Author + information
- Received September 14, 1985
- Revision received December 10, 1985
- Accepted December 26, 1985
- Published online May 1, 1986.
- Wade H. Martin III, MDa,1,
- Edward F. Coyle, PHD1,
- Susan A. Bloomfield, MA and
- Ali A. Ehsani, MD, FACC
- ↵aAddress for reprints: Wade H. Martin III, MD, Washington University School of Medicine, 4566 Scott Avenue, Campus Box 8113, 2nd Floor, West Building, St. Louis, Missouri 63110.
To determine the role of preload in maintaining the enhanced stroke volume of upright exercise-trained endurance athletes after deconditioning, six highly trained subjects undergoing upright and supine bicycle ergometry were characterized before and after 3, 8 and 12 weeks of inactivity that reduced oxygen uptake by 20%. During exercise, oxygen uptake, cardiac output by carbon dioxide rebreathing, cardiac dimensions by M-mode echocardiography, indirect arterial blood pressure and heart rate were studied simultaneously. Two months of inactivity resulted in a reduction in stroke volume, calculated as cardiac output/heart rate, during upright exercise (p < 0.005) without a significant change during supine exercise. A concomitant decrease in the left ventricular end-diastolic dimension from the trained to the deconditioned state was observed in the upright posture (5.1 ± 0.3 versus 4.6 ± 0.3 cm; p = 0.02) but not with recumbency (5.4 ± 0.2 versus 5.1 ± 0.3 cm; p = NS). There was a strong correlation between left ventricular end-diastolic dimension and stroke volume (r > 0.80) in all subjects. No significant changes in percent fractional shortening or left ventricular end-systolic dimension occurred in either position after cessation of training. Estimated left ventricular mass was 20% lower after 3 and 8 weeks of inactivity than when the subjects were conditioned (p < 0.05 for both).
Thus, the endurance-trained state for upright exercise is associated with a greater stroke volume during upright exercise because of augmented preload. Despite many years of intense training, inactivity for only a few weeks results in loss of this adaptation in conjunction with regression of left ventricular hypertrophy.
↵1 Dr. Martin and Dr. Coyle were postdoctoral research trainees supported by National Institutes of Health Institutional National Research Service Award AG00078.
This research was supported in part by Institutional National Research Service Award AG00078 from the National Institutes of Health, Bethesda, Maryland and Grant HL17646 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland, Specialized Center of Research in Ischemic Heart Disease.
- Received September 14, 1985.
- Revision received December 10, 1985.
- Accepted December 26, 1985.
- American College of Cardiology Foundation