Peripheral vasodilatation determines cardiac output in exercising humans: insight from atrial pacing

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.

Figure 1. Cardiac output (A), stroke volume (B), mean arterial pressure (C) and systemic vascular conductance (D) as a function of heart rate

Data are means ± SEM. *Significantly different from baseline within the same trial. †Significantly different from resting conditions. §Significantly different from exercise trial. (P < 0.05).

Figure 2. Central venous pressure (A), pulmonary arterial mean pressure (B), pulmonary capillary wedge pressure (C), sysolic blood pressure (D), diastolic blood pressure (E) and pulse pressure (F) as a function of heart rate

Data are means ± SEM. *Significantly different from baseline within the same trial. †Significantly different from resting conditions. §Significantly different from exercise trial. (P < 0.05).

Figure 3. The left ventricular contractility index dP/dt_max during resting conditions, exercise and femoral arterial ATP infusion with and without atrial pacing

Data are means ± SEM. *Significantly different from baseline within the same trial (P < 0.05). †Significantly different from resting conditions (P < 0.05).

Figure 4. Leg blood flow (A), leg vascular conductance (B), middle cerebral artery V_mean (C) and brain vascular conductance index (D) as a function of heart rate

Data are means ± SEM. *Significantly different from baseline within the same trial (P < 0.05). †Significantly different from resting conditions (A: P < 0.05; B: P < 0.001).

Figure 5. Acute changes in systolic, diastolic and mean arterial pressure in the seconds after initiation of the 1st pacing level in the three different trials: resting (A), exercising (B) and arterial ATP infusion at rest (C)

*Significantly different from baseline within the same trial (P < 0.05). †Significantly different from 5 s (P < 0.05). ‡Significantly different from 10 s (P < 0.05).