Exercise intensity-dependent contribution of β-adrenergic receptor-mediated vasodilatation in hypoxic humans

Brad W. Wilkins, Tasha L. Pike, Elizabeth A. Martin, Timothy B Curry, Maile L. Ceridon, Michael Joseph Joyner

Research output: Contribution to journalArticle

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Abstract

We previously reported that hypoxia-mediated reductions in α-adrenoceptor sensitivity do not explain the augmented vasodilatation during hypoxic exercise, suggesting an enhanced vasodilator signal. We hypothesized that β-adrenoceptor activation contributes to augmented hypoxic exercise vasodilatation. Fourteen subjects (age: 29 ± 2 years) breathed hypoxic gas to titrate arterial O2 saturation (pulse oximetry) to 80%, while remaining normocapnic via a rebreath system. Brachial artery and antecubital vein catheters were placed in the exercising arm. Under normoxic and hypoxic conditions, baseline and incremental forearm exercise (10% and 20% of maximum) was performed during control (saline), α-adrenoceptor inhibition (phentolamine), and combined α- and β-adrenoceptor inhibition (phentolomine/propranolol). Forearm blood flow (FBF), heart rate, blood pressure, minute ventilation, and end-tidal CO2 were determined. Hypoxia increased heart rate (P < 0.05) and minute ventilation (P < 0.05) at rest and exercise under all drug infusions, whereas mean arterial pressure was unchanged. Arterial adrenaline (P < 0.05) and venous noradrenaline (P < 0.05) were higher with hypoxia during all drug infusions. The change (Δ) in FBF during 10% hypoxic exercise was greater with phentolamine (Δ306 ± 43 ml min-1) vs. saline (Δ169 ± 30 ml min-1) or combined phentolamine/propranolol (Δ213 ± 25 ml min-1; P < 0.05 for both). During 20% hypoxic exercise, ΔFBF was greater with phentalomine (Δ466 ± 57 ml min-1; P < 0.05) vs. saline (Δ346 ± 40 ml min -1) but was similar to combined phentolamine/propranolol (Δ450 ± 43 ml min-1). Thus, in the absence of overlying vasoconstriction, the contribution of β-adrenergic mechanisms to the augmented hypoxic vasodilatation is dependent on exercise intensity.

Original languageEnglish (US)
Pages (from-to)1195-1205
Number of pages11
JournalJournal of Physiology
Volume586
Issue number4
DOIs
StatePublished - Feb 15 2008

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Phentolamine
Forearm
Vasodilation
Adrenergic Receptors
Propranolol
Ventilation
Heart Rate
Oximetry
Brachial Artery
Vasoconstriction
Vasodilator Agents
Pharmaceutical Preparations
Adrenergic Agents
Epinephrine
Veins
Norepinephrine
Arterial Pressure
Arm
Catheters
Gases

ASJC Scopus subject areas

  • Physiology

Cite this

Exercise intensity-dependent contribution of β-adrenergic receptor-mediated vasodilatation in hypoxic humans. / Wilkins, Brad W.; Pike, Tasha L.; Martin, Elizabeth A.; Curry, Timothy B; Ceridon, Maile L.; Joyner, Michael Joseph.

In: Journal of Physiology, Vol. 586, No. 4, 15.02.2008, p. 1195-1205.

Research output: Contribution to journalArticle

Wilkins, Brad W. ; Pike, Tasha L. ; Martin, Elizabeth A. ; Curry, Timothy B ; Ceridon, Maile L. ; Joyner, Michael Joseph. / Exercise intensity-dependent contribution of β-adrenergic receptor-mediated vasodilatation in hypoxic humans. In: Journal of Physiology. 2008 ; Vol. 586, No. 4. pp. 1195-1205.
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abstract = "We previously reported that hypoxia-mediated reductions in α-adrenoceptor sensitivity do not explain the augmented vasodilatation during hypoxic exercise, suggesting an enhanced vasodilator signal. We hypothesized that β-adrenoceptor activation contributes to augmented hypoxic exercise vasodilatation. Fourteen subjects (age: 29 ± 2 years) breathed hypoxic gas to titrate arterial O2 saturation (pulse oximetry) to 80{\%}, while remaining normocapnic via a rebreath system. Brachial artery and antecubital vein catheters were placed in the exercising arm. Under normoxic and hypoxic conditions, baseline and incremental forearm exercise (10{\%} and 20{\%} of maximum) was performed during control (saline), α-adrenoceptor inhibition (phentolamine), and combined α- and β-adrenoceptor inhibition (phentolomine/propranolol). Forearm blood flow (FBF), heart rate, blood pressure, minute ventilation, and end-tidal CO2 were determined. Hypoxia increased heart rate (P < 0.05) and minute ventilation (P < 0.05) at rest and exercise under all drug infusions, whereas mean arterial pressure was unchanged. Arterial adrenaline (P < 0.05) and venous noradrenaline (P < 0.05) were higher with hypoxia during all drug infusions. The change (Δ) in FBF during 10{\%} hypoxic exercise was greater with phentolamine (Δ306 ± 43 ml min-1) vs. saline (Δ169 ± 30 ml min-1) or combined phentolamine/propranolol (Δ213 ± 25 ml min-1; P < 0.05 for both). During 20{\%} hypoxic exercise, ΔFBF was greater with phentalomine (Δ466 ± 57 ml min-1; P < 0.05) vs. saline (Δ346 ± 40 ml min -1) but was similar to combined phentolamine/propranolol (Δ450 ± 43 ml min-1). Thus, in the absence of overlying vasoconstriction, the contribution of β-adrenergic mechanisms to the augmented hypoxic vasodilatation is dependent on exercise intensity.",
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