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

TY - JOUR

T1 - Maximal heart rate does not limit cardiovascular capacity in healthy humans

T2 - insight from right atrial pacing during maximal exercise

AU - Munch, G D W

AU - Svendsen, J H

AU - Damsgaard, R

AU - Secher, N H

AU - González-Alonso, J

AU - Mortensen, S P

PY - 2014/1/15

Y1 - 2014/1/15

N2 - 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 (HRmax) and stroke volume (SV) are unclear. To evaluate the effect of tachycardia and elevations in HRmax 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 (WLmax) 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 HRmax 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 HRmax 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.

AB - 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 (HRmax) and stroke volume (SV) are unclear. To evaluate the effect of tachycardia and elevations in HRmax 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 (WLmax) 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 HRmax 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 HRmax 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.

KW - Adult

KW - Atrial Function, Right

KW - Exercise

KW - Exercise Tolerance

KW - Heart

KW - Heart Rate

KW - Humans

KW - Male

KW - Oxygen Consumption

KW - Ventricular Function, Left

U2 - 10.1113/jphysiol.2013.262246

DO - 10.1113/jphysiol.2013.262246

M3 - Journal article

C2 - 24190933

SN - 0022-3751

VL - 592

SP - 377

EP - 390

JO - The Journal of Physiology

JF - The Journal of Physiology

IS - Pt 2

ER -