14 January 2010

How to preserve aging muscles

Scientists at the Universities of Texas and Michigan, working under the guidance of Dr. Holly Van Remmen, have identified an important cause of age-associated muscle atrophy (sarcopenia). The results of their work, published on December 29 in the preliminary on-line version of the FASEB journal in the article "Increased superoxide in vivo accelerates age-associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degeneration", demonstrate that free radicals, such as reactive oxygen species, damage the mitochondria of muscle cells, which leads to their death and gradual muscle atrophy. The authors believe that the data they have obtained will allow the development of drugs that slow down this process.

According to the authors, skeletal muscle atrophy associated with aging is inevitable, so the task of researchers is to study the mechanisms underlying its formation and develop therapeutic approaches that will slow down or limit this process.

In their experiments, the authors used genetically modified mice that were not capable of synthesizing a protective antioxidant – the enzyme copper-zinc superoxide dismutase (CuZnSOD). The accumulation of extremely high levels of free radicals in the body of such mice led to a significantly faster loss of muscle mass compared to normal animals. In addition, the muscles of the genetically modified mice were much smaller and weaker than the muscles of normal animals.

The researchers believe that the model they created allows "at an increased speed" to reproduce the effects of the normal human aging process. They note that the importance of the results obtained lies in the possibility of using this model to identify molecules responsible for muscle aging, blocking the activity of which will help people maintain full physical activity for longer and look younger.

Portal "Eternal youth" http://vechnayamolodost.ru based on the materials of ScienceDaily:
Discovery May Help Baby Boomers Get Buff: Free Radicals Damage Mitochondria in Muscle Cells.

14.01.2010


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