AMHERST, Mass. Muscle physiologist Edward Debold at the University of Massachusetts Amherst's School of Public Health and Health Sciences recently received a three-year, $198,000 grant from the American Heart Association to support studies to uncover the molecular mechanisms of skeletal muscle fatigue.
The work will advance basic understanding of muscle function and should lead to new drug therapies for individuals with fatigue that greatly limits physical function and quality of life, including the 5.7 million Americans living with chronic heart failure.
Medical researchers and physiologists believed for a long time that heart failure, a syndrome or collection of symptoms, involved only cardiac muscle, Debold points out. But in the late 1980s, they were surprised to find that function of skeletal muscle is also compromised and is much more susceptible to fatigue, he explains. "So for affected individuals the simplest tasks around the house become extremely arduous." It makes sense to study the basis of skeletal muscle function, he adds, "because if we can reduce the fatigue, we could enable them to live independently longer and increase activity levels, which can improve their long-term prognosis."
Muscle fatigue of this type is like a car engine with a bad exhaust system, unable to get rid of waste products, the physiologist says. By-products of metabolism build up inside the muscle cells and inhibit its ability to contract. "Our understanding of muscle fatigue is currently limited by our inability to directly observe this process at the molecular level," Debold says. "The really exciting aspect of this project is that it will overcome this limitation by using the latest technologies to directly visualize and characterize the process of muscle fatigue at the single-molecule level."
He and colleagues are experts in the use of a single molecule laser trap assay, which enables them to directly observe the nanoscale moti
|Contact: Janet Lathrop|
University of Massachusetts at Amherst