The original embargo on this release, (April 11 at 14:00 ET) has been lifted.
DALLAS April 12, 2002 A calcium-signaling protein transforms sedentary, easily fatigued muscles into energy-producing, fatigue-resistant muscles, UT Southwestern Medical Center at Dallas researchers report.
In a study published in todays issue of Science, the researchers found that by genetically expressing the protein in skeletal muscles of laboratory mice, easily fatigued, or type II, muscle fibers were transformed into fatigue-resistant and mitochondria-rich, or energy-producing, type I muscle fibers, which resemble muscles that have been exercised.
This research could lead to novel measures to stimulate muscles in patients with chronic diseases such as congestive heart failure or respiratory insufficiency, or individuals confined to bed rest.
The muscles of individuals who are on bed rest resemble type II muscle fibers; they fatigue quickly and the muscles are tired, said Dr. Rhonda Bassel-Duby, associate professor of internal medicine and co-author of the study. If we have a way of mimicking this protein, we can convert the muscle with a drug to a more fatigue-resistant, mitochondria-rich muscle.
Researchers expressed the active form of the calcium signaling protein called calcium/calmodulin-dependent protein kinase (CaMK) in the skeletal muscles of transgenic mice. CaMK controls production of mitochondria structures in cells that are responsible for energy production in mammalian muscle tissue.
Calcium signaling plays an essential role in muscle remodeling, said Dr. Hai Wu, lead author of the study and a postdoctoral research fellow in molecular biology.
CaMK has been intensely studied in neurons, where it is responsible for neuron plasticity and involved in learning and memory. Both neurons and muscle cells are excitable, and they share a lot of common signaling pathways in response to either brain activity or e
Contact: Amy Shields
UT Southwestern Medical Center