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

• Published in: The Journal of physiology 2008-02, Vol.586 (4), p.1195-1205
• Main Authors: Wilkins, Brad W., Pike, Tasha L., Martin, Elizabeth A., Curry, Timothy B., Ceridon, Maile L., Joyner, Michael J.
• Format: Article
• Language: English
• Subjects: Adult; Antihypertensive Agents; Blood Gas Analysis; Blood Pressure - drug effects; Blood Pressure - physiology; Epinephrine - blood; Exercise - physiology; Female; Forearm - blood supply; Heart Rate - drug effects; Heart Rate - physiology; Humans; Hypoxia - physiopathology; Integrative; Male; Norepinephrine - blood; Phentolamine - pharmacology; Propranolol - pharmacology; Receptors, Adrenergic, beta - physiology; Regional Blood Flow - drug effects; Regional Blood Flow - physiology; Vasodilation - drug effects; Vasodilation - physiology; Vasodilator Agents - pharmacology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2007.144113

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.