Effects of partial neuromuscular blockade on sympathetic nerve responses to static exercise in humans

R. G. Victor, S. L. Pryor, N. H. Secher, J. H. Mitchell

Research output: Contribution to journalArticle

164 Citations (Scopus)

Abstract

We used intraneural recordings of sympathetic nerve activity in conscious humans to determine if central command increases sympathetic discharge to resting skeletal muscle during static exercise. In nine healthy subjects, we measured arterial pressure, heart rate, and muscle sympathetic nerve activity with microelectrodes in the peroneal nerve of the resting leg during 1) static handgrip at 15% and 30% maximal voluntary contraction and 2) attempted handgrip during partial neuromuscular blockade produced by systemic administration of tubocurarine chloride (0.075 mg/kg i.v.). During curare, subjects reported that they used near-maximal motor effort to attempt a sustained handgrip contraction, but they generated almost no force. Without sustained contraction, the intent to exercise alone, that is, central command, caused statistically significant (p < 0.05) increases in muscle sympathetic nerve activity as well as in arterial pressure and heart rate. However, the increases in muscle sympathetic nerve activity (+56 ± 16% over control) and in mean arterial pressure (+12 ± 2 mm Hg) during attempted handgrip were much smaller (p < 0.05) than the sympathetic nerve response (+ 217 ± 37% over control) and pressor response (+25 ± 3 mm Hg) during an actual static handgrip at 30% maximal voluntary contraction. In contrast, heart rate increased as much during the attempted contraction (+18 ± 2 beats/min) as during the actual contraction at 30% maximal voluntary contraction (+16 ± 4 beats/min). In 11 additional subjects, the heart rate responses during curare were greatly attenuated (p < 0.05) by atropine but were not significantly affected by propranolol. From these observations, we conclude that during static handgrip in humans central command plays a major role in the regulation of parasympathetic outflow to the sinus node and a minor role in the activation of sympathetic outflow to nonexercising skeletal muscle. The new concept suggested by these data is that central command governs vagally mediated increases in heart rate at all levels of static exercise but contributes to activation of skeletal muscle sympathetic outflow only at near-maximal levels of static handgrip.

Original languageEnglish (US)
Pages (from-to)468-476
Number of pages9
JournalCirculation Research
Volume65
Issue number2
StatePublished - 1989

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Neuromuscular Blockade
Heart Rate
Exercise
Curare
Arterial Pressure
Skeletal Muscle
Tubocurarine
Muscles
Peroneal Nerve
Sinoatrial Node
Microelectrodes
Atropine
Propranolol
Leg
Myocardium
Healthy Volunteers

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Effects of partial neuromuscular blockade on sympathetic nerve responses to static exercise in humans. / Victor, R. G.; Pryor, S. L.; Secher, N. H.; Mitchell, J. H.

In: Circulation Research, Vol. 65, No. 2, 1989, p. 468-476.

Research output: Contribution to journalArticle

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abstract = "We used intraneural recordings of sympathetic nerve activity in conscious humans to determine if central command increases sympathetic discharge to resting skeletal muscle during static exercise. In nine healthy subjects, we measured arterial pressure, heart rate, and muscle sympathetic nerve activity with microelectrodes in the peroneal nerve of the resting leg during 1) static handgrip at 15{\%} and 30{\%} maximal voluntary contraction and 2) attempted handgrip during partial neuromuscular blockade produced by systemic administration of tubocurarine chloride (0.075 mg/kg i.v.). During curare, subjects reported that they used near-maximal motor effort to attempt a sustained handgrip contraction, but they generated almost no force. Without sustained contraction, the intent to exercise alone, that is, central command, caused statistically significant (p < 0.05) increases in muscle sympathetic nerve activity as well as in arterial pressure and heart rate. However, the increases in muscle sympathetic nerve activity (+56 ± 16{\%} over control) and in mean arterial pressure (+12 ± 2 mm Hg) during attempted handgrip were much smaller (p < 0.05) than the sympathetic nerve response (+ 217 ± 37{\%} over control) and pressor response (+25 ± 3 mm Hg) during an actual static handgrip at 30{\%} maximal voluntary contraction. In contrast, heart rate increased as much during the attempted contraction (+18 ± 2 beats/min) as during the actual contraction at 30{\%} maximal voluntary contraction (+16 ± 4 beats/min). In 11 additional subjects, the heart rate responses during curare were greatly attenuated (p < 0.05) by atropine but were not significantly affected by propranolol. From these observations, we conclude that during static handgrip in humans central command plays a major role in the regulation of parasympathetic outflow to the sinus node and a minor role in the activation of sympathetic outflow to nonexercising skeletal muscle. The new concept suggested by these data is that central command governs vagally mediated increases in heart rate at all levels of static exercise but contributes to activation of skeletal muscle sympathetic outflow only at near-maximal levels of static handgrip.",
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