New discovery shows how exercise increases muscle energy production

Although it is well known that exercise is good for us, many of the underlying molecular mechanisms remain to be identified. Now researchers at the University of Copenhagen have discovered new insights that will help us understand the health effects of exercise – and potentially pave the way for new treatments for many muscle diseases.

“We have identified a new, important mechanism for muscle cell energy production and shown that it is activated by physical exercise – regardless of age, gender and health status,” says Associate Professor Lykke Sylow from the Department of Biomedical Sciences and corresponding author of the new study.

In the study, the researchers show that a particular protein plays a key role in energy production in the cells’ energy factory, the mitochondria. And they were surprised that through fitness training (so-called aerobic training) it is actually possible to circumvent the role of this protein in energy production.

Our research shows that exercise can counteract genetic errors in muscle energy production. If this protein is missing, exercise can activate alternative processes that restore the muscle’s energy capacity and circumvent the genetic error. This is extremely interesting because it shows how useful exercise is in overcoming genetic defects.”

Postdoc Tang Cam Phung Pham, lead author of the study

An opportunity to develop new treatment methods

Researchers still don’t know exactly how exercise circumvents this process, but their discovery could help pave the way for new treatments for a range of muscle diseases. Their discovery could make it possible to develop a drug that mimics the health benefits of exercise in people who are unable to exercise, explains Lykke Sylow:

“It opens up the possibility of developing new treatments for more than 200 different diseases related to defects in muscle energy production. These include rare mitochondrial genetic disorders as well as more common diseases such as diabetes, cancer, cardiovascular disease and neurodegenerative diseases – where reduced muscle function is associated with increased mortality.”

Although loss of muscle mass is normal, it can be potentially fatal in some patient groups, including cancer patients.

“When cancer patients lose muscle mass, they may not be able to receive the best treatment available. This may prevent them from receiving the optimal chemotherapy to kill a tumor because the treatment is too toxic for patients who do not have enough muscle mass.” “So there is a strong connection between muscle mass and physical activity on the one hand and the chance of survival with cancer on the other hand,” says Lykke Sylow and adds:

“But if we could increase patients’ muscle mass even slightly as they begin their cancer treatment, it could mean the difference between life and death for some people.”

Can improve quality of life

The protein crucial to the newly discovered mitochondrial mechanism is known as SLIRP.

In the study, the researchers also show that SLIRP stabilizes genes found in the mitochondria. Among other things, SLIRP is responsible for translating so-called mRNA into proteins that are essential for healthy, energy-producing mitochondria. However, if SLIRP is missing, the mitochondria are damaged and cannot produce sufficient energy. This is the process that can be circumvented through physical exercise.

We won’t get a pill with the same beneficial effects as exercise in the near future, emphasizes Lykke Sylow, but these new findings bring researchers one step closer to developing drugs that target the mitochondria and mimic just some of the health benefits of physical Movement. And that could make a big difference.

“Physical exercise has a magical effect on the muscles. While most of us find it quite difficult to get up from the couch and exercise, it’s even more difficult when you’re sick. So it would be amazing if we could create some of this muscle magic.” “It could really improve the quality of life and health of many patients,” concludes Lykke Sylow.