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Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas
Submitted 20 June 2008 ; accepted in final form 19 November 2008
The purpose of this investigation was to determine whether cardiovascular adaptations characteristic of long-term endurance exercise compensate more effectively during cardioselective β1-adrenergic receptor blockade-induced reductions in sympathoadrenergic-stimulated contractility. Endurance-trained (ET) athletes (n = 8) and average-trained (AT; n = 8) subjects performed submaximal cycling exercise at moderate [45% maximum oxygen uptake (
O2max)] and heavy (70%
O2max) workloads, with and without metoprolol. Cardiac output (
c), heart rate (HR), and systolic blood pressure were recorded at rest and during exercise. Cardiac work was calculated from the triple product of HR, stroke volume, and systolic blood pressure, and myocardial efficiency is represented as cardiac work for a given total body oxygen consumption. Metoprolol reduced
c at 45%
O2max (P = 0.004) and 70%
O2max (P = 0.022) in ET subjects, but did not alter
c in the AT subjects. In ET subjects at 45%
O2max, metoprolol-induced reductions in
c were a result of decreases in HR (P < 0.05) and the absence of a compensatory increase in stroke volume (P > 0.05). The cardiac work and calculated cardiac efficiency were reduced with metoprolol in ET subjects at both exercise intensities and in the AT subjects during the high-intensity workload (P < 0.01). The cardiac work and the calculated cardiac efficiency were not affected by metoprolol in the AT subjects during the 45%
O2max exercise. Therefore, in AT subjects, β-blockade reduced the amount of pressure generation necessary to produce the same amount of work during moderate-intensity exercise. In patients with heart disease receiving metoprolol, a decrease in the generation of cardiac pressure necessary to perform a given amount of work during mild-to-moderate exercise would prove to be beneficial.
Frank-Starling mechanism; cardiac output; cardiac efficiency; acetylene rebreathe; exercise-induced cardiac hypertrophy
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