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.
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