Altered mechanisms of sympathetic activation during rhythmic forearm exercise in heart failure

David Silber, Greg Sutliff, Qing Yang, Michael B. Smith, Lawrence Sinoway, Urs Leuenberger

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Abstract

In congestive heart failure (CHF), the mechanisms of exercise-induced sympathoexcitation are poorly defined. We compared the responses of sympathetic nerve activity directed to muscle (MSNA) and to skin (SSNA, peroneal microneurography) during rhythmic handgrip (RHG) at 25% of maximal voluntary contraction and during posthandgrip circulatory arrest (PHG-CA) in CHF patients with those of an age-matched control group. During RHG, the CHF patients fatigued prematurely. At end exercise, the increase in MSNA was similar in both groups (CHF patients, n = 12; controls, n = 10). However, during PHG-CA, in the controls MSNA returned to baseline, whereas it remained elevated in CHF patients (P < 0.05). Similarly, at end exercise, the increase in SSNA was comparable in both groups (CHF patients, n = 11; controls, n = 12), whereas SSNA remained elevated during PHG-CA in CHF patients but not in the controls (P < 0.05). In a separate control group (n = 6), even high- intensity static handgrip was not accompanied by sustained elevation of SSNA during PHG-CA. 31P-nuclear magnetic resonance spectroscopy during RHG demonstrated significant muscle acidosis and accumulation of inorganic phosphate in CHF patients (n = 7) but not in controls (n = 9). We conclude that in CHF patients rhythmic forearm exercise leads to premature fatigue and accumulation of muscle metabolites. The prominent PHG-CA response of MSNA and SSNA in CHF patients suggests activation of the muscle metaboreflex. Because, in contrast to controls, in CHF patients both MSNA and SSNA appear to be under muscle metaboreflex control, the mechanisms and distribution of sympathetic outflow during exercise appear to be different from normal.

Original languageEnglish (US)
Pages (from-to)1551-1559
Number of pages9
JournalJournal of Applied Physiology
Volume84
Issue number5
StatePublished - May 1 1998

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Forearm
Heart Failure
Exercise
Muscles
Muscle Fatigue
Control Groups
Acidosis
Research Design
Magnetic Resonance Spectroscopy
Phosphates
Skin

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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title = "Altered mechanisms of sympathetic activation during rhythmic forearm exercise in heart failure",
abstract = "In congestive heart failure (CHF), the mechanisms of exercise-induced sympathoexcitation are poorly defined. We compared the responses of sympathetic nerve activity directed to muscle (MSNA) and to skin (SSNA, peroneal microneurography) during rhythmic handgrip (RHG) at 25{\%} of maximal voluntary contraction and during posthandgrip circulatory arrest (PHG-CA) in CHF patients with those of an age-matched control group. During RHG, the CHF patients fatigued prematurely. At end exercise, the increase in MSNA was similar in both groups (CHF patients, n = 12; controls, n = 10). However, during PHG-CA, in the controls MSNA returned to baseline, whereas it remained elevated in CHF patients (P < 0.05). Similarly, at end exercise, the increase in SSNA was comparable in both groups (CHF patients, n = 11; controls, n = 12), whereas SSNA remained elevated during PHG-CA in CHF patients but not in the controls (P < 0.05). In a separate control group (n = 6), even high- intensity static handgrip was not accompanied by sustained elevation of SSNA during PHG-CA. 31P-nuclear magnetic resonance spectroscopy during RHG demonstrated significant muscle acidosis and accumulation of inorganic phosphate in CHF patients (n = 7) but not in controls (n = 9). We conclude that in CHF patients rhythmic forearm exercise leads to premature fatigue and accumulation of muscle metabolites. The prominent PHG-CA response of MSNA and SSNA in CHF patients suggests activation of the muscle metaboreflex. Because, in contrast to controls, in CHF patients both MSNA and SSNA appear to be under muscle metaboreflex control, the mechanisms and distribution of sympathetic outflow during exercise appear to be different from normal.",
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Altered mechanisms of sympathetic activation during rhythmic forearm exercise in heart failure. / Silber, David; Sutliff, Greg; Yang, Qing; Smith, Michael B.; Sinoway, Lawrence; Leuenberger, Urs.

In: Journal of Applied Physiology, Vol. 84, No. 5, 01.05.1998, p. 1551-1559.

Research output: Contribution to journalArticle

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T1 - Altered mechanisms of sympathetic activation during rhythmic forearm exercise in heart failure

AU - Silber, David

AU - Sutliff, Greg

AU - Yang, Qing

AU - Smith, Michael B.

AU - Sinoway, Lawrence

AU - Leuenberger, Urs

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N2 - In congestive heart failure (CHF), the mechanisms of exercise-induced sympathoexcitation are poorly defined. We compared the responses of sympathetic nerve activity directed to muscle (MSNA) and to skin (SSNA, peroneal microneurography) during rhythmic handgrip (RHG) at 25% of maximal voluntary contraction and during posthandgrip circulatory arrest (PHG-CA) in CHF patients with those of an age-matched control group. During RHG, the CHF patients fatigued prematurely. At end exercise, the increase in MSNA was similar in both groups (CHF patients, n = 12; controls, n = 10). However, during PHG-CA, in the controls MSNA returned to baseline, whereas it remained elevated in CHF patients (P < 0.05). Similarly, at end exercise, the increase in SSNA was comparable in both groups (CHF patients, n = 11; controls, n = 12), whereas SSNA remained elevated during PHG-CA in CHF patients but not in the controls (P < 0.05). In a separate control group (n = 6), even high- intensity static handgrip was not accompanied by sustained elevation of SSNA during PHG-CA. 31P-nuclear magnetic resonance spectroscopy during RHG demonstrated significant muscle acidosis and accumulation of inorganic phosphate in CHF patients (n = 7) but not in controls (n = 9). We conclude that in CHF patients rhythmic forearm exercise leads to premature fatigue and accumulation of muscle metabolites. The prominent PHG-CA response of MSNA and SSNA in CHF patients suggests activation of the muscle metaboreflex. Because, in contrast to controls, in CHF patients both MSNA and SSNA appear to be under muscle metaboreflex control, the mechanisms and distribution of sympathetic outflow during exercise appear to be different from normal.

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