by ATP from sympathetic nerve endings (17). Although two recent studies (1,19) showed that P2X-receptor stimulation produces vasoconstriction in the hindlimb of anesthetized cats and rats, it is unknown whether stimulation of P2X receptors in the arterial vasculature of skeletal muscle will produce vasoconstriction during exercise.In the past, the ability of the sympathetic nervous system to restrain blood flow in active skeletal muscle has been questioned (14,24,26)...

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Functional Sympatholysis During Muscular Activity

Cited by 369 publications

References 24 publications

Changes of central haemodynamic parameters during mental stress and acute bouts of static and dynamic exercise

Changes of central haemodynamic parameters during mental stress and acute bouts of static and dynamic exercise

Neural control of muscle blood flow during exercise

Vasoconstriction in active skeletal muscles: a potential role for P2X purinergic receptors?

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