α-Adrenergic blockade unmasks a greater compensatory vasodilation in hypoperfused contracting muscle

Darren P. Casey, Michael Joseph Joyner

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

We previously demonstrated that acute hypoperfusion in exercising human muscle causes an immediate increase in vascular resistance that is followed by a partial restoration (less than 100% recovery) of flow. In the current study we examined the contribution of α-adrenergic vasoconstriction in the initial changes in vascular resistance at the onset of hypoperfusion as well as in the recovery of flow over time. Nine healthy male subjects (29 ±2) performed rhythmic forearm exercise (20% of maximum) during hypoperfusion evoked by intra-arterial balloon inflation. Each trial included; baseline, exercise prior to inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound), local (brachial artery), and systemic arterial pressure (MAP; Finometer) were measured. The trial was repeated during phentolamine infusion (α-adrenergic receptor blockade). Forearm vascular conductance (FVC; ml min-1 100 mmHg -1) and resistance (mmHg mlmin -1) was calculated from BF (mlmin -1) and local MAP (mmHg). Recovery of FBF and FVC (steady state inflation plus exercise value-nadir)/[steady state exercise (control) value - nadir] with phentolamine was enhanced compared with the respective control (no drug) trial (FBF = 97 ±5% vs. 81 ±6%, P<0.05; FVC = 126 ±9% vs. 91 ±5%, P<0.01). However, the absolute (0.05±0.01 vs. 0.06±0.01 mmHg ml min -1; P = 0.17) and relative (35±5% vs. 31 ±2%; P = 0.41) increase in vascular resistance at the onset of balloon inflation was not different between the α-adrenergic receptor inhibition and control (no drug) trials. Therefore, our data indicate that α-adrenergic mediated vasoconstriction restricts compensatory vasodilation during forearm exercise with hypoperfusion, but is not responsible for the initial increase in vascular resistance at the onset of hypoperfusion.

Original languageEnglish (US)
Article numberArticle 271
JournalFrontiers in Physiology
Volume3 JUL
DOIs
StatePublished - 2012

Fingerprint

Vasodilation
Adrenergic Agents
Economic Inflation
Exercise
Muscles
Forearm
Vascular Resistance
Phentolamine
Drug and Narcotic Control
Vasoconstriction
Adrenergic Receptors
Brachial Artery
Blood Vessels
Healthy Volunteers
Arterial Pressure

Keywords

  • Alpha-adrenergic receptors
  • Blood flow
  • Exercise
  • Hypoperfusion
  • Vascular resistance

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

α-Adrenergic blockade unmasks a greater compensatory vasodilation in hypoperfused contracting muscle. / Casey, Darren P.; Joyner, Michael Joseph.

In: Frontiers in Physiology, Vol. 3 JUL, Article 271, 2012.

Research output: Contribution to journalArticle

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abstract = "We previously demonstrated that acute hypoperfusion in exercising human muscle causes an immediate increase in vascular resistance that is followed by a partial restoration (less than 100{\%} recovery) of flow. In the current study we examined the contribution of α-adrenergic vasoconstriction in the initial changes in vascular resistance at the onset of hypoperfusion as well as in the recovery of flow over time. Nine healthy male subjects (29 ±2) performed rhythmic forearm exercise (20{\%} of maximum) during hypoperfusion evoked by intra-arterial balloon inflation. Each trial included; baseline, exercise prior to inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound), local (brachial artery), and systemic arterial pressure (MAP; Finometer) were measured. The trial was repeated during phentolamine infusion (α-adrenergic receptor blockade). Forearm vascular conductance (FVC; ml min-1 100 mmHg -1) and resistance (mmHg mlmin -1) was calculated from BF (mlmin -1) and local MAP (mmHg). Recovery of FBF and FVC (steady state inflation plus exercise value-nadir)/[steady state exercise (control) value - nadir] with phentolamine was enhanced compared with the respective control (no drug) trial (FBF = 97 ±5{\%} vs. 81 ±6{\%}, P<0.05; FVC = 126 ±9{\%} vs. 91 ±5{\%}, P<0.01). However, the absolute (0.05±0.01 vs. 0.06±0.01 mmHg ml min -1; P = 0.17) and relative (35±5{\%} vs. 31 ±2{\%}; P = 0.41) increase in vascular resistance at the onset of balloon inflation was not different between the α-adrenergic receptor inhibition and control (no drug) trials. Therefore, our data indicate that α-adrenergic mediated vasoconstriction restricts compensatory vasodilation during forearm exercise with hypoperfusion, but is not responsible for the initial increase in vascular resistance at the onset of hypoperfusion.",
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AB - We previously demonstrated that acute hypoperfusion in exercising human muscle causes an immediate increase in vascular resistance that is followed by a partial restoration (less than 100% recovery) of flow. In the current study we examined the contribution of α-adrenergic vasoconstriction in the initial changes in vascular resistance at the onset of hypoperfusion as well as in the recovery of flow over time. Nine healthy male subjects (29 ±2) performed rhythmic forearm exercise (20% of maximum) during hypoperfusion evoked by intra-arterial balloon inflation. Each trial included; baseline, exercise prior to inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound), local (brachial artery), and systemic arterial pressure (MAP; Finometer) were measured. The trial was repeated during phentolamine infusion (α-adrenergic receptor blockade). Forearm vascular conductance (FVC; ml min-1 100 mmHg -1) and resistance (mmHg mlmin -1) was calculated from BF (mlmin -1) and local MAP (mmHg). Recovery of FBF and FVC (steady state inflation plus exercise value-nadir)/[steady state exercise (control) value - nadir] with phentolamine was enhanced compared with the respective control (no drug) trial (FBF = 97 ±5% vs. 81 ±6%, P<0.05; FVC = 126 ±9% vs. 91 ±5%, P<0.01). However, the absolute (0.05±0.01 vs. 0.06±0.01 mmHg ml min -1; P = 0.17) and relative (35±5% vs. 31 ±2%; P = 0.41) increase in vascular resistance at the onset of balloon inflation was not different between the α-adrenergic receptor inhibition and control (no drug) trials. Therefore, our data indicate that α-adrenergic mediated vasoconstriction restricts compensatory vasodilation during forearm exercise with hypoperfusion, but is not responsible for the initial increase in vascular resistance at the onset of hypoperfusion.

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