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 -adrenoceptor activation contributes to augmented hypoxic exercise vasodilatation. Fourteen subjects (age: 29±2) breathed hypoxic gas to titrate arterial O₂ saturation (pulse oximetry) to 80%, while remaining normocapnic via a re-breath 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 -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±43ml min^-1) vs. saline (169±30ml min^-1) or combined phentolamine / propranolol (213±25ml min^-1; P>0.05 for both). During 20% hypoxic exercise, FBF was greater with phentalomine (466±57ml min^-1; P>0.05) vs. saline (346±40ml min^-1) but was similar to combined phentolamine / propranolol (450±43ml min^-1). Thus, in the absence of overlying vasoconstriction, the contribution of -adrenergic mechanisms to the augmented hypoxic vasodilatation is dependent on exercise intensity.