Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise

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Abstract
—To date, no studies have investigated coronary vasomotor control of myocardial O 2 delivery (MD o 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 (MV̇ o 2 ) from 163±16 μmol/min (mean±SE) at rest to 423±75 μmol/min ( P ≤0.05), which was paralleled by an increase in MD o 2 , so that myocardial O 2 extraction (79±1% at rest) and coronary venous O 2 tension (cvP o 2 , 23.7±1.0 mm Hg at rest) were maintained. β-Adrenoceptor blockade blunted the exercise-induced increase of MD o 2 out of proportion compared with the attenuation of the exercise-induced increase in MV̇ o 2 , so that O 2 extraction rose from 78±1% at rest to 83±1% during exercise and cvP o 2 fell from 23.5±0.9 to 19.6±1.1 mm Hg (both P ≤0.05). In contrast, α-adrenoceptor blockade, either in the absence or presence of β-adrenoceptor blockade, had no effect on myocardial O 2 extraction or cvP o 2 at rest or during exercise. Muscarinic receptor blockade resulted in a decreased O 2 extraction and an increase in cvP o 2 at rest, an effect that waned during exercise. The vasodilation produced by muscarinic receptor blockade was likely due to an increased β-adrenoceptor activity, since combined muscarinic and β-adrenoceptor blockade produced similar changes in O 2 extraction and cvP o 2 , as did β-adrenoceptor blockade alone. In conclusion, in swine myocardium, MV̇ o 2 and MD o 2 are matched during exercise, which is the result of feed-forward β-adrenergic vasodilation in conjunction with minimal α-adrenergic vasoconstriction. β-Adrenergic vasodilation is due to an increase in sympathetic activity but may also be supported by withdrawal of muscarinic receptor–mediated inhibition of β-adrenergic coronary vasodilation. The observation that cvP o 2 levels are maintained even during heavy exercise suggests that a decrease in cvP o 2 is not essential for coronary vasodilation during exercise.