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This Article Full Text Full Text (PDF) All Versions of this Article: 586/4/1195    most recent jphysiol.2007.144113v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wilkins, B. W. Articles by Joyner, M. J. Search for Related Content PubMed PubMed Citation Articles by Wilkins, B. W. Articles by Joyner, M. J. Related Collections Integrative

¹ Department of Human Physiology, University of Oregon, Eugene, OR, USA
² Department of Anaesthesiology, Mayo Clinic, Rochester, MN, USA

We previously reported that hypoxia-mediated reductions in -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), -adrenoceptor inhibition (phentolamine), and combined - 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 () in FBF during 10% hypoxic exercise was greater with phentolamine (306 ± 43 ml min^–1) vs. saline (169 ± 30 ml min^–1) or combined phentolamine/propranolol (213 ± 25 ml min^–1; P < 0.05 for both). During 20% hypoxic exercise, FBF was greater with phentalomine (466 ± 57 ml min^–1; P < 0.05) vs. saline (346 ± 40 ml min^–1) but was similar to combined phentolamine/propranolol (450 ± 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.

(Received 29 August 2007; accepted after revision 28 November 2007; first published online 29 November 2007)
Corresponding author B. W. Wilkins: Department of Human Physiology, 122 Esslinger Hall, 1240 University of Oregon, Eugene, OR 97403-1240, USA. Email: bwilkins{at}uoregon.edu