Ageing impairs skeletal muscle function, linked to reduced subsarcolemmal mitochondrial density, fragmented intermyofibrillar networks, and lower cristae density. These mitochondrial changes are strongly associated with diminished physical capacity, highlighting mitochondria’s role in age-related muscle decline.
December 2024 – Aging Cell
Key takeaways
- Mitochondrial fragmentation signals early ageing: Even in physically active middle-aged adults, skeletal muscle mitochondria show increased fragmentation. This disruption in the mitochondrial network is one of the earliest detectable signs of ageing and strongly correlates with reduced physical performance, suggesting it may precede visible muscle decline or loss of function
- Lower cristae density weakens energy output: Middle-aged individuals exhibit a significant reduction in mitochondrial cristae density, essential structures for energy production. While the total respiration remains similar due to increased mitochondrial number, each mitochondrion is less efficient. This subtle deterioration compromises the cell’s ability to generate energy effectively
- Subsarcolemmal mitochondria drive oxygen use: Mitochondria located near the muscle cell membrane, known as subsarcolemmal mitochondria, play a vital role in oxygen extraction during exercise. Their reduced density in middle-aged individuals impairs this function, directly affecting exercise tolerance and aerobic capacity which are key markers of vitality and longevity
- Intramuscular fat worsens mitochondrial health: An increase in intramuscular lipid droplets was linked to higher mitochondrial fragmentation and lower cristae density. This suggests a feedback loop where fat accumulation inside muscle cells accelerates mitochondrial dysfunction, compounding the decline in energy capacity with age
Read the article at: Goulding, Richie P., et al. “Skeletal muscle mitochondrial fragmentation predicts age‐associated decline in physical capacity.” Aging Cell, vol. 24, no. 2, 2025, e14386. https://doi.org/10.1111/acel.14386.