Good News for Lifelong Exercisers
Along with its salutary effects on the heart, weight, and other facets of health, physical activity also helps to regenerate muscle mass, which tends to diminish as people age. That’s the finding of research done at the University of Utah and other institutions published in the March 6th 2014 in the journal Free Radical Biology and Medicine.
A release from the university quotes senior author Raj Soorappan, Ph.D. as saying, "Physical activity is the key to everything. After this study, we believe that moderate exercise could be one of the key ways to induce stem cells to regenerate especially during senescence."
The release notes that sarcopenia – age-related loss of skeletal muscle mass – occurs naturally and begins in most people around age 30. However the body produces antioxidants, which are molecules that help maintain muscle mass through the regeneration of stem cells that become muscle cells.
For reasons not yet entirely known, as people age, their bodies produce fewer antioxidants. This can result in oxidative stress, a condition in which the level of molecules called free radicals – rogue electrons that travel through the body triggering chemical reactions that damage proteins and cells – exceeds that of antioxidants. When this happens, stem cell regeneration and, consequently, formation of muscle cells doesn't keep up with muscle mass loss.
Nrf2 is a protein and transcription factor that turns on and off the genes that produce antioxidants. To test the role of Nrf2 in regeneration of skeletal muscle during aging, Soorappan tested two groups of mice that were 23 months or older – the rodent equivalent of senior citizens. In one group of mice, the gene that codes for Nrf2 had been knocked out while the other group of mice was able to produce the protein. Each group underwent endurance training to create a profound oxidative stress setting.
Typically, regeneration, maintenance and repair of adult skeletal muscle damage due to aging and/or chronic stress states require activation of satellite cells (stem cells). In the group that couldn't produce Nrf2, endurance exercise stress on the treadmills affected stem cell protein expression and limited skeletal muscle regenerative capacity.
"Now we know that the antioxidant protein Nrf2 guards the muscle regeneration process in the elderly mice and loss of Nrf2, when combined with endurance exercise stress, can cause severe muscle stem cell impairment," said Madhusudhanan Narasimhan, Ph.D., a U of U senior research associate and the study's first author.
Understanding Nfr2's role on muscle regeneration is essential to optimize effective strategies for muscle repair during aging, Soorappan said.
Going forward, Soorappan plans to continue his studies to see whether spontaneous exercise (active lifestyle) favors stem cells and muscle regeneration. But he's also looking into studies to see whether exercise affects Nfr2 activation in people.
Although the results of this study haven't been replicated in people yet, Soorappan believes there's a clear message for couch potatoes: "If you don't use your muscles, you will lose them. At the same time, overdoing endurance training may detract from muscle regeneration," he cautions.