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

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 vasodilatat...

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Published in:The Journal of physiology 2008-02, Vol.586 (4), p.1195
Main Authors: Brad W. Wilkins, Tasha L. Pike, Elizabeth A. Martin, Timothy B. Curry, Maile L. Ceridon, Michael J. Joyner
Format: Article
Language:English
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Summary: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 O 2 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 CO 2 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.
ISSN:0022-3751
1469-7793
DOI:10.1113/jphysiol.2007.144113