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Coronary pressure-flow relationship and exercise: contributions of heart rate, contractility, and alpha 1-adrenergic
D J Duncker1, N S Van Zon, M Crampton
1Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.
Insights
Exercise impedes coronary blood flow by increasing heart rate, alpha 1-adrenergic vasoconstriction, and left ventricular filling pressure. Contractility plays a minimal role in these exercise-induced reductions in maximal coronary blood flow.
Area of Science:
- Cardiovascular Physiology
- Exercise Physiology
Background:
- Exercise increases myocardial oxygen demand, necessitating enhanced coronary blood flow.
- Understanding factors limiting coronary blood flow during exercise is crucial for cardiovascular health.
Purpose of the Study:
- To investigate the mechanisms by which exercise reduces maximal coronary blood flow.
- To quantify the contributions of heart rate, contractility, and alpha 1-adrenergic vasoconstriction to these reductions.
Main Methods:
- Utilized chronically instrumented dogs to analyze the coronary pressure-flow relationship during maximal vasodilation induced by adenosine.
- Manipulated heart rate (treadmill exercise, atrial pacing), contractility (dobutamine), and alpha 1-adrenergic activity (prazosin).
Main Results:
- Exercise decreased maximal coronary blood flow by altering the pressure-flow relationship (reduced slope, increased pressure at zero flow).
- Increased heart rate and alpha 1-adrenergic vasoconstriction were primary contributors to reduced maximal coronary blood flow.
- Increased left ventricular filling pressure also contributed to the observed effects.
Conclusions:
- Exercise-induced reductions in maximal coronary blood flow are primarily mediated by increased heart rate, alpha 1-adrenergic vasoconstriction, and elevated left ventricular filling pressure.
- Contractility has a minimal impact on exercise-induced limitations in coronary blood flow.
Abstract:
We examined the impeding effects of exercise on coronary blood flow by analyzing exercise-induced changes in the pressure-flow relationship during maximal coronary vasodilation with adenosine in chronically instrumented dogs and assessed the individual contributions produced by heart rate, contractility, and alpha 1-adrenergic vasoconstriction. Treadmill exercise that increased heart rate from 118 +/- 6 beats/min at rest to 213 +/- 8 beats/min (P < 0.01) decreased maximum coronary blood flows by decreasing the slope of the linear part of the pressure-flow relationship for coronary pressures > or = 30 mmHg (slopeP > or = 30) from 12.3 +/- 0.9 to 10.9 +/- 0.9 ml.min-1 x g-1 x mmHg-1 (P < 0.01) and increasing the measured coronary pressure at zero flow (P zf,measured) from 12.6 +/- 1.2 to 23.3 +/- 2.0 mmHg (P < 0.01). Atrial pacing at 200 beats/min caused an increase of P zf,measured from 15.0 +/- 1.6 to 18.3 +/- 2.1 mmHg (P < 0.05) with no change in slopeP > or = 30. While pacing continued, infusion of dobutamine (20 micrograms.kg-1 x min-1 i.v.) increased contractility to levels similar to those during exercise but caused no significant change in coronary blood flow, as a decrease of the slopeP > or = 30 was compensated for by a slight decrease in P zf,measured. alpha 1-Adrenergic blockade with intracoronary prazosin (10 micrograms/kg) did not prevent the exercise-induced increase of P zf,measured but abolished the decrease of the slopeP > or = 30. When the increases in heart rate, contractility, and alpha 1-adrenergic vasoconstriction were prevented, exercise still increased P zf,measured from 15.8 +/- 2.1 to 21.8 +/- 2.6 mmHg (P < 0.05) but had no effect on the slopeP > or = 30. This residual increase in P zf,measured correlated with the concomitant increase in left ventricular filling pressure. In conclusion, exercise-induced decreases of maximum coronary blood flow were explained by increases in heart rate, alpha 1-adrenergic vasoconstriction, and left ventricular filling pressure, with a minimal contribution of contractility.