As we approach middle age, most of us start to notice some physical changes. Our previously 20/20 eyesight seems a little less clear. Wrinkles or gray hairs pop up here and there. Weight management is likely more challenging. In addition, when we exercise, we do so with less intensity and our muscles tend to wear out faster. Just look at our professional athletes in most any highly active sport—maintaining muscle as you age is even challenging for them as you don’t see many playing too far into their 30s, and most are at their prime in their 20s.
So in regards to physical activity, why is it that we seem to peak in our 20s and lose strength as we age? The short answer is muscle decline (more specifically, neuromuscular-junction degeneration). But what causes this decline, and is there anything you can do to maintain muscle as you age? A new study suggests these answers may lie not in our motor neurons (nerve cells), as is commonly thought, but in our stem cells.
What Are Stem Cells and Motor Neurons?
Stem cells are cells that can differentiate, which means they can turn into other types of cells in the body. This makes them the body’s ideal repairmen, and they work 24/7 doing just that: repairing damage as we go about our day none the wiser. But beyond just repairing, what really makes stem cells stem cells is that they also function as the general contractor, so they have the unique functions of both directing and fulfilling every step of the repair process. In addition, they have a gift for navigation, being able to mobilize and travel great distances to find the part that needs fixing. This process is called “homing.”
Many things can damage our stem cells. Smoking, for example has been shown to not only damage stem cells but also disrupt their ability to find and repair whatever needs fixing. Mitochondrial burnout (mitochondria are the batteries that live inside and power our cells) is a major force that happens as we age, causing our stem cells to slow down and stop fixing things. Medications, such as steroids, anesthetics, statins, and even the hair-loss drug Propecia, can damage or slow the growth of stem cells.
Stem cells reside in just about every body tissue. In our muscles, they not only repair but in the process aid in growth of the muscle. Motor neurons (those nerve cells), on the other hand, carry signals from our spine to our muscles, with muscle fibers being linked to the neurons via the neuromuscular junction. This connection is what allows our muscles to move when our central nervous system wants them to, and the common theory has been that it’s the loss of these motor neurons that causes muscle decline as we age. But is this the case? Let’s review the study.
Inability to Maintain Muscle as You Age May Be Due to Loss of Stem Cells, not Motor Neurons
The study set out to test the common idea that motor neurons are responsible for muscle decline against the new idea that stem cell loss is actually to blame. Leaving motor neurons intact and undisrupted, researchers depleted the stem cells in the muscles in one group of mice. In another group of mice, they prevented any stem cell loss. The results? The group with muscle stem cell loss (with no disruption of neurons) experienced muscle decline earlier (in middle age) rather than later (in old age), while the group without stem cell loss did not experience this middle-age decline. Researchers concluded that this loss of stem cells, not motor neuron loss, actually caused the neuromuscular junction degeneration (muscle decline) in these middle-age mice.
The upshot? We are learning more and more about the power of our stem cells and the importance of keeping them healthy as we age. The discovery in this new study that the loss of stem cells, not motor neurons, may be the primary cause of muscle decline is certain to lead to more research in the future. And perhaps this will generate new ways to slow muscle decline and allow us to more effectively maintain muscle as you age. Who knows?…In 20 years, we may be reaching our physical peaks in our 40s instead of our 20s.