Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise Evidence for Feed-Forward b-Adrenergic Control

To date, no studies have investigated coronary vasomotor control of myocardial O2 delivery (MDO2) and its modulation by the autonomic nervous system in the porcine heart during treadmill exercise. We studied 8 chronically instrumented swine under resting conditions and during graded treadmill exercise. Exercise up to 85% to 90% of maximum heart rate produced an increase in myocardial O2 consumption (MV̇O2) from 163616 mmol/min (mean6SE) at rest to 423675 mmol/min (P#0.05), which was paralleled by an increase in MDO2, so that myocardial O2 extraction (7961% at rest) and coronary venous O2 tension (cvPO2, 23.761.0 mm Hg at rest) were maintained. b-Adrenoceptor blockade blunted the exercise-induced increase of MDO2 out of proportion compared with the attenuation of the exercise-induced increase in MV̇O2, so that O2 extraction rose from 7861% at rest to 8361% during exercise and cvPO2 fell from 23.560.9 to 19.661.1 mm Hg (both P#0.05). In contrast, a-adrenoceptor blockade, either in the absence or presence of b-adrenoceptor blockade, had no effect on myocardial O2 extraction or cvPO2 at rest or during exercise. Muscarinic receptor blockade resulted in a decreased O2 extraction and an increase in cvPO2 at rest, an effect that waned during exercise. The vasodilation produced by muscarinic receptor blockade was likely due to an increased b-adrenoceptor activity, since combined muscarinic and b-adrenoceptor blockade produced similar changes in O2 extraction and cvPO2, as did b-adrenoceptor blockade alone. In conclusion, in swine myocardium, MV̇O2 and MDO2 are matched during exercise, which is the result of feed-forward b-adrenergic vasodilation in conjunction with minimal a-adrenergic vasoconstriction. b-Adrenergic vasodilation is due to an increase in sympathetic activity but may also be supported by withdrawal of muscarinic receptor–mediated inhibition of b-adrenergic coronary vasodilation. The observation that cvPO2 levels are maintained even during heavy exercise suggests that a decrease in cvPO2 is not essential for coronary vasodilation during exercise. (Circ Res. 1998;82:1312-1322.)