Episode Transcript
[00:00:00] Speaker A: And when you think about design, one aspect of design is you work with the materials available.
In the case of the body, the only thing available to work with were molecules that existed at the scale of nanometers.
Those were the raw materials and you had to make something work that would move massive large bodies. And so muscle solves that problem of how tiny molecules at the nanometer scale and could be assembled to move things that are billions of times larger and heavier than they are.
[00:00:34] Speaker B: ID the Future, a podcast about evolution and intelligent Design.
[00:00:40] Speaker C: Welcome to ID the Future. I'm your host, Andrew McDermott. Today I get to conclude my conversation with Dr. Robert Walter about the amazing molecular machinery and systems that allow muscles to generate force and movement.
Dr. Walter is currently the Chair and Professor of Biology at Belhaven University in Jackson, Mississippi, where he has been teaching for over 30 years. He has a PhD in anatomy from the Ohio State University where he focused on the anatomy of the brain. He teaches courses in human biology and is a leader in the Division of History and Philosophy of Sciences at the Mississippi Academy of Sciences, where he was recently awarded the designation for Fellow of the Academy. He is the co author, with four others, of the book Evolution and Intelligent Design in a Nutshell. He has been doing research and has given presentations on intelligent design, often at secular conferences, for close to 30 years. Welcome back, Dr. Walzer.
[00:01:38] Speaker A: Good to be back.
[00:01:40] Speaker C: Well, we have been talking about muscles and I want to review a little bit with folks, but then I want to jump into even more depth and detail because it's truly amazing as you get right down to the molecular level and see the structures that are responsible for giving us movement and that strength that we all enjoy. Now, you've taught and studied muscle physiology for many years. In part one, you told us how you came to focus on muscle strain. Can you just briefly remind us of that here?
[00:02:11] Speaker A: Well, I had mentioned that a number of interest converged. One was my experience teaching courses on muscle from the organ level to the cellular level. The second was my interest in the properties of protein, including the potential of them to have multiple shapes in consecutive order.
And the third was my interest in motor proteins and how they generate force.
All this set the backdrop for my interest in muscle. And I first looked at the molecules in muscle that generate force. But then as I studied muscle, more realized that there were muscles that were receiving the force and incurring a great deal of strain in receiving that force.
[00:02:56] Speaker C: Yeah, and you've, you've been unpacking now for us, you actually argue that normal muscle function involves continual Microscopic damage.
Can you explain what you mean by that?
[00:03:07] Speaker A: The structure of muscle is such that the molecules are getting pulled. Pulled on incredibly much greater in a sense than they're able to handle. But you know, in design, that's all we have to work with.
You have to work with the available materials, and those are the available materials.
So they are getting pulled on with tremendous forces and they're not able to handle it. And so they get overstrained and damaged.
And so that damage has to be detected and repaired or replaced at the rate that it occurs for normal function to continue to maintain.
[00:03:46] Speaker C: Wow. And you will unpack that with us a little more as we go through this?
[00:03:52] Speaker A: Absolutely.
[00:03:52] Speaker C: Now let's take a closer look at the repair, the replacement, and the stabilization mechanisms that keep muscle functioning. Muscle faces a major problem. Every contraction places components under tremendous stress. And yet our muscles don't just collapse or destroy themselves.
How is the continual damage kept under control?
[00:04:14] Speaker A: I think it's fair to say this is not fully understood, but there's a lot going on in muscle. But some of the mechanisms are just basic cell biology which all cells have, where they have roving damage detection molecules that sense that a protein is damaged, target it for destruction, and then I guess in the normal course of things, that protein gets replaced. But in addition to the things that all cells have, there are much more complex systems in muscle that muscle cells have where they have special detection mechanisms and special signaling mechanisms to trigger a response to initiate repair and replacement.
[00:05:00] Speaker C: Wow.
Okay, so muscle isn't static. It's more like, I don't know, an active construction site. Or perhaps a better analogy would be an emergency room during a natural disaster or a pandemic. You know, you've got all this, this action happening because of something that's going on, you know, in the, in the outside world. And it's a lot, but it, it, it's still managed, seemingly overwhelming, but know able to run consistently with good planning and management.
Are those useful analogies to help us understand what's happening?
[00:05:36] Speaker A: I think those analogies come as close as the, as any analogy can to characterize what's going on in muscle.
And I think what's good about them is their kind of extremely busy, if not frenzied level of activity that's still maintained in an orderly way.
Where the analogies are limited is that in constructing a building, you don't yet have the building, you're constructing it, but with muscle, you have it already. It's already constructed, but yet that same level of activity or pretty Close to that same level of activity is still continuously going on. And the same with the pandemic or the natural disaster.
Those are unnatural things. They don't happen all the time.
But in the normal course of muscle function, this is happening all the time where you're needing that level of responsiveness to fix things.
So it's just. There's nothing like it, really.
[00:06:40] Speaker C: And by the way, the damage and repair, this is happening in real time as the muscle's being used, right?
[00:06:47] Speaker A: Absolutely. It's happening in real time. This is during normal function.
And a way of thinking about it, it's almost humor, but it's like fixing the plane while it's flying, you know, which. Which seems kind of really dicey. And so that's kind of a whole subject in and of itself. How it maintains.
I think the. The general idea would be that any portion, it's only a small percentage of it, that's being replaced at any given time, so everything else is still intact and kind of doing the work. It's kind of like you have multiple engines on a plane, so you're fixing one of them or something.
[00:07:23] Speaker C: Yeah. And if it's completely built, you know, the, The. The muscle system, why does it require such a high level of activity all the time?
[00:07:32] Speaker A: Yeah, that's. I think that's a good question. And I think this is due to one of the features that got me interested in muscle initially, and that is the tremendous amount of force generated by tiny molecules. And these molecules are strained beyond their capacities by the nature of the task, both in the generation and the receiving of the force.
Therefore, they're continuously damaged and require repair and replacement continuously.
And when you think about design, one aspect of design is you work with the materials available. In the case of the body, the only thing available to work with were molecules that existed at the scale of nanometers, that those were the raw materials. And you had to make something work that would move massive large bodies. And so muscle solves that problem of how tiny molecules at the nanometer scale could be assembled to move things that are billions of times larger and heavier than they are.
[00:08:35] Speaker C: Yeah. And that's part of understanding the.
This system at the molecular level. You know, we know muscles as this, you know, but you go right down to the molecular level, and you have to know what is. What is, you know, exercising that force and what is receiving that force.
[00:08:55] Speaker A: Right.
[00:08:56] Speaker C: Now, one of the most fascinating structures you touched on in part one of our conversation is the Z disc. Remind us what that is and why it captured your attention so to talk
[00:09:09] Speaker A: about the Z disc, we have to kind of rewind the tape a little bit and talk about a little bit of what we mentioned in the first podcast. And that is the sarcomere.
The sarcomere is the unit of contraction in muscle, and it's like a tubular segment and they are lined up end to end with a bunch of other of these tubular segments in something called a myofibril.
So the boundaries of the sarcomere are Z discs.
And so since there is one Z disk between two adjacent sarcomeres, that the structures in both sarcomeres are anchored to that Z disk.
And so for instance, what we have is we have actin filaments extending out of the Z disc into the sarcomere. Those filaments get pulled on by a molecule called myosin and that pulls the Z disc toward the center of the sarcomere, shortening it.
Well, the same thing is happening in the other sarcomere. So really, the Z disc is in the middle of a tug of war, getting pulled on by actin filaments from both sides.
And the molecules inside that Z disk get exceedingly strained and have to be replaced very rapidly.
[00:10:33] Speaker C: Now, you compare the Z disc structure to a mattress box spring or shock absorber. Why are those helpful analogies?
[00:10:42] Speaker A: Actually, I got that from the literature. Authors have examined it themselves and used that terminology.
They have gotten special high tech images of the Z disk where a slice is made through the sarcomere right at the Z disc. So you could look at it head on, and they find this amazingly intricate pattern of either little squares or kind of oval shaped structures.
And so anyway, that really kind of shocked people in terms of how highly organized it was.
And then they were trying to figure out what's going on between the shapes, which we can talk about in a bit.
But because that, because it's getting pulled on in both directions, it's going through a lot of strain. Now, I mentioned a mattress box spring and the mattress box spring. I think if you've ever seen the box springs in the complicated pattern, that that suggests the structure of that pattern in the Z disc.
So I think there's a lot of similarity.
When you compare those. The difference is that a box spring, you sit on it, so you're actually pushing on it and you're pushing on it from one side.
The Z disc has different stresses and strains because it's getting pulled on and pulled on from both sides.
[00:12:10] Speaker C: Okay, now one thing you note in your presentation of this topic is that these structures actually change shape under the stress that they're. They're receiving. Tell us about that.
[00:12:22] Speaker A: What. What you have are photos of electron micrograph images of these amazingly complicated, evenly spaced patterns. And they come in two varieties, either what's called the small square or the basket weave. The small squares, as it suggests little squares. While the basket weave is more of an oval shape with the ends a little bit more expanded than the middle.
It was initially thought that the small square was the relaxed state of the muscle and the basket weave was the contracted state.
That may be true, but it's come into question.
And right now I think there are some factors that have made it a bit more complex to explain the difference in states.
But what I think, no matter what's going on, I think we can be confident that there is strain on that Z disk. And the molecules that are making up that lattice work are getting bent in different ways.
That pushes them beyond their limit. And so it's those molecules that are the most rapidly replaced of any molecules that are forming this lattice work in the Z disk.
[00:13:39] Speaker C: One statistic you actually share is quite astonishing. You note that individual alpha actinin molecules are replaced roughly every 25 seconds. Why is that significant?
[00:13:50] Speaker A: Yeah, and if we have that illustration, you'll see that there are yellow and black bars that represent actin filaments, and they are anchored together by alpha actinin molecules. And those are what form the lattice. So it's believed that the lattice is made up of those different alpha actinin molecules.
And so obviously they're going through extreme distortion because of something happening during contraction.
And so, so they. It's been studied and it's been shown that they are replaced every 25 seconds. Why that is significant is cause alpha actin is a big protein. It's not small. It's 1800amino acids.
And I don't know if people have a sense of the size of proteins, but hemoglobin, which holds oxygen inside of your red blood cells, alpha actin is about four times bigger than that or enzymes. People maybe know a little bit about enzymes that digest your food and about five times bigger than an enzyme. So these are large proteins, and so it's not an easy job to replace such a big protein. And yet it's done at an astonishingly rapid rate.
[00:15:05] Speaker C: Huh, that's very interesting. Now, what happens when these repair and replacement systems break down, such as with muscle diseases?
[00:15:15] Speaker A: Well, muscle diseases are a whole big complicated topic, and to some extent they're not even fully understood.
But in general, if the repair and replacement mechanisms aren't operational, then the damage isn't detected and it's not fixed.
And very often, not only does it remain and get in the way of function, but it'll lead to more damage, which will lead to more damage. There'll be a downward spiral which could lead to the complete failure of the muscle.
[00:15:49] Speaker C: Okay. When that balance is lost and weakness starts to accumulate.
Okay, that makes sense. Now, you implied there are some delicate balances maintained in muscle. Can you elaborate on that, give us a better picture of the balances going on in real time?
[00:16:06] Speaker A: Yeah. When you look at muscle, there are so many molecules that are so uniform and evenly distributed, it's astonishing. It's been referred to as a paracrystalline array, but it's not like a polymer or a chemical that just assembles by itself. I mean, these are things that are built by very detailed sort of mechanisms of assembly which aren't understood themselves.
So you see tremendous balance in the structure, particularly of individual sarcomeres as well as the surrounding sarcomeres. The myosinhic filaments are equal length within a sarcomere, and they have the same number of molecules in them.
And myosin are kind of mirror image of molecules. They have two sides, the thick filaments, and there's about the same on one side as there is on the other.
And then they interdigitate with actin filaments coming in from both sides of the sarcomere. And if you just look at one side for a moment, those actin filaments are uniform in their size. Exact.
And likewise, the ones on the other side of the sarcomere are uniform. And in fact, the two sides are uniform with each other.
And not only that, but if you look over to the next sarcomere, remember we mentioned that the Z disc is a boundary between two sarcomeres, and the actin filaments are extending out of that Z disc on both sides.
The Z disk in the next sarcomere, the actins in the next sarcomere are uniform and equal in size to the ones in the sarcomere they're connected to. And in fact, if you look all the way down the line of sarcomeres connected to one another, they're like carbon copies, just almost as perfect as they can be. As well as parallel myofibrils with parallel sarcomeres, they look as fine as they can be also.
And in fact, they are even in register with one another.
So the amount of balancing that goes on is incredible.
And one other thing to mention about that Take the myosin thick filament.
If you, instead of looking at it from the side, kind of look on it like you're looking down the shaft. You'll see the head stick out in even intervals of 120 degrees. There's like three pairs going around the myosin, and then there are six actin filaments surrounding that one myosin molecule. So there will always be an available actin filament for those heads to grab. And that way, if they're grabbing evenly around the filament, then it doesn't get strained and twisted and distorted.
So that's another aspect of the amazement.
I have an analogy here of if things were. Weren't quite right, what would happen? Can I share it?
[00:19:16] Speaker C: Yeah, yeah, let's hear it.
[00:19:17] Speaker A: So let's say that you had a myofibril with a number of sarcomeres lined up, but one of them was much weaker and smaller than the others.
So what kind of analogy could we give for that? Well, I imagine you took a hundred equally strong Olympic bodybuilders and they linked arm in arm to pull a Mack truck.
Now, it's hard to know whether they could succeed or not, but there'd be a lot of force going on.
Now, let's say that you took me. You or me, who is not a bodybuilder by any stretch, and put. Put us right in the middle between the two, the sets of 50. Right. We're number 51 in that, and 50 on each side, 50 on the other side pulling on that Mack truck. Well, we would be in for a rough time. We'd have our arms pulled out of our body. I mean, there'd be so much force. And then when we collapsed and were useless, then all of a sudden the whole chain would fail because the link was broken.
And so if things aren't perfectly balanced, you get this downward spiral which gets worse and worse and worse until it leads to massive destruction, which sometimes occurs in disease processes.
[00:20:41] Speaker C: Wow. Yeah, that does paint the picture and shows just how important that delicate balance is in these microscopic muscle structures.
Wow. Now, even with the latest imaging techniques, there are still lots of unanswered questions when it comes to muscle.
What mysteries remain about muscle that you think will continue to be studied and pursued?
[00:21:07] Speaker A: I think there are a lot of mysteries that still remain to be studied and pursued. And in fact, I think that they don't even know all the mysteries because as they find new things, it not only answers a question, but raises multiple new questions. But as far as some of the Ones that we know right now just producing enough proteins close enough to the locations where they were needed for replacement.
Because muscle is a big thing and if you produce proteins at a distance, they might take a long time to diffuse all the way through to where they need to get to. So how do you get these proteins to where they need to get to in a timely way? And how do you produce them in a timely way? And then removing large proteins from muscle alpha actin are big enough, but they're even bigger proteins that need to be replaced and removed.
And it, it becomes a logistical problem.
These things are so big. How do you get them out of there and then, then putting new proteins in the place of old ones. It's one thing if you're assembling some, assembling something from scratch, but if you have a, if you, if, let's say a shelf or something like that, and you are, and it's all fixed in place and you're trying to take apart out, but there's like nails and screws and things, how do you remove that and how do you get a new one in?
And that's kind of the problem in muscle. I don't know how it's done really, and I don't know if that's known. I don't think it is.
And all the regulation of all the lengths and the balancing of all the things that I just spoke about a moment ago, that really is unknown. And it's thought that some muscles, their actin filaments will be shorter uniformly in that particular muscle. But then in another muscle, the actin filaments are going to be longer and that relates to the function of that muscle. So how is that determined and how is that regulated? I mean, there's just myriads of questions related to this kind of stuff.
[00:23:11] Speaker C: Yeah, well, and as you're talking, I'm just envisioning that. And you bring up some good points about the logistics involved in these engineer structures. You know, how often do we think about that?
Just like in a, in a factory, you know, there's lots of logistics when there's lots of moving parts and lots of processes going on. And we know that molecular machines are at work, you know, transporting things to different parts of the cell. And you know, we've, we've seen some of those animations.
[00:23:42] Speaker A: Right.
[00:23:43] Speaker C: But these are still great research questions.
[00:23:46] Speaker A: Sure.
[00:23:47] Speaker C: So it's good to know there's still a lot to study when it comes to muscle.
Right now. Can you summarize for us as we wrap up today just how the systems involved in muscle demonstrate intelligent design.
[00:24:00] Speaker A: Well, I think that what I've discussed today, there are many ways that those systems demonstrate intelligent design and many that I haven't considered related to what we've discussed today. But then there are many other things related to muscle that we haven't even touched upon that also show lots of intelligent design. But let's just focus on what we've been talking about, what, what I mentioned.
Muscle solves the problem of moving massive bodies using tiny molecules that really aren't, aren't designed in a sense to handle that stress.
So they are overstressed. But muscle still gets the job done because it has these repair and replacement mechanisms that are johnny on the spot that get those new molecules in, in the nick of time so that the function of muscle isn't interrupted.
Also, these repair and replacement mechanisms are built into muscle as if muscle is anticipating those failures.
And they're built in at a scale where it can keep up with the damage. All right, so there's just an amazing amount of fine tuning. Right. Whenever you have things that are breaking down and things that are getting repaired, you have to make sure that those are both in balance. Because if one exceeds the other, then you either have a lot of unfixed damage or you're fixing stuff that doesn't need to be fixed, which could be a whole different kind of problem.
[00:25:35] Speaker C: Yeah.
[00:25:36] Speaker A: And then in the, in the biological world, the layout of the structures and muscle is just so incredibly ordered. It I think exceeds anything that's seen in the biological world as far as it's being functionally significant. The exact placement of every molecule in the exact way that it is placed. And not only that, but there are things that are expecting the molecules to get moved and shifted and distorted.
And these aren't, I'm not even talking about the repair and replacement mechanism. Those are kind of countering the forces and trying to hold things together, but even they can't do the job completely. And so things do get damaged.
So it's just a whole world of dealing with intense forces that are handled and managed.
So it's just absolutely incredible, I think, how it all works well.
[00:26:38] Speaker C: And my follow up question to that obviously would be in your personal as well as your professional scientific opinion, is it possible that an unguided evolutionary process could originate and develop muscle through, as Darwin once said, numerous successive slight modifications?
[00:26:58] Speaker A: Yeah. So let me answer this two ways. One is, let me kind of pose as a man on the street and not as a professional scientist.
If I'm just a man on the street. And you're presenting all this stuff to me and then saying, and by the way, did this come about by unguided evolutionary processes? I would say, what are you talking about?
There's no way that unguided process, you know, these numerous successive, slight modifications can produce all this organization.
It strikes me as, as insane that you're claiming such, there's such a high level of organization without an organizer.
That's, that's not common sense. So that's my man on the street answer. But my professional answer is also no.
But it's a bit maybe more dignified if I could say that. I'd put it this way. I have yet to see any detailed evidence showing how a step by step process could have created the complexity found in muscle.
And in the absence of that evidence, I see no reason to hold that an unguided mechanism produced it.
[00:28:10] Speaker C: Wow. Well, and with that last question, I feel a bit like, you know, the lawyer in the courtroom summoning an expert witness to provide an authoritative opinion on the facts of the case. But you really do have to look at it that way. You have to put all competing hypotheses in the doc, so to speak, and measure them up, don't you?
[00:28:30] Speaker A: Yes.
And as we were discussing before the show, and you asked, does this show irreducible complexity? And I answered, it shows nested irreducible complexities where one system that's irreducibly complex is in another that's irreducible complex. It's in another that's irreducibly complex. It's like irreducible complexity on steroids.
So, yes, you have to look at these meaningful competing hypotheses and they have to be something more than what are called just so stories, you know, kind of like fairy tales.
But I'm not even sure that they have just so stories for muscle. I mean, they can't even imagine, like if you're given as much license as possible for speculation, how an unguided step by step process could produce it.
So it's hard for me to answer that question about the competing hypothesis when I'm not really given anything to sink my teeth into as far as meaningful competing hypotheses.
[00:29:37] Speaker C: Hmm, interesting point. Yeah. Well, Rob, what's next for you in your research? You know, you've done a lot with muscle. You've studied it a lot. Where are you going to take it next?
[00:29:47] Speaker A: Well, you know, I'm like a kid in a candy store. I'm so interested in it. So I.
There's a lot of different options that I'm thinking about as I read about these proteins. They are really getting a handle on the exact 3D structure, like the surface contours and all that, and the surface contours of one and how another one can fit into those contours and where they attach and how they attach. And so I'd love to delve into it, try to get a handle on that. And we have some great 3D printing labs at Belhaven, both in the art and math departments. Maybe I could even try printing some of this stuff out and seeing how it would look, you know, if you're holding the objects in front of you. I've always personally found that a model, a physical model in front of you could always give additional insights. But I'm also thinking about writing a book, and I'm not sure where I want to go with the book, because I could start like with the general public and just start from the body and how muscles are on bones and then build my. Build things onto that.
Or I could just. Just get into the world of proteins. Because the set of proteins, for instance, in the Z disk, I left most of them out, right. I just mostly mentioned actin and alpha actinin, but there's at least 20 other proteins that are critical parts of the Z disc. And then there are multiple parts, you could say spheres of the cell which have their own sets of proteins in muscle. And there's probably at least a half a dozen of them that are all doing different things. And I would like to get into, you know, all of them if I could.
And that could take up a whole book in and of itself. So not sure where I want to go, but I'll probably just start going and see where it takes me.
[00:31:45] Speaker C: Yeah, well, and that's a great idea about the physical models of some of these things. Like, let's hold a sarcomere in our hand and get a feel for all the different parts, you know. Yeah, that. That would be pretty amazing.
[00:31:58] Speaker A: Yeah.
[00:31:58] Speaker C: Well, really appreciate you sharing your insight today. And over two episodes, sort of just touching on this enough to give us a little, little bit of complexity and understanding about these amazing systems. So thank you.
[00:32:13] Speaker A: Sure. Glad to do it.
[00:32:15] Speaker C: Well, audience, if you haven't yet, enjoy the first half of our conversation. It's available separate episode. And remember, you can listen and watch ID the Future. Now, you do have a choice. You can subscribe to our YouTube channel to see our latest interviews. That's at YouTube.com d the future.
So there you can go to watch these interviews. And as I said, we're trying to put little pictures and maybe some animation into this series, at least to show you what, what we're talking about. Well, until next time, I'm Andrew McDermott. Thank you for joining us.
[00:32:50] Speaker B: Visit us at idthefuture. Com and intelligentdesign.
[00:32:54] Speaker A: Org.
[00:32:55] Speaker B: This program is copyright Discovery Institute and recorded by its center for Science and Culture.
