Researchers Find New Way To Jump Start Tired Muscles

In a discovery that could help bed-ridden patients get back on their feet faster, a research team led by a Harvard Medical School (HMS) professor has found that a protein once associated only with liver function also plays an important role in muscle formation.

Bruce M. Spiegelman, professor of cell biology at HMS, joined researchers at University of Texas-Southwestern in publishing a study in the Aug. 15 issue of Nature demonstrating that the protein PGC-1 can supply certain muscles with the mitochondria that power their contractions.

Skeletal muscle is divided into two different types. PGC-1 is found naturally in type I, or “slow-twitch,” fibers, which are responsible for endurance and are fueled primarily by oxygen.

Easily fatigued type II muscle fibers, known as “fast-twitch” muscles, are fueled by the breakdown of sugar. When the protein is introduced to fatigued type II muscles, it supplies the fibers with the mitochondria they need to produce energy from oxygen.

Researchers in Spiegelman’s lab at the Dana-Farber Cancer Institute, a teaching affiliate of HMS, discovered the transformation of muscle types after genetically introducing PGC-1 into mice.

“Our goal was to learn more about muscle fiber type switching and development,” Spiegelman said. “We knew that the protein was expressed in muscle, and we thought that its function had to do with metabolism.”

Spiegelman said he was surprised at the result—the effects of the genetic modification in the mice resembled those of exercise.

“This discovery has made me more interested in the applications of this protein,” he said.

Since the presence of PGC-1 can change the composition of muscle fibers without a patient engaging in physical exercise, it may be possible to reinvigorate fatigued muscle just by injecting the protein into a patient.

Rhonda Bassel-Duby, a molecular biologist at UT-Southwestern who collaborated on the study, said that the findings may have implications for invalid patients whose inactivity has led to muscle atrophy.

Spiegelman also said the protein could eventually play a role in the treatment of obese patients who have difficulty exercising.