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Peripheral vasodilatation determines cardiac output in exercising humans: insight from atrial pacing
A A Bada1, J H Svendsen, N H Secher
1The Copenhagen Muscle Research Centre, Rigshospitalet, Denmark.
Insights
In humans, increasing heart rate during exercise does not boost cardiac output. Instead, blood flow to muscles and venous return are key regulators of cardiac output during exercise.
Area of Science:
- Cardiovascular Physiology
- Exercise Physiology
- Human Haemodynamics
Background:
- Studies in dogs suggest heart rate manipulation doesn't affect exercise-induced cardiac output increases.
- Human cardiovascular systems differ significantly from dogs, necessitating direct investigation.
- Understanding cardiac output regulation during exercise is crucial for cardiovascular health.
Purpose of the Study:
- To investigate the roles of heart rate and peripheral vasodilation in regulating cardiac output during steady-state exercise in humans.
- To determine if findings from canine studies are applicable to human cardiovascular responses.
Main Methods:
- Measured central and peripheral haemodynamics in 10 healthy males.
- Utilized atrial pacing to control heart rate (100–150 beats/min) during rest, one-legged knee extensor exercise (24 W), and femoral arterial ATP infusion.
- Monitored cardiac output, leg blood flow, vascular conductance, mean arterial pressure, and pressures within the heart and pulmonary artery.
Main Results:
- Exercise and ATP infusion increased cardiac output, leg blood flow, and vascular conductance, without altering cerebral perfusion.
- Atrial pacing, despite increasing heart rate, did not change cardiac output due to a compensatory decrease in stroke volume.
- Atrial pacing affected pressures within the heart and pulmonary artery, and altered left ventricular contractility and noradrenaline levels.
Conclusions:
- Elevated cardiac output during steady-state exercise in humans is primarily regulated by increased skeletal muscle blood flow and venous return.
- The increase in heart rate during exercise appears secondary to the regulation of cardiac output, rather than a primary driver.
- Human cardiovascular responses to heart rate manipulation during exercise differ from those observed in dogs.
Abstract:
In dogs, manipulation of heart rate has no effect on the exercise-induced increase in cardiac output. Whether these findings apply to humans remain uncertain, because of the large differences in cardiovascular anatomy and regulation. To investigate the role of heart rate and peripheral vasodilatation in the regulation of cardiac output during steady-state exercise, we measured central and peripheral haemodynamics in 10 healthy male subjects, with and without atrial pacing (100–150 beats min(−1)) during: (i) resting conditions, (ii) one-legged knee extensor exercise (24 W) and (iii) femoral arterial ATP infusion at rest. Exercise and ATP infusion increased cardiac output, leg blood flow and vascular conductance (P < 0.05), whereas cerebral perfusion remained unchanged. During atrial pacing increasing heart rate by up to 54 beats min(−1), cardiac output did not change in any of the three conditions, because of a parallel decrease in stroke volume (P < 0.01). Atrial pacing increased mean arterial pressure (MAP) at rest and during ATP infusion (P < 0.05), whereas MAP remained unchanged during exercise. Atrial pacing lowered central venous pressure (P < 0.05) and pulmonary capillary wedge pressure (P < 0.05) in all conditions, whereas it did not affect pulmonary mean arterial pressure. Atrial pacing lowered the left ventricular contractility index (dP/dt) (P < 0.05) in all conditions and plasma noradrenaline levels at rest (P < 0.05), but not during exercise and ATP infusion. These results demonstrate that the elevated cardiac output during steady-state exercise is regulated by the increase in skeletal muscle blood flow and venous return to the heart, whereas the increase in heart rate appears to be secondary to the regulation of cardiac output.
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