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Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, Texas 75235-9034
Received 11 November 1996; accepted in final form 28 April 1997.
Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712-717, 1997.
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.
echocardiography; pacemaker; left ventricular volume; Frank-Starling mechanism; myocardial contractility
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