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α‐Adrenergic Vascular Responsiveness during Postexercise Hypotension in Humans
Author(s) -
Halliwill John R.,
Dinenno Frank A.,
Dietz Niki M.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.042838
Subject(s) - phenylephrine , medicine , clonidine , brachial artery , blood pressure , forearm , vasodilation , vascular resistance , femoral artery , mean arterial pressure , anesthesia , plethysmograph , cardiology , heart rate , surgery
In sedentary individuals, postexercise hypotension following a single bout of aerobic exercise is due to an unexplained peripheral vasodilatation. We tested the hypothesis that α‐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 % V̇ O 2, 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 α 1 ‐agonist phenylephrine and the α 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 α‐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 α‐adrenergic responsiveness is the cause.