In older adults without diabetes, skeletal muscle mitochondrial oxidative capacity, as measured by phosphocreatine recovery time (τPCr), is significantly slower in individuals with prediabetes than in those with normal glucose tolerance.

In muscle cells, when the energy-producing machinery called mitochondria works less efficiently, it produces less ATP and leaks more harmful molecules. This forces the muscle to rely more on stored phosphocreatine to keep energy flowing during activity. After exercise, the damaged mitochondria take longer to rebuild phosphocreatine because they cannot regenerate ATP fast enough, so the muscle recovers more slowly.