Researchers studying how oxidative stress in cells impacts sarcopenia, a loss of muscle mass and strength that occurs in all humans as they age, found that mice lacking a protective antioxidant protein did not have reduced size or number of muscles cells but they were weaker than normal ones.
The antioxidant protein is called SOD1 and the researchers developed mice that did not have SOD1 in their muscles, though it was still present in other types of cells. They found that the lack of SOD1 at the muscle was not enough to cause atrophy, the total muscle mass in this mouse was larger, but they were still weak.
Sarcopenia in people has two components: loss of muscle mass and loss of function (weakness). This study supports the idea that oxidative stress has a role in these detrimental effects. If a way can be found to curb the effects, then healthier, more productive aging could result, Dr. Van Remmen said.
The oxidative stress hypothesis of aging holds that oxidation from molecules called "free radicals" causes damage to cells over time, resulting in sarcopenia and other decline.
"We think that lack of SOD1 could be priming the muscle to use all of its survival skills," said senior author Holly Van Remmen, Ph.D., professor of cellular and structural biology in The University of Texas Health Science Center San Antonio. "The muscle knows things aren't quite right. Its rescue mechanisms are pulled into play."
Citation: Yiqiang Zhang, Carol Davis, George K. Sakellariou, Yun Shi, Anna C. Kayani, Daniel Pulliam, Arunabh Bhattacharya, Arlan Richardson, Malcolm J. Jackson, Anne McArdle, Susan V. Brooks, and Holly Van Remmen, 'CuZnSOD gene deletion targeted to skeletal muscle leads to loss of contractile force but does not cause muscle atrophy in adult mice', FASEB J fj.13-228130; published ahead of print May 31, 2013, doi:10.1096/fj.13-228130