Research could ease the transition to an active lifestyle
If you don’t exercise regularly, your muscles become less able to support physical activity, so you tire out quickly. That makes it extremely difficult for sedentary people to change their lifestyle to improve their health. Because being sedentary is a risk factor for metabolic disorders like obesity and diabetes, many scientists are trying to find ways to help lower the barrier to getting into an exercise routine—to make muscles work more like those of an athlete without years of training.
Two such researchers are Steven R. Smith, M.D., scientific director of the Florida Hospital Translational Research Institute for Metabolism and Diabetes (TRI-MD), an affiliate of Sanford Burnham Prebys Medical Discovery Institute (SBP), and Daniel Kelly, M.D., scientific director of SBP’s Lake Nona campus. Together with Rick Vega, Ph.D., research assistant professor in Dr. Kelly’s group, they recently contributed to a study published in the Journal of Biological Chemistry that identifies one way that muscle becomes better at generating the energy needed for strenuous exercise.
“Our findings are a key step toward a thorough understanding of how muscle increases capacity to burn fuel with exercise training,” said Kelly. “Such an understanding could allow us to develop a drug or a supplement that makes it easier for people with metabolic disease to adopt a more active lifestyle.”
The new research builds on a previous investigation from Kelly’s lab, which found that mice engineered for better exercise performance had more of an enzyme called lactate dehydrogenase B (LDHB) in their muscle. LDHB levels were linked to fuel-burning efficiency, suggesting that LDHB does something important even though it’s not directly involved in burning fuels.
In the new study, the team, led by Zhenji Gan, Ph.D., a professor at Nanjing University (previously a postdoc in Kelly’s lab), engineered another strain of mice that have extra LDHB in their muscle. These mice could run longer than normal mice because the mitochondria in their muscles were more efficient.
“Now that we know LDHB is a key regulator of mitochondrial efficiency, the next step is to figure out how the LDHB gene is turned on and how that leads to enhanced mitochondrial function,” said Smith. “Delineating those signaling steps should point to potential therapeutic targets aimed at obesity and a variety of muscle diseases.”
The paper is available online here.