Skeletal muscle metaboreceptor stimulation opposes peak metabolic vasodilation in humans

Lawrence Sinoway, S. Prophet

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

The total blood flow requirements of a large muscle mass can exceed the maximal cardiac output generated by the heart during exercise. Therefore, to maintain blood pressure, muscle vasodilation must be opposed by sympathetic vasoconstriction. The primary neural signal that increases sympathetic outflow is unclear. In an effort to isolate the vasoconstricting mechanism that opposes vasodilation, we measured the peak forearm vascular conductance response after the release of 10 minutes of forearm circulatory arrest under five separate study conditions: 1) no leg exercise, 2) low-level supine leg exercise, 3) low-level supine leg exercise with leg circulatory arrest after exercise, 4) high-level supine leg exercise, and 5) high-level supine leg exercise with leg circulatory arrest after exercise. We found that both high-workload conditions reduced peak forearm conductance below the no-leg exercise condition (a 34% reduction during leg exercise and a 52% reduction during leg exercise followed by leg circulatory arrest). In addition, at each workload, leg circulatory arrest after exercise, which isolated the skeletal muscle metaboreceptor contribution to vasoconstriction, reduced forearm conductance by approximately 20% below the values noted for leg exercise alone (combined central command and metaboreceptor stimulation). In a separate group of subjects, peak forearm blood flow was measured during lower-body negative pressure to levels up to -40 mm Hg, a maneuver that unloads high- and low-pressure baroreceptors. This intervention did not affect peak forearm blood flow. We conclude that 1) metaboreceptor stimulation is the crucial mechanism causing the vasoconstriction that opposes metabolic vasodilation, 2) some volitional influence during exercise acts to oppose metaboreceptor-mediated constriction, and 3) baroreceptor unloading does not influence maximal forearm conductance.

Original languageEnglish (US)
Pages (from-to)1576-1584
Number of pages9
JournalCirculation Research
Volume66
Issue number6
DOIs
StatePublished - Jan 1 1990

Fingerprint

Vasodilation
Leg
Skeletal Muscle
Forearm
Vasoconstriction
Pressoreceptors
Workload
Lower Body Negative Pressure
Pressure
Muscles
Constriction
Cardiac Output
Blood Vessels
Blood Pressure

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Skeletal muscle metaboreceptor stimulation opposes peak metabolic vasodilation in humans",
abstract = "The total blood flow requirements of a large muscle mass can exceed the maximal cardiac output generated by the heart during exercise. Therefore, to maintain blood pressure, muscle vasodilation must be opposed by sympathetic vasoconstriction. The primary neural signal that increases sympathetic outflow is unclear. In an effort to isolate the vasoconstricting mechanism that opposes vasodilation, we measured the peak forearm vascular conductance response after the release of 10 minutes of forearm circulatory arrest under five separate study conditions: 1) no leg exercise, 2) low-level supine leg exercise, 3) low-level supine leg exercise with leg circulatory arrest after exercise, 4) high-level supine leg exercise, and 5) high-level supine leg exercise with leg circulatory arrest after exercise. We found that both high-workload conditions reduced peak forearm conductance below the no-leg exercise condition (a 34{\%} reduction during leg exercise and a 52{\%} reduction during leg exercise followed by leg circulatory arrest). In addition, at each workload, leg circulatory arrest after exercise, which isolated the skeletal muscle metaboreceptor contribution to vasoconstriction, reduced forearm conductance by approximately 20{\%} below the values noted for leg exercise alone (combined central command and metaboreceptor stimulation). In a separate group of subjects, peak forearm blood flow was measured during lower-body negative pressure to levels up to -40 mm Hg, a maneuver that unloads high- and low-pressure baroreceptors. This intervention did not affect peak forearm blood flow. We conclude that 1) metaboreceptor stimulation is the crucial mechanism causing the vasoconstriction that opposes metabolic vasodilation, 2) some volitional influence during exercise acts to oppose metaboreceptor-mediated constriction, and 3) baroreceptor unloading does not influence maximal forearm conductance.",
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Skeletal muscle metaboreceptor stimulation opposes peak metabolic vasodilation in humans. / Sinoway, Lawrence; Prophet, S.

In: Circulation Research, Vol. 66, No. 6, 01.01.1990, p. 1576-1584.

Research output: Contribution to journalArticle

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