Is it possible to maintain muscle strength and integrity through the duration of life? Sarcopenia may be against you. Can you battle against sarcopenia? Maybe. If not today, perhaps soon.
There’s an old Grimm fable that when living things asked God about longevity, God like the number 30 years.With a little negotiating, humans got 70 years but at a price. Sometimes these fairy tales are true. At age 30, lean muscle tissue decreases and is replaced by fat. This decrease is partly caused by a loss of muscle tissue (atrophy). The speed and amount of skeletal muscle changes seem to be caused by genes. This muscle loss happens very slowly yet gradually – usually noticed un 10 year differences. The process is Sarcopenia that, thus far, is an untestable condition.
Barring genetic diseases such as Muscular Dystrophy and DDNX3, sarcopenia is a normal process of aging. Body builders have been using a pseudo-genetic chemical called Myostatin, that some believe may help slow sarcopenia muscle loss with aging.
Myostatin (also known as growth differentiation factor 8, abbreviated GDF-8) is a myokine, a protein produced and released by myocytes that acts on muscle cells’ function to inhibit myogenesis: muscle cell growth and differentiation. In humans it is encoded by the MSTN gene. Myogenesis is a form of regeneration as the process by which damaged skeletal, smooth or cardiac muscle undergoes biological repair and formation of new muscle when other muscle fibers waste or die due to disease. This process may slow with aging and hormonal changes.
When discussing sarcopenia and myostatin, there are two sides of a coin. Muscle atrophy is a decrease in muscle mass; muscle hypertrophy is an increase in muscle mass due to an increase in muscle cell size. Hypertrophy is a very rare condition and sarcopenia is more associated with aging and conditions like muscular dystrophies. As a possible method at treating sarcopenia, myostatin inhibitors are being explored by doctors albeit at mouse level experiments.
The potential side effects of using myostatin inhibitors provoke heated debates in research communities. With few studies, there are some negative side effects reported:
One potential concern is that increased muscle growth will lead to an increased risk of injury due to increased stress on the muscle fibers. This is especially true for individuals using myostatin inhibitors as workout supplements instead of as part of a medical treatment for muscular dystrophy or other disorders.
Other possible side effects of myostatin inhibitors include increased the chance of tendon rupture, heart failure due to inflamed cardiac muscle, and rhabdomyolysis, a breakdown of muscle fibers that often leads to kidney failure
Despite few thorough clinical trials, Myostatin has become a main target for the development of drugs for cachexia and muscle wasting diseases. While sarcopenia behaves at wasting skeletal muscles, The cachectic state is observed in many pathological conditions such as cancer, chronic obstructive pulmonary disease (COPD), sepsis, or chronic heart failure. These are also muscles. The other problem associated with Myostatin is it is not targeted for research by the US Food and Drug Administration for testing and approval. It is available as a supplement.
In the United Kingdom, use of a myostatin inhibitor is targeted for experimentation for Duchenne Muscular Dystrophy, one of many muscular dystrophy diseases.
While muscle wasting is associated with muscular dystrophies and other emerging genetic conditions, including sarcopenia, there is no certainty whether myostatin might reverse muscle wasting that has already happened. Among small and possibly skewed studies it is generally accepted that age-related changes in skeletal muscle structure and function are inevitable, whether these deleterious effects on skeletal muscle can be stopped or reversed is debatable.Some studies support myostatin inhibitor supplementation, most studies agree that more research is needed. In 2017, a reasonably thorough German study of myostatin inhibitors as treatment for muscle wasting concluded with interest but for further experimentation required.
The general wisdom is that muscle integrity within normal sarcopenia is activity – virtually any activity – may reduce muscle wasting over time. Activity may also benefit hippocampus growth for cognitive support. Unused muscles can waste away if you are not active. Even after it begins, this type of atrophy can often be reversed with exercise and improved nutrition. Muscle atrophy can also happen if you are bedridden or unable to move certain body parts due to a medical condition.
Muscle wasting with age varies but sarcopenia may not be considered a leading cause of death in aging. There are some foods that include flavonoids that dietitians believe may work as myostatin inhibitors. They are: green tea, chocolate (especially dark chocolate and raw cocoa powder),
blackberries, pomegranates, and broad beans, broccoli, cauliflower, and spinach.
There are genetic tests to evaluate your myostatin levels. Discuss with your doctor to determine whether you need one.
Aging well seems to many a fantasy as new diseases and conditions creep in unrelenting succession. Living is an activity. Damned genetic muscle wasting diseases may one day be curbed. Will it be myostatin related? There seem to be many promises but all we can do is wait. Might as well go for a walk while waiting. Wisdom points that activity may be helpful. Sarcopenia and many other neuromuscular disease treatments is definitely worth researching as the aging population increases.
As you battle with the bulges and size upgrades as you grow older, sarcopenia might be the cause behind the results.