α-adrenergic vascular responsiveness during postexercise hypotension in humans

In sedentary individuals, postexercise hypotension following a single bout of aerobic exercise is due to an unexplained peripheral vasodilatation. We tested the hypothesis that alpha-adrenergic responsiveness in the forearm and leg vasculatures is blunted during postexercise hypotension. We studied 12 men and two women before and 30 min after a 60 min bout of cycling at 60 % (V) over dot (O2,peak). In the first five subjects, arterial pressure (brachial artery catheter) and forearm blood flow (plethysmography) were measured and vascular conductance was calculated during intraarterial infusions of the alpha(1)-agonist phenylephrine and the alpha(2)-agonist clonidine. Exercise reduced mean arterial pressure (89 +/- 2 vs. 95 +/- 2 mmHg, P < 0.05) and increased forearm vascular conductance 77 33 % (P < 0.05). Despite these changes in baseline vascular conductance, vasoconstrictor responses in the forearm to phenylephrine and clonidine were similar (or enhanced) postexercise vs. preexercise. In the remaining nine subjects, arterial pressure (femoral artery catheter) and leg blood flow (Doppler ultrasound of the femoral artery) were measured and vascular conductance was calculated during intraarterial infusions of phenylephrine and clonidine. Exercise reduced mean arterial pressure (80 +/- 2 vs. 89 +/- 2 mmHg, P < 0.05) and increased leg vascular conductance 94 +/- 16 % (P < 0.05). Despite these changes in baseline vascular conductance, vasoconstrictor responses in the leg to phenylephrine and clonidine were similar (or enhanced) postexercise vs. preexercise. These results suggest that vascular responsiveness to alpha-adrenergic agonists is maintained during postexercise hypotension in humans. Thus, while postexercise hypotension is associated with increased vascular conductance in the forearm and leg, it does not appear that blunting of alpha-adrenergic responsiveness is the cause.