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-adrenergic vasoconstriction in exercising human thigh muscles
1 Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX 76107, USA2 Copenhagen Muscle Research Center, Rigshospitalet, DK-2200, Copenhagen N, Denmark
The mechanisms underlying metabolic inhibition of sympathetic responses within exercising skeletal muscle remain incompletely understood. The aim of the present study was to test whether 
2-adrenoreceptor-mediated vasoconstriction was more sensitive to metabolic inhibition than 1-vasoconstriction during dynamic knee-extensor exercise. We studied healthy volunteers using two protocols: (1) wide dose ranges of the -adrenoreceptor agonists phenylephrine (PE, 1 selective) and BHT-933 (BHT, 2 selective) were administered intra-arterially at rest and during 27 W knee-extensor exercise (n= 13); (2) flow-adjusted doses of PE (0.3 µg kg-1 l-1) and BHT (15 µg kg-1 l-1) were administered at rest and during ramped exercise (7 W to 37 W; n= 10). Ultrasound Doppler and thermodilution techniques provided direct measurements of femoral blood flow (FBF). PE (0.8 µg kg-1) and BHT (40 µg kg-1) produced comparable maximal reductions in FBF at rest (-58 ± 6 versus-64 ± 4%). Despite increasing the doses, PE (1.6 µg kg-1 min-1) and BHT (80 µg kg-1 min-1) caused significantly smaller changes in FBF during 27 W exercise (-13 ± 4 versus-3 ± 5%). During ramped exercise, significant vasoconstriction at lower intensities (7 and 17 W) was seen following PE (-16 ± 5 and -16 ± 4%), but not BHT (-2 ± 4 and -4 ± 5%). At the highest intensity (37 W), FBF was not significantly changed by either drug. Collectively, these data demonstrate metabolic inhibition of -adrenergic vasoconstriction in large postural muscles of healthy humans. Both 1- and 2-adrenoreceptor agonists produce comparable vasoconstriction in the resting leg, and dynamic thigh exercise attenuates 1- and 2-mediated vasoconstriction similarly. However, 2-mediated vasoconstriction appears more sensitive to metabolic inhibition, because 2 is completely inhibited even at low workloads, whereas 1 becomes progressively inhibited with increasing workloads.
(Received 16 September 2003;
accepted after revision 19 December 2003;
first published online 23 December 2003)
Corresponding author M. Sander: Rigshospitalet, section 7652, Blegdamsvej 9, DK-2100 Copenhagen Ø, Denmark. Email: sanders{at}dadlnet.dk
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