CLINICAL STUDIES
Capillary density of skeletal muscle
A contributing mechanism for exercise intolerance in class II–III chronic heart failure independent of other peripheral alterations
Brian D. Duscha, MS*,
William E. Kraus, MD*  ,
Steven J. Keteyian, PhD ,
Martin J. Sullivan, MD*,
Howard J. Green, PhD ,
Fred H. Schachat, PhD,
Anne M. Pippen, BS*,
Clinton A. Brawner, BS,
Jason M. Blank, BS and
Brian H. Annex, MD*
* Division of Cardiology, Duke University Medical Center, Durham, North Carolina, USA
Division of Cell Biology, Duke University Medical Center, Durham, North Carolina, USA
Henry Ford Heart and Vascular Institute, Detroit, Michigan, USA
Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada
Manuscript received September 9, 1998;
revised manuscript received January 21, 1999,
accepted February 10, 1999.
Reprint requests and correspondence: Brian D. Duscha, Duke University Medical Center, Box 3022, Duke Center for Living, Durham, North Carolina 27710
Dusch001{at}mc.duke.edu
OBJECTIVES
The study was conducted to determine if the capillary density of skeletal muscle is a potential contributor to exercise intolerance in class II–III chronic heart failure (CHF).
BACKGROUND
Previous studies suggest that abnormalities in skeletal muscle histology, contractile protein content and enzymology contribute to exercise intolerance in CHF.
METHODS
The present study examined skeletal muscle biopsies from 22 male patients with CHF compared with 10 age-matched normal male control patients. Aerobic capacities, myosin heavy chain (MHC) isoforms, enzymes, and capillary density were measured.
RESULTS
The patients with CHF demonstrated a reduced peak oxygen consumption when compared to controls (15.0 ± 2.5 vs. 19.8 ± 5.0 ml·kg–1·min–1, p <0.05). Using cell-specific antibodies to directly assess vascular density, there was a reduction in capillary density in CHF measured as the number of endothelial cells/fiber (1.42 ± 0.28 vs. 1.74 ± 0.35, p = 0.02). In CHF, capillary density was inversely related to maximal oxygen consumption (r = 0.479, p = 0.02). The MHC IIx isoform was found to be higher in patients with CHF versus normal subjects (28.5 ± 13.6 vs. 19.5 ± 9.4, p <0.05).
CONCLUSIONS
There was a significant reduction in microvascular density in patients with CHF compared with the control group, without major differences in other usual histologic and biochemical aerobic markers. The inverse relationship with peak oxygen consumption seen in the CHF group suggests that a reduction in microvascular density of skeletal muscle may precede other skeletal muscle alterations and play a critical role in the exercise intolerance characteristic of patients with CHF.
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Abbreviations and Acronyms
| | A-VO2 | = arteriovenous-oxygen difference | | CHF | = chronic heart failure | | LVEF | = left ventricular ejection fraction | | MET | = metabolic equivalent | | MHC | = myosin heavy chain | | NMR | = nuclear magnetic resonance |
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