Dr. Mike Roberts

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1,217 appearances 1 recordings 1 series first heard Jul 2026 last heard 8 Jul

Dr. Mike Roberts’s voice in public audio — every appearance, attributed to the second.

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Perform with Dr. Andy Galpin · What Drives Muscle Growth & What Doesn't | Dr. Mike Roberts · 8 Jul 2026 podcast

There's also some other studies, and I want to say they're in like Petri dish, embryonic, fibroblasts, but VIM has been linked to stimulating mTORC1, which we know is needed for bolstering MPS or protein synthesis in any cell.

And so there's that linkage between this protein and mTOR.

So we're really excited.

That seems to be

part of the mechanical tension story that we think needs to be further investigated, if that makes sense.

Other than that, Marnie Bopart does elegant work with the integrins that are spanning the cell membrane.

The notion being you have this integrin protein that sort of communicates with the extracellular matrix.

And then once tugged upon, we'll start this phosphorylation cascade that can transduce the tension signal into anabolic signaling in muscle cells.

And so that's always been in the backdrop.

I'd say for the past decade in terms of potentially being a driver of how we get tension into anabolic signaling.

Other candidates, and we talk about this stuff in the review that we wrote in 2023, Karen and I's review.

Other candidates would be calcium, so stretch-activated calcium channels.

When you contract muscle, you have this influx of intracellular calcium.

Now, some of that is used to activate calpain, which are calpain proteases, and you see this proteolytic response.

But in addition to that, there's a tie-in with the influx of calcium and mTOR activation.

So there's a little bit of that going on as well.

But all of this sort of, you know, mechanisms aside, this is cool stuff.

These are academic questions.

These are just sort of reinforcing the notion that it is a mechanical tension, right, that is feeding into this anabolic signaling, which is then bolstering MPS, muscle protein synthesis, which is then leading to the deposition of more myofibrils, which is then leading to the expansion of the myofiber.

And once we reach a critical threshold, call it like a 10% increase in mild fiber size, we have the stem cells fusing, starting to tether additional nuclei so that more proteins can be produced and so on and so forth, right?

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