Key result
Treadmill exercise in swine increased myocardial O2 consumption from 163 to 423 μmol/min (P≤0.05), which was matched by beta-adrenergic-mediated increases in O2 delivery.
In swine myocardium, myocardial oxygen consumption and delivery are matched during exercise primarily through feed-forward beta-adrenergic vasodilation.
Findings in swine should not guide human therapy; extends evidence for beta-adrenergic control of myocardial O2 delivery during exercise.
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 (MVO2) from 163+/-16 micromol/min (mean+/-SE) at rest to 423+/-75 micromol/min (P< or =0.05), which was paralleled by an increase in MDO2, so that myocardial O2 extraction (79+/-1% at rest) and coronary venous O2 tension (cvPO2, 23.7+/-1.0 mm Hg at rest) were maintained. Beta-adrenoceptor blockade blunted the exercise-induced increase of MDO2 out of proportion compared with the attenuation of the exercise-induced increase in MVO2, so that O2 extraction rose from 78+/-1% at rest to 83+/-1% during exercise and cvPO2 fell from 23.5+/-0.9 to 19.6+/-1.1 mm Hg (both P< or =0.05). In contrast, alpha-adrenoceptor blockade, either in the absence or presence of beta-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 beta-adrenoceptor activity, since combined muscarinic and beta-adrenoceptor blockade produced similar changes in O2 extraction and cvPO2, as did beta-adrenoceptor blockade alone. In conclusion, in swine myocardium, MVO2 and MDO2 are matched during exercise, which is the result of feed-forward beta-adrenergic vasodilation in conjunction with minimal a-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 cvPO2 levels are maintained even during heavy exercise suggests that a decrease in cvPO2 is not essential for coronary vasodilation during exercise.
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Duncker et al. (1998) studied Healthy (chronically instrumented swine) (n=8). Graded treadmill exercise and autonomic receptor blockades vs. Resting conditions / unblocked state was evaluated on Myocardial O2 consumption (MVO2), O2 extraction, and coronary venous O2 tension (cvPO2) (p=≤0.05). Treadmill exercise in swine increased myocardial O2 consumption from 163 to 423 μmol/min (P≤0.05), which was matched by beta-adrenergic-mediated increases in O2 delivery.
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