Maximal heart rate does not limit cardiovascular capacity in healthy humans: insight from right atrial pacing during maximal exercise

In humans, maximal aerobic power (V̇O2 max ) is associated with a plateau in cardiac output (Q̇), but the mechanisms regulating the interplay between maximal heart rate (HR _max) and stroke volume (SV) are unclear. To evaluate the effect of tachycardia and elevations in HR _max on cardiovascular function and capacity during maximal exercise in healthy humans, 12 young male cyclists performed incremental cycling and one-legged knee-extensor exercise (KEE) to exhaustion with and without right atrial pacing to increase HR. During control cycling, Q̇ and leg blood flow increased up to 85% of maximal workload (WL _max) and remained unchanged until exhaustion. SV initially increased, plateaued and then decreased before exhaustion (P < 0.05) despite an increase in right atrial pressure (RAP) and a tendency (P = 0.056) for a reduction in left ventricular transmural filling pressure (LVFP). Atrial pacing increased HR _max from 184 ± 2 to 206 ± 3 beats min ^-1 (P < 0.05), but Q̇ remained similar to the control condition at all intensities because of a lower SV and LVFP (P < 0.05). No differences in arterial pressure, peripheral haemodynamics, catecholamines or V̇O2 were observed, but pacing increased the rate pressure product and RAP (P < 0.05). Atrial pacing had a similar effect on haemodynamics during KEE, except that pacing decreased RAP. In conclusion, the human heart can be paced to a higher HR than observed during maximal exercise, suggesting that HR _max and myocardial work capacity do not limit V̇O2 max in healthy individuals. A limited left ventricular filling and possibly altered contractility reduce SV during atrial pacing, whereas a plateau in LVFP appears to restrict Q̇ close to V̇O2 max.