Inhibition of α₂-adrenergic vasoconstriction during contraction of glycolytic, not oxidative, rat hindlimb muscle

Previous studies have produced conflicting evidence as to whether sympathetic vasoconstriction is impaired in active skeletal muscle. Because α₂-, not α₁-, adrenergic vasoconstriction is attenuated by mild acidosis, we hypothesized that α₂-mediated sympathetic vasoconstriction would be attenuated in contracting glycolytic muscle, which produces more acidosis than oxidative muscle. We compared effects of lumbar sympathetic nerve stimulation and α-adrenergic agonists on arterial pressure femoral blood flow, and force output during contractions of oxidative or glycolytic muscles in anesthetized rats. We found that 1) sympathetic vasoconstriction was preserved during contractions of oxidative soleus muscle and during low- intensity contractions of glycolytic gastrocnemius-plantaris muscles but was abolished during maximal contractions of these glycolytic muscles; 2) this sympatholytic effect was caused by impaired α₂-, not α₁-, vasoconstriction; and 3) the increased muscle blood flow resulting from a combination of impaired vasoconstriction and increased arterial pressure was paralleled by increased force of gastrocnemius-plantaris muscle contraction. Thus contraction-induced impairment of α₂-vasoconstriction can augment muscle blood flow and muscle contraction, but the degree of impairment depends on fiber type and intensity of muscle contraction.