Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans.
Ten patients with preserved inotropic function having a dual-chamber (right atrium and right ventricle) pacemaker placed for complete heart block were studied. They performed static one-legged knee extension at 20% of their maximal voluntary contraction for 5 min during three conditions: 1) atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HR fixed at the resting value (DOO-Rest; 73 +/- 3 beats/min), and 3) HR fixed at peak exercise rate (DOO-Ex; 107 +/- 4 beats/min). During control exercise (DDD mode), mean arterial pressure (MAP) increased by 25 mmHg with no change in stroke volume (SV) or systemic vascular resistance. During DOO-Rest and DOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of a SV-dependent increase in cardiac output (+1.3 and +1.8 l/min, respectively). The increase in SV during DOO-Rest utilized a combination of increased contractility and the Frank-Starling mechanism (end-diastolic volume 118-136 ml). However, during DOO-Ex, a greater left ventricular contractility (end-systolic volume 55-38 ml) mediated the increase in SV.
Nóbrega
A C
AC
Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, Texas 75235-9034, USA.
Williamson
J W
JW
Garcia
J A
JA
Mitchell
J H
JH
D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D004562:Electrocardiography; D015444:Exercise / Q000502:physiology*; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D010138:Pacemaker, Artificial; D013318:Stroke Volume / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology