{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,27]],"date-time":"2026-06-27T03:03:45Z","timestamp":1782529425556,"version":"3.54.5"},"reference-count":35,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2008,2,18]],"date-time":"2008-02-18T00:00:00Z","timestamp":1203292800000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2008,2,15]]},"abstract":"<jats:p>We previously reported that hypoxia\u2010mediated reductions in \u03b1\u2010adrenoceptor sensitivity do not explain the augmented vasodilatation during hypoxic exercise, suggesting an enhanced vasodilator signal. We hypothesized that \u03b2\u2010adrenoceptor activation contributes to augmented hypoxic exercise vasodilatation. Fourteen subjects (age: 29 \u00b1 2 years) breathed hypoxic gas to titrate arterial O<jats:sub>2<\/jats:sub> 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), \u03b1\u2010adrenoceptor inhibition (phentolamine), and combined \u03b1\u2010 and \u03b2\u2010adrenoceptor inhibition (phentolomine\/propranolol). Forearm blood flow (FBF), heart rate, blood pressure, minute ventilation, and end\u2010tidal CO<jats:sub>2<\/jats:sub> were determined. Hypoxia increased heart rate (<jats:italic>P<\/jats:italic> &lt; 0.05) and minute ventilation (<jats:italic>P<\/jats:italic> &lt; 0.05) at rest and exercise under all drug infusions, whereas mean arterial pressure was unchanged. Arterial adrenaline (<jats:italic>P<\/jats:italic> &lt; 0.05) and venous noradrenaline (<jats:italic>P<\/jats:italic> &lt; 0.05) were higher with hypoxia during all drug infusions. The change (\u0394) in FBF during 10% hypoxic exercise was greater with phentolamine (\u0394306 \u00b1 43 ml min<jats:sup>\u22121<\/jats:sup>) <jats:italic>vs.<\/jats:italic> saline (\u0394169 \u00b1 30 ml min<jats:sup>\u22121<\/jats:sup>) or combined phentolamine\/propranolol (\u0394213 \u00b1 25 ml min<jats:sup>\u22121<\/jats:sup>; <jats:italic>P<\/jats:italic> &lt; 0.05 for both). During 20% hypoxic exercise, \u0394FBF was greater with phentalomine (\u0394466 \u00b1 57 ml min<jats:sup>\u22121<\/jats:sup>; <jats:italic>P<\/jats:italic> &lt; 0.05) <jats:italic>vs.<\/jats:italic> saline (\u0394346 \u00b1 40 ml min<jats:sup>\u22121<\/jats:sup>) but was similar to combined phentolamine\/propranolol (\u0394450 \u00b1 43 ml min<jats:sup>\u22121<\/jats:sup>). Thus, in the absence of overlying vasoconstriction, the contribution of \u03b2\u2010adrenergic mechanisms to the augmented hypoxic vasodilatation is dependent on exercise intensity.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.144113","type":"journal-article","created":{"date-parts":[[2007,11,30]],"date-time":"2007-11-30T01:46:03Z","timestamp":1196387163000},"page":"1195-1205","source":"Crossref","is-referenced-by-count":55,"title":["Exercise intensity\u2010dependent contribution of \u03b2\u2010adrenergic receptor\u2010mediated vasodilatation in hypoxic humans"],"prefix":"10.1113","volume":"586","author":[{"given":"Brad W.","family":"Wilkins","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tasha L.","family":"Pike","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth 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