Autonomic control of vasomotion in the porcine coronary circulation during treadmill exercise -: Evidence for feed-forward β-adrenergic control

To date, no studies have investigated coronary vasomotor control of myocardial O-2 delivery (MDo(2)) 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 O-2 consumption (MVo(2)) from 163+/-16 mu mol/min (mean+/-SE) at rest to 4-23+/-75 mu mol/min (P less than or equal to 0.05), which was paralleled by an increase in MDo(2), so that myocardial O-2 extraction (79+/-1% at rest) and coronary venous O-2 tension (cvPo(2), 237+/-1.0 mm Hg at rest) were maintained. beta-Adrenoceptor blockade blunted the exercise-induced increase of MDo(2) out of proportion compared with the attenuation of the exercise-induced increase in MVO2 so that O-2 extraction rose from 78+/-1% at rest to 83+/-l% during exercise and cvPo(2) fell from 23.5+/-0.9 to 19.6+/-1.1 mm Hg (both P less than or equal to 0.05). In contrast, alpha-adrenoceptor blockade, either in the absence or presence of beta-adrenoceptor blockade, had no effect on myocardial 0(2) extraction or cvPo(2) at rest or during exercise. Muscarinic receptor blockade resulted in a decreased O-2 extraction and an increase in cvPo(2) at rest, an effect that waned during exercise. The vasodilation produced by muscarinic receptor blockade was Likely due to an increased beta-adrenoceptor activity, since combined muscarinic and alpha-adrenoceptor blockade produced similar changes in O-2 extraction and cvPo(2), as did beta-adrenoceptetr blockade alone. In conclusion, in swine myocardium, MVo(2) and MDo(2) are matched during exercise, which is the result of feed-forward beta-adrenergic vasodilation in conjunction with minimal alpha-adrenergic vasoconstriction. beta-Adrenergic vasodilation is due to an increase in sympathetic activity but may also be supported by withdrawal of muscarinic receptor-mediated inhibition of beta-adrenergic coronary vasodilation. The observation that cvPo(2) levels are maintained even during heavy exercise suggests that a decrease in cvPo(2) is not essential for coronary vasodilation during exercise.