doi: 10.1161/01.RES.0000231259.29646.74
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© 2006 American Heart Association, Inc.
Editorials |
When Hearts Fail So Does Skeletal Muscle
Breaking a Vicious Cycle
From the Center for Cardiovascular Research, University of Illinois at Chicago Department of Physiology & Biophysics.
Correspondence to R. John Solaro, PhD, Department of Physiology & Biophysics (M/C 901), University of Illinois at Chicago, College of Medicine, 835 S Wolcott Ave, Chicago, IL 60612. E-mail solarorj@uic.edu
See related article, pages 1514–1519
Key Words: hypertrophy • congestive heart failure • animal models of human disease • heart failure
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
 |
Introduction |
|---|
In heart failure, keeping up with the oxygen demands of working skeletal muscles becomes compromised during exercise. As if this situation is not bad enough, as with many aspects of the heart failure syndrome, there are more vicious mechanisms at work. It has been known for some time that skeletal muscle function is also depressed in patients and animals in heart failure. The depression has been attributed to disuse atrophy, changes in fiber types, and abnormal metabolism.1,2 Thus the impaired cardiac function in patients not only limits exercise, but depressed skeletal muscle function itself inhibits the ability to exercise causing further depression of cardiac function.
In the current issue of Circulation Research, Lunde et al3 report evidence which supports the concept that heart failure leads to a primary depression in the force generating capacity of skeletal muscle, and which provides new insights into the mechanism. Their approach involved investigation of single living fibers isolated from the soleus muscle of rats whose hearts had been stressed by ligation of the coronary arteries (MI mice) 6 weeks before the experiments. In technically demanding experiments, Lunde et al3 simultaneously determined the force and intracellular Ca2+ ([Ca2+]i) in single soleus cells under nonfatiguing and fatiguing conditions. Under nonfatiguing conditions contraction and Ca2+- transients of sham and MI-fibers were not significantly different, but there was a depression in the levels of [Ca2+]i during the tetani. Compared with controls, MI-fibers had no major changes in expression of membrane proteins involved in
Related Article:
Circ. Res. 2006 98: 1514-1519.