Muscle aging is not simply a passive decline but a deliberate sacrifice of strength to protect cells from damage, according to a research team led by the University of Copenhagen that studied why muscle fibers change type in old age, infohub.kz reports.
Human muscles are made up of fast fibers responsible for sharp, powerful movements and slow fibers built for sustained exertion. Over the years, fast tissue is converted into slow tissue, even though the latter depends more heavily on mitochondria — the intracellular power plants that begin to fail with age.
The biologists focused on a special fat molecule, cardiolipin, which shapes the inner membrane of mitochondria. Its levels in the cells of humans and mice decline with age. When the researchers artificially lowered cardiolipin levels in young rodents, their muscles began to age rapidly. Damage to the organelles caused them to produce reactive oxygen species, which triggered a protective restructuring of the fibers. The cells actively absorbed glucose from the blood not to generate energy but to produce their own antioxidants for survival.
The restructuring of fibers is controlled by a specific protein, ERRγ. In experiments on mice, the scientists restored cardiolipin concentrations to roughly two-thirds of normal, which halted tissue atrophy and prevented the animals' early death. The authors expect that targeting this protein and stabilizing membrane fats could in the future form the basis of drugs against age-related muscle loss.