J Physiol Sign Up for eTOC
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Physiol Volume 586, Number 4, 1195-1205, February 15, 2008 DOI: 10.1113/jphysiol.2007.144113
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
586/4/1195    most recent
jphysiol.2007.144113v1
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Wilkins, B. W.
Right arrow Articles by Joyner, M. J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wilkins, B. W.
Right arrow Articles by Joyner, M. J.
Related Collections
Right arrow Integrative

INTEGRATIVE

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

 Brad W. Wilkins1, Tasha L. Pike2, Elizabeth A. Martin2, Timothy B. Curry2, Maile L. Ceridon2 and Michael J. Joyner2

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






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2008 The Physiological Society.