Sympathetic nerve activity during prolonged rhythmic forearm exercise

Batman, B.; Hardy, Joanne; Leuenberger, Urs A.; Smith, Michael B.; Yang, Qing; Sinoway, Lawrence I.

doi:10.1152/jappl.1994.76.3.1077

Cited by 57 publications

(54 citation statements)

References 21 publications

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“…Thus the accentuated MSNA responses to EOW in the control trials should not be caused by the pain sensation. Although these observations (3,5,10,20) suggested that the mechanosensitive nerve endings could be sensitized by accumulating metabolites, the causative metabolite(s) was not identified in these human studies.…”

Section: Discussionmentioning

confidence: 90%

“…Recently, we demonstrated that the static passive stretch of muscles via the extension of the wrist (EOW) evoked significant increases in mean MSNA and blood pressure when the muscle metabolites were accumulated under post-exercise muscle ischemia (PEMI), whereas the static passive stretch of the muscles had no significant effects on mean MSNA and blood pressure under a freely perfused condition (10). Although these data suggest that muscle metabolites sensitize the mechanoreceptors in the muscles, the causative metabolite(s) was not tested in these reports (3,5,10,20).…”

mentioning

confidence: 96%

“…Previous human studies (3,20) speculated that the mechanosensitive nerve endings were sensitized by the chemical products of the muscle contraction during active exercise. The study of Bell and White (5) showed that external pressure applied to the leg muscles during post-exercise circulatory occlusion evoked further increases in blood pressure and suggested that exercise metabolites sensitized a population of mechanosensitive afferents in human muscles.…”

mentioning

confidence: 99%

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Cyclooxygenase inhibition attenuates sympathetic responses to muscle stretch in humans

Cui¹,

Moradkhan²,

Mascarenhas³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Cui J, Moradkhan R, Mascarenhas V, Momen A, Sinoway LI. Cyclooxygenase inhibition attenuates sympathetic responses to muscle stretch in humans. Am J Physiol Heart Circ Physiol 294: H2693-H2700, 2008. First published April 25, 2008; doi:10.1152/ajpheart.91505.2007.-Passive muscle stretch performed during a period of post-exercise muscle ischemia (PEMI) increases muscle sympathetic nerve activity (MSNA), and this suggests that the muscle metabolites may sensitize mechanoreceptors in healthy humans. However, the responsible substance(s) has not been studied thoroughly in humans. Human and animal studies suggest that cyclooxygenase products sensitize muscle mechanoreceptors. Thus we hypothesized that local cyclooxygenase inhibition in exercising muscles could attenuate MSNA responses to passive muscle stretch during PEMI. Blood pressure (Finapres), heart rate, and MSNA (microneurography) responses to passive muscle stretch were assessed in 13 young healthy subjects during PEMI before and after cyclooxygenase inhibition, which was accomplished by a local infusion of 6 mg ketorolac tromethamine in saline via Bier block. In the second experiment, the same amount of saline was infused via the Bier block. Ketorolac Bier block decreased prostaglandin synthesis to ϳ34% of the baseline. Before ketorolac Bier block, passive muscle stretch evoked significant increases in MSNA (P Ͻ 0.005) and mean arterial blood pressure (P Ͻ 0.02). After ketorolac Bier block, passive muscle stretch did not evoke significant responses in MSNA (P ϭ 0.11) or mean arterial blood pressure (P ϭ 0.83). Saline Bier block had no effect on the MSNA or blood pressure response to ischemic stretch. These observations indicate that cyclooxygenase inhibition attenuates MSNA responses seen during PEMI and suggest that cyclooxygenase products sensitize the muscle mechanoreceptors.exercise pressor reflex; passive exercise; autonomic nervous system; muscle afferents; regional intravenous anesthesia EXERCISE IS A POTENT STIMULUS to activate the sympathetic nervous system (36). Increases in muscle sympathetic nerve activity (MSNA) during exercise are caused, reflexively, by the stimulation of mechanosensitive and chemosensitive afferents within the contracting muscle (27). Groups III and IV afferent fibers in muscles are suggested to be involved in this reflex (28,43). Whereas group III muscle afferents are predominantly mechanically sensitive, unmyelinated group IV muscle afferents are mainly chemically sensitive (1,2,22,24).A number of animal studies have shown that mechanoreceptor stimulation in cats activates sympathetic efferents to muscles (21) and kidneys (17, 42) and can evoke pressor responses to exercise (16,25,39). Recently, we demonstrated in healthy humans that passive stretch of leg or arm muscles evokes a significant increase in MSNA during the first few seconds of the muscle stretch; however, under freely perfused conditions, the magnitude of the response is small and transient, and the evoked hemodynamic consequences are limited (9, 10).Animal st...

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Section: Discussionmentioning

confidence: 90%

mentioning

confidence: 96%

mentioning

confidence: 99%

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Cyclooxygenase inhibition attenuates sympathetic responses to muscle stretch in humans

Cui¹,

Moradkhan²,

Mascarenhas³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…Isometric HG exercise causes repetitive increases in forearm flow and sympathetic nerve traffic [18]. Isometric HG training may have therefore improved basal nitric oxide-related endothelial function in the resistance vessels of the forearm.…”

Section: Effects Of Isometric Hg Training On Vascular Reactivitymentioning

confidence: 99%

Isometric handgrip training does not improve flow-mediated dilation in subjects with normal blood pressure

et al. 2007

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Isometric HG (handgrip) training lowers resting arterial BP (blood pressure), yet the mechanisms are elusive. In the present study, we investigated improved systemic endothelial function as a mechanism of arterial BP modification following isometric HG training in normotensive individuals. This study employed a within-subject repeated measures design primarily to assess improvements in BA FMD (brachial artery flow-mediated dilation; an index of endothelium-dependent vasodilation), with the non-exercising limb acting as an internal control. Eleven subjects performed four 2-min unilateral isometric HG contractions at 30% of maximal effort, three times per week for 8 weeks. Pre-, mid- and post-training resting ABP and BA FMD (exercised arm and non-exercised arm) were measured via automated brachial oscillometry and ultrasound respectively. BA FMD (normalized to the peak shear rate experienced in response to the reactive hyperaemic stimulus) remained unchanged [exercised arm, 0.029+/-0.003 to 0.026+/-0.003 to 0.029+/-0.004%/s(-1) (pre- to mid- to post-training respectively); non-exercised arm, 0.023+/-0.003 to 0.023+/-0.003 to 0.024+/-0.003%/s(-1) (pre- to mid- to post-training respectively); P=0.22]. In conclusion, improved systemic endothelial function is unlikely to be responsible for lowering arterial BP in this population.

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“…Central command plays a supporting role, underlying increases in muscle sympathetic nerve activity (MSNA) only during extreme, or near maximal, effort (33). Recent reports support the notion that the muscle mechanoreceptors also underlie the increase in MSNA during exercise, especially rhythmic exercise, in healthy humans (3,11). We (19,20) reported that cyclooxygenase products, but not lactic acid or adenosine, sensitize muscle mechanoreceptors in healthy humans.…”

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confidence: 94%

Cyclooxygenase products sensitize muscle mechanoreceptors in humans with heart failure

Middlekauff

Chiu

Hamilton

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Prior work in animals and humans suggests that muscle mechanoreceptor control of sympathetic activation [muscle sympathetic nerve activity (MSNA)] during exercise in heart failure (HF) patients is heightened compared with that of healthy humans and that muscle mechanoreceptors are sensitized by metabolic by-products. We sought to determine whether cyclooxygenase products and/or endogenous adenosine, two metabolites of ischemic exercise, sensitize muscle mechanoreceptors during rhythmic handgrip (RHG) exercise in HF patients. Indomethacin, which inhibits the production of prostaglandins, and saline control were infused in 12 HF patients. In a different protocol, aminophylline, which inhibits adenosine receptors, and saline control were infused in 12 different HF patients. MSNA was recorded (microneurography). During exercise following saline, MSNA increased in the first minute of exercise, consistent with baseline heightened mechanoreceptor sensitivity. MSNA continued to increase during 3 min of RHG, indicative that muscle mechanoreceptors are sensitized by ischemia metabolites. Indomethacin, but not aminophylline, markedly attenuated the increase in MSNA during the entire 3 min of low-level rhythmic exercise, consistent with the sensitization of muscle mechanoreceptors by cyclooxygenase products. Interestingly, even the early increase in MSNA was abolished by indomethacin infusion, indicative of the very early generation of cyclooxygenase products after the onset of exercise in HF patients. In conclusion, muscle mechanoreceptors mediate the increase in MSNA during low-level RHG exercise in HF. Cyclooxygenase products, but not endogenous adenosine, play a central role in muscle mechanoreceptor sensitization. Finally, muscle mechanoreceptors in patients with HF have heightened basal sensitivity to mechanical stimuli, which also appears to be mediated by the early generation of cyclooxygenase products, resulting in exaggerated early increases in MSNA.

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Sympathetic nerve activity during prolonged rhythmic forearm exercise

Cited by 57 publications

References 21 publications

Cyclooxygenase inhibition attenuates sympathetic responses to muscle stretch in humans

Cyclooxygenase inhibition attenuates sympathetic responses to muscle stretch in humans

Isometric handgrip training does not improve flow-mediated dilation in subjects with normal blood pressure

Cyclooxygenase products sensitize muscle mechanoreceptors in humans with heart failure

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