Muscle Hypertrophy: What Limits the Ability of Your Muscles to Grow?

 

 

Muscle Hypertrophy – Why do you lift weights? You’re probably doing it to increase the size of your muscles, build strength, or preserve the muscle you have. All good reasons! You lose muscle mass at a steady rate after the age of 30 and the muscle loss accelerates for women after menopause. Between the ages of 50 and 70, the average person loses a whopping 30% of their muscle mass.

The consequences of muscle loss are sobering. Later in life, it can lead to frailty, falls, and disability. Plus, loss of metabolically active muscle tissue is harmful to your metabolic health and can lead to weight gain. Not a very optimistic picture, is it? Sarcopenia, the age-related loss of muscle tissue, is fast becoming an epidemic that rivals the growing problem of obesity. Fortunately, strength training can offset the loss of muscle tissue and help preserve strength. That’s why no exercise program is complete without strength training.

Muscle Hypertrophy: Why Muscles Stop Growing: Blame it on Myostatin

We know that there are limits to how large muscles can grow and that it becomes more difficult to build muscle after the age of 50. Have you ever wondered what limits the ability of muscles to grow beyond a certain point? Why don’t your muscles continue to get larger and larger in response to training? After all, the amount of fat tissue an individual can gain from overeating and under-exercising seems almost limitless. In fact, the heaviest man in the world tipped the scales at 1,400 pounds and the heaviest woman 1,200 pounds. Your body has almost a boundless ability to store body fat. Why not muscle?

Muscle growth is limited by a protein called myostatin. Although myostatin has hormone-like properties, it is, actually, a myokine, a protein released by myocytes or muscle cells. Myostatin limits muscle growth by blocking the ability of muscle cells to grow and mature. In experimental studies, animals that have low levels of myostatin develop an increased number of muscle fibers during early development and, as adults, have greater hypertrophy of their muscle fibers. This persists throughout life.

The amount of myostatin you have is partially determined by genetics. You inherit two copies of a gene involved in making myostatin, one from your mother and one from your father. Humans and animals that have mutations in both copies of the myostatin gene have myostatin proteins that don’t work properly. In other words, they don’t work as well to limit muscle growth. As a result, these individuals have larger muscles and greater muscle strength, sometimes freakishly so. Cattle breeders have developed genetically a strain of cow called Belgian blue that have inactive myostatin genes. These cows are exceptionally lean and muscular. There are also cases of humans born with two defective genes for myostatin that also have remarkable strength and muscle size, even without training.

Muscle Hypertrophy: Can Myostatin Explain Differences in Muscle Development Between Individuals?

It’s no secret that some people develop muscle easily and are capable of putting on new muscle with less effort while others struggle to develop any muscle at all. What role does myostatin play? It’s possible that some people who are naturally strong and pile on muscle easily have myostatin genes that don’t function well and therefore, limit muscle hypertrophy less. These guys and gals have no problem reaching their strength-training goals!

As you might expect, there’s interest in how to limit the impact of myostatin on muscle growth. One study showed that supplementing with creatine monohydrate in conjunction with the amino acid leucine reduced inhibition of muscle growth by myostatin. So, getting enough essential amino acids, especially leucine, along with creatine supplementation could help overcome inhibition of muscle growth.

What about age-related muscle loss? How much of a role does myostatin play? Scientists are currently exploring this question. One study showed that myostatin increases with age in women but decreases in men. The researchers point out that this may explain why women experience more age-related loss of muscle than men.

What happens if you block the action of myostatin? Researchers used an antibody in mice to interfere with the action of myostatin. Four weeks of this treatment reversed age-related sarcopenia and muscle loss and improved muscle strength and sensitivity to insulin. So, interfering with the activity of myostatin might be one way to prevent sarcopenia. The improvements in insulin sensitivity would also be favorable for metabolic health.

Myostatin may have other implications for health and longevity as well. Mouse studies show that modest reductions in myostatin prolong lifespan by as much as 15%, but beyond a certain point, greater decreases in myostatin can shorten lifespan because it increases the size of cardiac muscle cells as well. Plus, humans that have very low levels of myostatin have muscle pain and muscle cramps due to their excess muscle tissue.

Muscle Hypertrophy: Myostatin Inhibitors?

With myostatin playing an important role in muscle and strength gains, it’s not surprising that so-called myostatin inhibitors that block that activity of myostatin have hit the market. Are they effective? The short answer is no. There’s no evidence that these supplements work. However, researchers are trying to develop a legitimate myostatin inhibitor to help people with muscle wasting diseases, like muscular dystrophy, be more functional.

The Bottom Line

Myostatin plays a role in muscle development but, at this point, there’s no way to lower your level by taking a supplement. There’s some evidence that supplementing with leucine and creatine may lower the impact of myostatin and aid muscle growth. However, there really isn’t enough data to say that it works. Still, the best approach to building new muscle tissue and preserving what you have is with good nutrition and challenging strength training. Of course, you already knew that!

 

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Curr Genomics. 2007 Nov; 8(7): 415–422. doi: 10.2174/138920207783591672
Cell Mol Life Sci. 2014 Nov;71(22):4361-71. doi: 10.1007/s00018-014-1689-x. Epub 2014 Jul 31.
Mol Cell Endocrinol. 2010 Apr 12;317(1-2):25-30. doi: 10.1016/j.mce.2009.12.019. Epub 2009 Dec 22.
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