Medical News Today reports that the professor of Systems Biology in the School of Sport, Exercise, and Health Sciences at Loughborough University recently issued a press statement that overturned a concept that was long held true by the scientific and medical community.
Professor Timmons and her colleagues have observed that physical exercise has very little to no control over how well the muscles age in the human body. It has been found that genetic pathways have been identified as the largest deciding factor as to how well your muscles actually age. These processes are completely distinct from the processes that are regulated by physical activity. In other words, no matter how much you exercise, genetics wins again… Physical activity has NOT been observed to alter age-related biological changes.
A test trial on endurance took place over a 20 week time period with a group of volunteers. It was discovered that through a specific pathway known as mTOR, only those select few who can genetically suppress this pathway are able to gain more lean muscle tissue mass with exercise. For the majority of the people who could not genetically suppress the mTOR pathway, no amount of exercise could stop or slow their muscle aging.
According to Daily science studies done by scientist at the Salk Institute for Biological Studies “Tweaking a Gene Makes Muscles Twice as Strong: New Avenue for Treating Muscle Degeneration in People Who Can’t Exercise”, studies shows dramatically enhanced muscle tissue in a high performing mouse, which has greater numbers of mitochondria (brown), the energy factories of cells. Through genetic engineering, the mouse developed stronger muscles than normal, even though it was inactive. In the image, a blood vessel (seen in cross section) is red and muscle fibers are blue.”
Collaboration between researchers at the Salk Institute for Biological Studies, and two Swiss institutions, Ecole Polytechnique Federale de Lausanne (EPFL) and the University of Lausanne researchers’ team of scientists has created super-strong, high-endurance mice and worms by suppressing a natural muscle-growth inhibitor, suggesting treatments for age-related or genetics-related muscle degeneration are within reach. The scientists found that a tiny inhibitor may be responsible for determining the strength of our muscles. By acting on a genome regulator (NCoR1), they were able to modulate the activity of certain genes, creating a strain of mighty mice whose muscles were twice a strong as those of normal mice. This Gene can aid as an induced drug for diabetic, obesity patience or any other health complications, such as diabetes, immobility and frailty,” says Ronald M. Evans, a professor in Salk’s Gene Expression Lab, who led the Salk team.
Researchers at Salk Univeristy, Ecole Polytechnique Federale de Lausanne, and University of Lausanne have tweaked a few sets of genes that made a certain group of mice twice as strong as regular mice. The researchers have identified a genome regular, NCoR1, that allowed them to create these super strong mice. They believe that with this discover, drugs can be made for people who have a degeneration of the muscle and obese people that are unable to exercise. With taking away this inhibtor, mice were able to run for an extended amount of time. The drug that could be created will decrease the effectiveness of NCoR1 since in the research NCoR1 was genetically modified. It is interesting to see that people with muscle degeneration may now have increased hope to be able to use their body as a normal person would, along with people with an obesity problem allow to function better.
Scientists at the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), found cells that could repair muscle loss. These cells called, satellite cells are cells that activate themselves to build muscle mass after muscle has been lost over a long period of time or injury. If someone loses muscle then begins to gain it back after a long period of time then these satellite cells will kick in. People who have Duchenne muscular dystrophy have an increase in muscle loss. So, with the help of satellite cells regenerating themselves, these patients are able to gain muscle mass back. Eventually satellite cells will stop working as people age but they can help elderly people from hurting themselves by falling and also those with arthritis. Research has shown that the gene Ezh2 may be able to promote satellite cell degeneration. With this research within the gene, Ezh2, scientists may be able to treat a muscles disease patient’s lifespan by expanding the satellites cell life. This is good news for those with muscle disease and arthritis.
As the title suggest, the article that I chose looks at studies done that shows a correlation between age and muscle break down caused by the expression of these particular genes, primarily in men, as they age. Essentially the expression of these genes cause more of a release of certain enzymes, called atrogin-1 and MuRF-1,which break down muscle tissue. Researchers also noticed that the greater the expression of the MuRF-1 enzyme the lower the levels of IGF-1 (Insulin Growth-like Factors) which increase the growth of cells and tissues in the human body. However to minimize these effects, specialized weight training routines can help to counter act muscular atrophy and maintain muscle mass.
This is interesting because it is common knowledge that as you get older you lose muscle mass exponentially, however now it appears that there may be genes that control how much mass you actually lose. I wonder how they would control the expression of this gene and if there are other problems attributed to this gene beyond muscular atrophy, such as low testosterone levels in men. Testosterone, or other hormones, when used as prescribed, would help to negate muscle loss and overall heath in older men and women as well. Do you think it is plausible to use human hormones to control the effects of this gene’s expression?