This study examined how β-hydroxybutyrate (β-HB), the primary ketone body produced during ketosis, affects skeletal muscle mitochondria. In both cultured muscle cells and rats fed a ketogenic diet, β-HB increased mitochondrial respiration while reducing the production of reactive oxygen species (H₂O₂), suggesting that mitochondria were producing energy more efficiently with less oxidative stress. Muscle cells exposed to β-HB also showed greater viability, indicating a protective effect beyond simply serving as an alternative fuel.

The researchers found that β-HB shifted mitochondria toward a more fused, interconnected network by reducing the fission protein DRP1. This was accompanied by lower levels of several ceramide species, lipids that have previously been linked to mitochondrial dysfunction and insulin resistance. Together, these changes suggest that β-HB influences mitochondrial health through both metabolic and signaling pathways.

Although the animal study was relatively short and performed in rodents, the findings support the idea that ketosis improves skeletal muscle function by enhancing mitochondrial efficiency rather than simply increasing the number of mitochondria. The authors conclude that ketones act as beneficial metabolic signals that help protect muscle cells and maintain a healthier metabolic environment.