How Exercise Reverses Muscle Aging

First things first, let’s quickly cover that biological age is not one thing but quite a lot of things, each of which can age at different rates, for example:

• Visual markers of aging (e.g. wrinkles, graying hair)
• Performative markers of aging (e.g. mobility tests)
• Internal functional markers of aging (e.g. tests for cognitive decline, eyesight, hearing, etc)
• Cellular markers or aging (e.g. telomere length)
• …and more, but we only have so much room here and we do want to get on to the topic of muscle aging

For what we can do about each of those other ones we mentioned, see: Age & Aging: What Can (And Can’t) We Do About It?

So, what’s this about exercise vs muscle aging?

You can rebuild you; you have the (bio)technology

Your body is constantly rebuilding itself, in fact. Every single cell gets regularly replaced—some kinds more quickly than others, but yes, all of them (yes, even brain cells, per: Building Your Brain At Every Age).

Even the inorganic minerals of your bones, teeth, etc are constantly being added and removed by active processes (see: Which Osteoporosis Medication, If Any, Is Right For You?, for an explainer on that, since it has to do with acting on your body’s specialized cells that, respectively, destroy and rebuild bone for you).

Your muscles are also very much part of the constant destroy-and-rebuild processes of your body, as the mTORC1 growth pathway helps maintain muscle by regulating protein production, but healthy muscles must also remove damaged proteins to remain functional.

In aging muscles, mTORC1 becomes overactive, shifting the balance towards producing new proteins while reducing the removal of damaged ones. You would think that would result in bigger muscles, but no: allowing defective proteins to accumulate actively makes the muscles weaker, and biologically older.

The new discovery we want to talk about is the role of DEAF1 (that’s a gene)*. Researchers (Dr. Weiyi Jiang et al.) found that DEAF1 levels rise with age, driving excessive mTORC1 activity and worsening the imbalance between protein production and protein clearance, accelerating muscle deterioration.

^{*Specifically, a genetic transcription factor, and nothing to do with deafness (although certain mutations of DEAF1 can cause speech impairments, but that’s a separate matter). The name comes from “Deformed Epidermal Autoregulatory Factor 1”.}

To explain in few words why this matters:

• Why DEAF1 increases: under normal conditions, FOXO proteins keep DEAF1 under control, but FOXO activity naturally declines with age, allowing DEAF1 levels to increase.
• How exercise helps: exercise activates proteins that lower DEAF1 levels, restoring a healthier balance in mTORC1 activity so muscles can remove damaged proteins more effectively, repair themselves, and remain stronger and more resilient. Yay!

There are some limitations still: when DEAF1 levels become extremely high, or FOXO activity falls too far, exercise alone might not fully restore muscle repair, potentially explaining why some older adults benefit more from exercise than others, but research is still ongoing in this regard.

Meanwhile, if you’d like to read the paper in full, here it is: Exercise suppresses DEAF1 to normalize mTORC1 activity and reverse muscle aging

Want to learn more?

For more practical pointers than just “exercise more”, see:

Age & Strength Loss: What Happens When, & How Much Is Unavoidable?

Take care!