Muscle Wasting and Aging: What Do We Know? | Sunday Observer

Muscle Wasting and Aging: What Do We Know?

18 April, 2021

Most strength-based records are held by people in their thirties. There are exceptions, but at that age muscle tissue has matured, years of training have reached their peak, and the decline of strength and muscle mass has not yet set in.

Decline? Yes. Unfortunately, it becomes increasingly hard to build and maintain muscle mass as we age. Sure, there are individual differences in the rate and onset of this decline and some people who start resistance training later in life will still notice gains. There are certain — not always legal — chemical means of support as well.

Overall, though, muscles eventually will start to waste away. Sarcopenia is the term used to denote this muscle wasting. Sarcopenia refers to muscle loss both in terms of strength and mass due to aging.

Primary sarcopenia is caused simply by the aging of our bodies, while secondary sarcopenia is a corollary of other issues such as immobility, disease, or nutritional inadequacy. These potential causes tend to overlap as we grow old, compounding the problem. The composition of muscle changes too as more fat is deposited within the muscle, compromising muscle function.

The effects of sarcopenia on elderly patients are quite substantive: mobility disorders, increased risk of falls and fractures, impaired ability to perform daily activities, poor quality of life, loss of independence…

Preventing the decline of muscle mass and strength is why exercise and eating sufficient (but not too much) protein is even more important as we grow old. There is also work on stem cells and enzyme targeting that investigates possible ways to address the issue.

How the muscle crumbles

A new review tallies all we know about our failing physiques.

The authors characterize sarcopenia at different levels, from the overall composition of muscle fibers, over neuromuscular connections and changes in satellite cells, to changes within muscle cells. They also take into account systemic effects where whole-body changes affect muscle.

A very brief look at each one:

Muscle fibers

Lean muscle is made up out of two types of fiber: type I (slow-twitch, aka endurance), and type II (fast-twitch, aka explosive power, further divided into IIa and IIb). As we age, we seem to lose relatively more of the type II ones. There are also confused fibers that are stuck somewhere between I and II. Finally, in young tissue, the fibers are fairly randomly distributed whereas in older people the fiber types tend to cluster together. Add the intrusion of fat cells into the muscle, and all this reduces muscle functionality.

Neuromuscular connection

Neurons that run from the spinal cord to the muscle fibers and form different motor units (Wikimedia commons, Daniel Walsh and Alan Sved) Anyone experienced in resistance training knows that the mind-muscle connection is important. After all, we need neurons to activate the muscle. As we age — you’ve guessed it by now — that declines. The older we get, the fewer motor units (a motor neuron + the muscle fibers it connects to) we have. It’s not fully clear what happens, but it’s likely to be a combination of instability in the connections between nerves and muscles, as well as the general decrease in neurons that comes with age.

Satellite cells

Myo-satellite cells are the stem cells that give rise to skeletal muscle cells. They’re important for both building and maintaining muscle. The theme, I’m sure, is clear by now: as we age, both the number and regenerative capacity of myo-satellite cells decrease — in humans, this is especially so in type II fibers.

(Wikimedia commons, Zammit PS, Partridge TA, Yablonka-Reuveni Z)

Inside the cells

Time to zoom in and cast a brief glance at what happens inside the muscle cells.

Muscle and protein go together like peanut butter and jelly, so let’s look at protein first. The balance between protein synthesis and breakdown is called protein homeostasis. In old muscle cells, protein synthesis goes down. So, homeostasis is off and less muscle is built. Homeostasis becomes proteolysis (protein breakdown).

Next, the mitochondria (energy producers of the cell), which are especially prevalent in muscle cells. Throughout our bodies, mitochondrial function is compromised as we age, and muscle tissue is no exception. Fewer mitochondria are produced, and the ones that remain are more prone to damage and breakdown. These dysfunctional mitochondria are also an important source of oxidative stress.

Systemic issues

Now, we’ll zoom out and take a look at the entire body.

Aging is often accompanied by systemic low-grade inflammation, a weakened immune system, and lower production of anabolic hormones. Inflammation engenders the release of cytokines (signal molecules) by the immune system. these cytokines may induce muscle protein degradation (although there is still some uncertainty about the mechanism and extent of this).

Keep pushing on those pushups

All is lost, then? Not quite. There are several things you can do to slow down the decline of muscle strength and mass.

The first one is obvious: do some resistance training. No need to go all-out bodybuilding (after all, training breaks down muscle and as you grow older, you need more time to recover).

Second: diet. Make sure to get enough protein — but here too, don’t go crazy. Find a balance. Add fruits and vegetables to keep the systemic inflammation at bay. (Ugh, that sounded very insta-influencer-like, didn’t it?). Likewise, omega 3 fatty acids, polyphenols, and vitamin D seem to be good focuses to keep inflammation in check. Third: drugs.

There are certain performance-enhancing drugs and hormone replacement therapies that might be helpful, but absolutely discuss this with your doctor to make sure it’s a good idea.

There are more targeted approaches for sarcopenia specifically under investigation (factors for inhibiting TNF, SHIP-2, GSK3, or proteasome activity; or interventions to activate Akt or mTOR), but those need more work before they can make it to the market.

The hope, of course, is that:

By further elucidating relevant mechanisms involved in sarcopenia development and exacerbation, we hope to gradually get closer to being able to identify efficient lifestyle and therapeutic interventions for preventing age-related loss of muscle mass and function