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J Appl Physiol (July 11, 2003). doi:10.1152/japplphysiol.00194.2003
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Submitted on February 25, 2003
Accepted on June 2, 2003

Attenuation of Cardiovascular Adaptations to Exercise in Frail Octogenarians

Ali A Ehsani1*, Robert J Spina2, Linda R Peterson1, Morton R Rinder1, Kathryn L Glover2, Dennis T Villareal2, Ellen F Binder3, and John O Holloszy2

1 Section of Applied Physiology, Washington University School of Medicine, St. Louis, MO, USA; Division of Geriatrics and Nutritional Sciences an d Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA; Cardiovascular Division, Washington University School of Medicine, St. Louis, MO, USA
2 Section of Applied Physiology, Washington University School of Medicine, St. Louis, MO, USA; Division of Geriatrics and Nutritional Sciences an d Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA
3 Division of Geriatrics and Nutritional Sciences an d Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA

* To whom correspondence should be addressed. E-mail: aehsani{at}im.wustl.edu.

To determine the mechanisms underlying increased aerobic power in response to exercise training in octogenarians, we studied mildly frail elderly men and women randomly assigned to a) an exercise group (n = 22) who participated in a training program consisting of 6 mo of physical therapy, strength training and walking exercises followed by 3 mo of more intense endurance exercise at 78% of peak heart rate; and b) a control sedentary group (n = 24). Peak O2 consumption (VO2) increased 14% in the exercise group (p < 0.0001) but decreased slightly in the controls. Training induced 14% increase (p = 0.027) in peak exercise cardiac output, determined with the acetylene-rebreathing method, and no change in a-v O2 content difference. The increase in cardiac output was mediated by increases in heart rate (p = 0.009) and probably stroke volume (p = 0.096). Left ventricular stroke work also increased significantly. In the men the increase in peak VO2 was exclusively due to a large increase in peak cardiac output (22%). In the women, the gain in peak VO2 was due to small increases in cardiac output and O2 extraction from skeletal muscles. Pulse pressure normalized for stroke volume and arterial elastance during peak effort did not change with training. Controls showed no changes. The results suggest that while frail octogenarians have a diminished capacity for improvement in aerobic power in response to exercise training this adaptation is mediated mostly by an increase in cardiac output during peak effort. Furthermore, cardiac output is likely to play a greater role in the adaptive increase in peak VO2 in the old men than old women.




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