Scientists have uncovered a pivotal mechanism within our cells that is crucial for muscle energy production, potentially opening the door to innovative treatments for muscle-related ailments such as diabetes, cancer, and cardiovascular diseases.
While exercise is widely recognized for its health benefits, many underlying molecular processes remain unidentified. Researchers at the University of Copenhagen have shed light on these processes, enhancing our understanding of exercise’s impact on health and potentially revolutionizing treatment for numerous muscle-related conditions.
“We’ve discovered a novel, critical mechanism for muscle cell energy production, showing it activates with physical activity across ages, genders, and health statuses,” states Associate Professor Lykke Sylow from the Department of Biomedical Sciences, lead author of the new research.
This investigation reveals that a unique protein plays a significant role in mitochondrial energy production. Remarkably, aerobic exercise can manage to bypass this protein’s function. According to Postdoc Tang Cam Phung Pham, first author of the study, “Our findings indicate that exercise can offset genetic issues hampering muscle energy production. In cases where this protein is lacking, exercise can trigger alternative pathways to restore energy capacity, skirting the genetic malfunction. This insight highlights exercise’s efficacy in addressing genetic anomalies.”
Although the precise mechanism by which exercise averts this process remains unknown, this discovery could lead to novel treatment options for multiple muscle disorders. Lykke Sylow suggests that this knowledge could facilitate the development of pharmaceuticals replicating exercise’s health benefits for those unable to engage in physical activity: “It paves the way for new treatments for over 200 muscle energy production-related disorders, including rare mitochondrial genetic conditions and common diseases such as diabetes, cancer, cardiovascular, and neurodegenerative disorders — all linked to diminished muscle function and elevated mortality rates.”
Muscle mass reduction, though expected, can be fatal for specific patient populations, such as those with cancer.
“When cancer patients lose muscle mass, it could hinder their ability to undergo optimal treatments like chemotherapy, owing to its toxicity in individuals lacking sufficient muscle mass,” explains Lykke Sylow. “There’s a significant link between muscle mass, physical activity, and cancer survival odds. Increasing muscle mass, even marginally, before commencing cancer treatment could be life-saving for some.”
Central to the newly identified mitochondrial mechanism is the protein SLIRP.
The study reveals that SLIRP helps stabilize mitochondrial genes, playing a crucial role in translating mRNA into proteins necessary for robust, energy-efficient mitochondria. In SLIRP’s absence, mitochondrial functionality is compromised, and energy production suffers. Exercise, however, can mitigate this deficiency.
Though replicating exercise’s effects via medication isn’t imminent, this new insight moves researchers closer to developing drugs that target mitochondria, capturing some health benefits of exercise. “Exercise is incredibly beneficial for our muscles, yet initiating it is challenging for many, especially the sick. Finding ways to invoke some of exercise’s benefits without physical activity would markedly enhance patients’ quality of life,” concludes Lykke Sylow.