Submitted on October 8, 2007
Accepted on January 14, 2008
Skeletal Muscle Contractile Protein Function is Preserved in Human Heart Failure
Yoko Okada1, Michael J. Toth1, and Peter VanBuren1*
1 Medicine, University of Vermont, Burlington, Vermont, United States
* To whom correspondence should be addressed. E-mail: vanburen{at}physiology.med.uvm.edu.
Skeletal muscle weakness is a commonly finding in patients with chronic heart failure (CHF). This functional deficit cannot be accounted for by muscle atrophy alone, suggesting that the syndrome of heart failure induces a myopathy in the skeletal musculature. To determine if decrements in muscle performance are related to alterations in contractile protein function, biopsies were obtained from the vastus lateralis muscle of 4 CHF patients and 4 controls. CHF patients exhibited reduced peak aerobic capacity (peak VO2) and knee extensor muscle strength. Decrements in whole muscle strength persisted after statistical control for muscle size. Thin filaments and myosin were isolated from biopsies and mechanically assessed using the in vitro motility assay. Isolated skeletal muscle thin filament function, however, did not differ between CHF patients and controls with respect to unloaded shortening velocity, calcium sensitivity, or maximal force. Similarly, no difference in maximal force or unloaded shortening velocity of isolated myosin was observed between CHF patients and controls. From these results, we conclude that skeletal contractile protein function is unaltered in CHF patients. Other factors, such as a decrease in total muscle myosin content, are likely contributors to the skeletal muscle strength deficit of heart failure.
