Skeletal muscle metaboreceptor exercise responses are attenuated in heart failure

D. A. Sterns, Steven Ettinger, K. S. Gray, S. K. Whisler, Timothy Mosher, M. B. Smith, Lawrence Sinoway

Research output: Contribution to journalArticle

123 Citations (Scopus)

Abstract

Background. Resting sympathetic nervous system activity is increased in heart failure. Whether sympathetic nervous system responses during exercise are increased is controversial. Futhermore, the role of muscle metaboreceptors and central command in regulating sympathetic outflow has been largely unexplored. Methods and Results. Muscle sympathetic nerve activity (MSNA, peroneal nerve) measured in nine heart failure subjects and eight age-matched control subjects during static exercise (30% maximal voluntary contraction) for 2 minutes and during a period of posthandgrip regional circulatory arrest. This maneuver isolates the metaboreceptor contribution to sympathetic nervous system responses. MSNA responses were similar during static exercise in the two groups. During posthandgrip regional circulatory arrest we observed a marked attenuation in MSNA responses in the heart failure subjects (15% increase in heart failure versus 57% increase in control subjects). A cold pressor test demonstrated a normal MSNA response to a potent nonspecific stimulus in the heart failure subjects (heart failure subjects, 141% increase; control subjects, 215% increase; NS). Nuclear magnetic resonance spectroscopy studies in five separate heart failure subjects and five control subjects suggested that the attenuated metaboreceptor response in heart failure was not due to reduced H+ production. Conclusions. Skeletal muscle metaboreceptor responses are impaired in heart failure. Because MSNA responses during static exercise are similar in the two groups, mechanisms aside from metaboreceptor stimulation must be important in increasing sympathetic nervous system activity.

Original languageEnglish (US)
Pages (from-to)2034-2039
Number of pages6
JournalCirculation
Volume84
Issue number5
DOIs
StatePublished - Jan 1 1991

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Skeletal Muscle
Heart Failure
Sympathetic Nervous System
Muscles
Peroneal Nerve
Magnetic Resonance Spectroscopy

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Sterns, D. A. ; Ettinger, Steven ; Gray, K. S. ; Whisler, S. K. ; Mosher, Timothy ; Smith, M. B. ; Sinoway, Lawrence. / Skeletal muscle metaboreceptor exercise responses are attenuated in heart failure. In: Circulation. 1991 ; Vol. 84, No. 5. pp. 2034-2039.
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abstract = "Background. Resting sympathetic nervous system activity is increased in heart failure. Whether sympathetic nervous system responses during exercise are increased is controversial. Futhermore, the role of muscle metaboreceptors and central command in regulating sympathetic outflow has been largely unexplored. Methods and Results. Muscle sympathetic nerve activity (MSNA, peroneal nerve) measured in nine heart failure subjects and eight age-matched control subjects during static exercise (30{\%} maximal voluntary contraction) for 2 minutes and during a period of posthandgrip regional circulatory arrest. This maneuver isolates the metaboreceptor contribution to sympathetic nervous system responses. MSNA responses were similar during static exercise in the two groups. During posthandgrip regional circulatory arrest we observed a marked attenuation in MSNA responses in the heart failure subjects (15{\%} increase in heart failure versus 57{\%} increase in control subjects). A cold pressor test demonstrated a normal MSNA response to a potent nonspecific stimulus in the heart failure subjects (heart failure subjects, 141{\%} increase; control subjects, 215{\%} increase; NS). Nuclear magnetic resonance spectroscopy studies in five separate heart failure subjects and five control subjects suggested that the attenuated metaboreceptor response in heart failure was not due to reduced H+ production. Conclusions. Skeletal muscle metaboreceptor responses are impaired in heart failure. Because MSNA responses during static exercise are similar in the two groups, mechanisms aside from metaboreceptor stimulation must be important in increasing sympathetic nervous system activity.",
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Skeletal muscle metaboreceptor exercise responses are attenuated in heart failure. / Sterns, D. A.; Ettinger, Steven; Gray, K. S.; Whisler, S. K.; Mosher, Timothy; Smith, M. B.; Sinoway, Lawrence.

In: Circulation, Vol. 84, No. 5, 01.01.1991, p. 2034-2039.

Research output: Contribution to journalArticle

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T1 - Skeletal muscle metaboreceptor exercise responses are attenuated in heart failure

AU - Sterns, D. A.

AU - Ettinger, Steven

AU - Gray, K. S.

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AU - Mosher, Timothy

AU - Smith, M. B.

AU - Sinoway, Lawrence

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N2 - Background. Resting sympathetic nervous system activity is increased in heart failure. Whether sympathetic nervous system responses during exercise are increased is controversial. Futhermore, the role of muscle metaboreceptors and central command in regulating sympathetic outflow has been largely unexplored. Methods and Results. Muscle sympathetic nerve activity (MSNA, peroneal nerve) measured in nine heart failure subjects and eight age-matched control subjects during static exercise (30% maximal voluntary contraction) for 2 minutes and during a period of posthandgrip regional circulatory arrest. This maneuver isolates the metaboreceptor contribution to sympathetic nervous system responses. MSNA responses were similar during static exercise in the two groups. During posthandgrip regional circulatory arrest we observed a marked attenuation in MSNA responses in the heart failure subjects (15% increase in heart failure versus 57% increase in control subjects). A cold pressor test demonstrated a normal MSNA response to a potent nonspecific stimulus in the heart failure subjects (heart failure subjects, 141% increase; control subjects, 215% increase; NS). Nuclear magnetic resonance spectroscopy studies in five separate heart failure subjects and five control subjects suggested that the attenuated metaboreceptor response in heart failure was not due to reduced H+ production. Conclusions. Skeletal muscle metaboreceptor responses are impaired in heart failure. Because MSNA responses during static exercise are similar in the two groups, mechanisms aside from metaboreceptor stimulation must be important in increasing sympathetic nervous system activity.

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