Author + information
- Received August 13, 2001
- Revision received November 14, 2001
- Accepted January 9, 2002
- Published online April 3, 2002.
- Brian D Duscha, MS*,*,
- Brian H Annex, MD*,‡,
- Howard J Green, PhD§,
- Anne M Pippen, MS* and
- William E Kraus, MD†
- ↵*Reprint requests and correspondence:
Brian D. Duscha, MS, Duke University Medical Center, Box 3022, Duke Center for Living, Durham, North Carolina 27710, USA.
Objectives It remains controversial whether the skeletal muscle alterations in chronic heart failure (CHF) are due to disease pathophysiology or result from chronic deconditioning. The purpose of this study was to compare the skeletal muscle of CHF patients to peak oxygen consumption (peak VO2) matched sedentary controls.
Background It has been established that skeletal muscle abnormalities are related to the exercise intolerance observed in patients with CHF.
Methods We studied the skeletal muscle of sedentary controls and patients with CHF matched for age, gender and peak VO2.
Results Hypothesis testing for the effects of group (CHF vs. normal), gender, and the interaction group × gender were performed. For capillary density only gender (p = 0.002) and the interaction of group × gender (p = 0.007) were significantly different. For 3-hydroxyl coenzyme A (CoA) dehydrogenase only group effect (p = 0.004) was significantly different. Mean values for capillary density were 1.46 ± 0.28 for CHF men versus 1.87 ± 0.32 for sedentary control men, 1.40 ± 0.32 for CHF women versus 1.15 ± 0.35 for sedentary control women. The activities for 3-hydroxyl CoA dehydrogenase were 3.09 ± 0.88 for CHF men versus 4.05 ± 0.42 for sedentary control men, 2.93 ± 0.72 for CHF women versus 3.51 ± 0.78 for sedentary control women.
Conclusions This study suggests that women and men adapt to CHF differently: men develop peripheral skeletal muscle abnormalities that are not attributable to deconditioning; women do not develop the same pathologic responses in skeletal muscle when compared with normal women matched for aerobic capacity.
☆ Supported by Grant HLI7670 (to Dr. Kraus) from the National Heart, Lung, and Blood Institute, Bethesda, Maryland, and by a Merit Review Grant from the Office of Research and Development, Medical Research Service, Department of Veterans Affairs (to Dr. Annex). Dr. Kraus and Dr. Annex received support from an Established Investigator Award from the American Heart Association.
- Received August 13, 2001.
- Revision received November 14, 2001.
- Accepted January 9, 2002.
- American College of Cardiology Foundation