As a recovering muscle physiologist (from my PhD days), I get pretty excited by anything to do with muscle and healthy ageing.

Some things about muscle and ageing aren't really that surprising - like the fact we tend to lose it, especially if we aren’t physically active.

But what I find incredible is we are still uncovering new knowledge about how muscle loss actually happens.

We’ve known for decades that muscle loss is explained (at least partly) by a decrease in the size of the individual fibres within that muscle.

But as for how those fibres decrease in size - that’s been somewhat of a mystery.

That’s until an important new study in The Journal of Physiology used new technology to capture what happens to the contractile machinery in muscle with ageing for the first time.

The question is - what does this new knowledge mean for how we can best maintain our muscle?

But first… Let’s go on a journey inside your muscles

Take a look at one of your muscles now (perhaps your biceps or quadriceps).

Those larger muscles are made up of hundreds of thousands of cylindrical muscle fibres, packed together to form a larger whole muscle.

Inside each of those muscle fibres are even smaller cylindrical filaments - known as myofibrils. Each myofibril is essentially a chain of tiny contractile units - called sarcomeres - arranged end-to-end.

Each sarcomere contains tiny contractile proteins, including actin and myosin, arranged in filaments.

When a muscle contracts, these filaments slide over one another, causing the sarcomeres in each myofibril to shorten. In turn, the myofibrils themselves shorten, as do the muscle fibres they lie inside.

This “sliding filament” mechanism is how our muscles produce the force we need to move, walk, lift, run, etc.

But the key question that’s gone unanswered for decades is this:

When a muscle fibre decreases in size due to ageing and/or inactivity, what happens to the contractile machinery (myofibrils) inside them? Do they also get smaller, or is there just less of them?

Enter this fascinating new work from Troy Hornberger and team at The University of Wisconsin-Madison.

So what actually happens when a muscle shrinks?

The researchers studied the muscles of both younger (aged 19-40) and older (aged 64-80) humans, as well age young and old mice, to work out what was happening to muscle at three different levels:

The whole muscle, down to the individual muscle fibres, and the individual myofibrils inside them.

In humans, MRI scans revealed the older adults had on average ~34% lower quadriceps muscle volume and ~32% lower cross-sectional area (CSA) than younger adults.

They also found the decrease in muscle fibre size (atrophy) was mainly confined to the faster type II fibres, which were about -23% smaller than in younger muscle, whereas the size of the slower type I fibres weren’t significantly different between age groups.

But the most interesting finding was WHY those type II fibres were smaller.

The researchers used a relatively new imaging method (known as FIM-ID) to look inside those fibres to measure the size of the myofibrils and estimate how many there were.

Surprisingly, they found the average size of an individual myofibril wasn’t significantly different between young and older adults, in either type I or type II fibres.

BUT, the type II fibres in older muscle had significantly fewer myofibrils than younger muscle.

That means these fibres weren’t getting smaller because the contractile machinery inside them was shrinking - rather, they were actually losing some of that machinery.

The animal study broadly supported this finding too. When the researchers immobilised one hindlimb of young and old mice for 10 days, the resulting muscle fibre atrophy again seemed mainly due to a loss of myofibrils - with relatively little change in the size of the remaining myofibrils.

It’s important to mention this new finding doesn’t explain everything about why we lose muscle with age. Because ageing is also associated with a loss of muscle fibres, not just a reduction in their size.

So together, this suggests muscle loss is likely a combination of a) muscle fibre loss (less total fibres) and b) myofibril loss (which is why the remaining fibres get smaller).

Question is, does this actually change what we should do to preserve our muscles as we age?

I think there are three main takeaways from this new data.

#1: Keep giving your type II fibres a reason to stick around

This isn’t the first study to reveal age-related muscle loss is mainly confined to the faster type II fibres.

That’s a big problem, since these fibres are critical for producing large amounts of force quickly. Since that’s something we do less and less as we age, it makes sense why these fibres decline in size the most - because we just don’t recruit these fibres as much anymore.

The “use it or lose it” principle really holds true here.

So to keep these fibres healthy (and larger), you need to ask your muscles to produce more force rapidly every so often.

To that point: when was the last time you lifted something heavy, moved quickly, or did something explosively?

#2: Regardless of WHY muscles shrink, resistance training still matters

While this study focused on muscle loss (atrophy), we still don’t know if the opposite occurs with muscle growth (hypertrophy).

That is, if building muscle involves the addition of new myofibrils that explain the increase in muscle fibre size.

This study didn’t look at whether resistance training could prevent the loss of myofibrils with ageing (though it’s a ripe question for future research).

But regardless, it probably doesn’t matter all that much for what to do in practice. We already know resistance training is our primary tool for preserving not just muscle size, but muscle function too.

This new mechanism is interesting, but I don’t think it really changes what you should do in practice.

#3: Remember, more muscle isn’t the only goal

It’s easy to get a bit too focused on muscle.

After all, it’s what we can see on the outside, and we’re taught to believe more muscle = more strength. So it’s only natural we might use it to judge if we’re winning the fight against ageing and inactivity.

Don’t get me wrong, muscle matters for many reasons. But declines in physical performance with ageing is a failure of the entire motor system, not just muscle.

Muscle contraction is the final link in a chain that begins with a signal from the motor cortex in the brain, travels down the spinal cord, and through motor neurons that deliver that signal to the muscle. Deficits anywhere in this chain can influence our ability to produce the force and coordination between muscles needed for movement.

This is why gains in muscle size do not always accompany improvements in muscle function (strength or power) or physical performance (e.g., walking speed or sit-to-stand performance) with resistance training.

Again, muscle matters - but it’s not the only thing determining how well you move.

The biology is interesting… but so what?

This new understanding of how the muscle contractile machinery changes when we lose muscle is fascinating, for sure.

But I’m always coming back to the “so what” question. Mechanisms are cool… but does it actually change what we should do in practice?

In this case, I don’t think so (yet). But there are still many unanswered questions here.

Questions like: is the loss of myofibrils a reversible process, and if so, can we “rescue” lost myofibrils with resistance training? Or if not, could this be one reason why some studies have shown a limited muscle growth response in older adults? And what might this mean about the importance of acting earlier to preserve muscle mass?

These are interesting questions, but this is why I emphasise it’s not all about muscle.

Because whether or not your muscle fibres have already lost some of their myofibrils, you can still improve your motor (movement) system without big changes to your muscle mass.

You just have to keep giving your muscles (and the rest of your motor system) a reason to produce force.

Once again, thanks for reading!

Until next week,

Jackson

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