I have run into a question about muscle building at the cellular level and was wondering about peoples opinions. I know a lot of you don’t give a crap about this. I totally understand. In that case, just walk away.
Given: A myofibril is composed of many sarcomeres lying end to end in a series from one end of the cell to the other, then
Question: When a muscle cell builds a myofibril, a) does it just lay down all the sarcomeres necessary to span the entire cell all at once/in a very short period of time or b) are there “unfinished” myofibrils sitting around in muscle cells that do not span the entire length of the cell?
Never given it particular thought before, but I’m fairly certain that actin and myosin proteins are added one/few at a time in different locations along the length of the cell rather than a bunch at once the whole length. I’m basing this off of some photos of muscle cells I’ve seen that seem to demonstrate the idea of nuclear domain; some areas are much more developed than others along the same fiber. Given that, it seems that different sarcomeres would build at different rates and it’d be possible for some to be temporarily disconnected. I wouldn’t think for long, though, the body isn’t in the habit of building useless structures.
I’ll see if I can dig up anything definitive tomorrow.
[quote]buffalokilla wrote:
Never given it particular thought before, but I’m fairly certain that actin and myosin proteins are added one/few at a time in different locations along the length of the cell rather than a bunch at once the whole length. I’m basing this off of some photos of muscle cells I’ve seen that seem to demonstrate the idea of nuclear domain; some areas are much more developed than others along the same fiber.
-Dan[/quote]
Do you mean that some regions are more highly nucleated?
Do you mean that some regions are more highly nucleated?
[/quote]
A little bit, as nuclei don’t seem to be distributed uniformly along a fiber. That’s not the main part of the nuclear domain theory as I understand it though - it looks like certain nuclei are effected to express proteins to a greater extent than others along the same fiber in response to chronic stimuli.
This is the best pic I could find in a quick search online, the differences are subtle:
The host site also has a short discussion about how removing the connective tissue about the fiber appears to discount nuclear domain theory a bit as the fiber shown was more dramatic in variation before clearing the tissue, but I’m not sure I buy that since connective tissue is part of adaptation.
In any case, a prof of mine has a few other pictures that show much more dramatic width fluctuations, I’ll see if he has digital versions if you’re interested.
[quote]buffalokilla wrote:
Never given it particular thought before, but I’m fairly certain that actin and myosin proteins are added one/few at a time in different locations along the length of the cell rather than a bunch at once the whole length. I’m basing this off of some photos of muscle cells I’ve seen that seem to demonstrate the idea of nuclear domain; some areas are much more developed than others along the same fiber. Given that, it seems that different sarcomeres would build at different rates and it’d be possible for some to be temporarily disconnected. I wouldn’t think for long, though, the body isn’t in the habit of building useless structures.
I’ll see if I can dig up anything definitive tomorrow.
-Dan[/quote]
I’m agreeing with this idea. The body goes through great extent with all its checkpoints to make sure nothing useless or nonfunctional is built. I too will have to do a search on this tomorrow. Probably the most interesting question I’ve seen here in days.
Hope this helps. From my knowledge. The muscle fibre spans the lengs of the cell, but the myofibrils don’t. In reality the myofibril doesn’t necessarily look like the neat and tidy thing you see in the textbooks.
So when you get microtrauma breaking the sarcomere, they wont just grow to join at the middle again (increasing sarcomeric length); the ends will branch out like the dendrites of a tree, all a bit skew-if reattaching where the can and thereby increasing the cross-sectional diameter of the fibre as well.
When you ‘zoom’ out of this level of ‘chaos’ it all looks a bit neater. And If you tried to represent what is really happening in a textbook it would all look a bit of a bloody mess TBH.
I was thinking about this overnight last night and this morning while I was working and had my own counter question. Now I may be way off, but don’t we not build new muscle cells, but simply make the ones we have longer? If thats the case are we really building new myofibrils and sarcomeres, or are we expanding the ones we already have. If we’re expanding the existing ones then we would have the answer. You dont build new myofibrils. Just curious.
[quote]TrainerinDC wrote:
I was thinking about this overnight last night and this morning while I was working and had my own counter question. Now I may be way off, but don’t we not build new muscle cells, but simply make the ones we have longer? If thats the case are we really building new myofibrils and sarcomeres, or are we expanding the ones we already have. If we’re expanding the existing ones then we would have the answer. You dont build new myofibrils. Just curious.[/quote]
The muscle cell grows thicker by adding more myofibrils along its length.
[quote]sootybaby wrote:
So when you get microtrauma breaking the sarcomere, they wont just grow to join at the middle again (increasing sarcomeric length); the ends will branch out like the dendrites of a tree, all a bit skew-if reattaching where the can and thereby increasing the cross-sectional diameter of the fibre as well.
-sooty[/quote]
That does make a lot of sense.
My original question actually stemmed from one of the so called training “myths” that you couldn’t preferrentially build part of a muscle like the inner pecs.
If sarcomeres can be added preferrentially to one end, the other, or the middle, then it is possible, and I’d say even likely that a particular exercise could result in more sarcomere density on one end of a muscle than another.
In other words, crossovers may indeed build the inner area of the pec fibers.
Anyway, it turned into a more interesting question I think.
Oh lord, I wouldn’t want to perpetuate or add fuel to the ‘inner pec’ debate.
I would have to ask one of my muscle physiologist colleagues for an absolute answer to this, but whilst x-sectional area increase will for sure result from this response to microtrauma I am pretty sure that the loading over a muscle fibre and gross muscle itself is more uniform. As in, even a static load in one position would spread the force over the length of the muscle.
But I will get back to youse all on that point.
[quote]TrainerinDC wrote:
I was thinking about this overnight last night and this morning while I was working and had my own counter question. Now I may be way off, but don’t we not build new muscle cells, but simply make the ones we have longer? If thats the case are we really building new myofibrils and sarcomeres, or are we expanding the ones we already have. If we’re expanding the existing ones then we would have the answer. You dont build new myofibrils. Just curious.[/quote]
Sorry, I re-read what you wrote and I understand now. You do not add sarcomeres (right?) but you might add contractile units unequally to different sarcomeres in the same myofibril.
Just to be clear on definitions, a muscle fiber is made up of a bundle of myofibrils, which are like small muscle fibers. A myofibril is made up of a long row of sarcomeres, and a sarcomere is the smallest contractile unit in a muscle.
My understanding is that we generally do not grow new muscle fibers (hyperplasia) but we do get more myofibrils (increasing muscle fibers is debated). Essentially myofibrils split under tension and then each one grows bigger, kind of like cutting a worm in half. This makes the muscle fiber ultimately thicker which results in the increase in size (hypertrophy). If this is correct then when the myofibril splits and grows the sarcomeres would grow, so we would make new sarcomeres. I am not sure if they grow from the middle or at the ends.
This probably means that you might be able to target a specific part of a muscle, however it would work better in some muscles than others. Namely I would think pennate muscles and not parallel muscles would work better, and probably longer rather than shorter muscles. But given that tension is somewhat distributed through the muscle this probably wouldn’t be huge.
[quote]nptitim wrote:
Just to be clear on definitions, a muscle fiber is made up of a bundle of myofibrils, which are like small muscle fibers. A myofibril is made up of a long row of sarcomeres, and a sarcomere is the smallest contractile unit in a muscle.
[/quote]
So, what I am not clear on is this: My old textbooks show a sarcomere as being at least several actin/myosin chains thick. Is this correct?
I can’t contribute much more than has already been said (though I do recall reading something regarding Desmin/Titin in its earlier mentioned role). I do want to say to all who have posted so far, excelent work! People like you are the reason I continue to come to T-Nation.
[quote]mertdawg wrote:
So, what I am not clear on is this: My old textbooks show a sarcomere as being at least several actin/myosin chains thick. Is this correct?
[/quote]
A sarcomere has actin and myosin in it, I think the typical sarcomere is made up of 3 myosin with 8 actin. The actin are connected to the ends of the sarcomere and when they slide towards each other they pull the ends of sarcomere toward each other, thus shortening it. The length of the myosin is essentially the minimal length the sarcomere can get. Of note is that the actin and myosin do not actually change length, they slide against one another, hence the Sliding Filament Theory.
[quote]nptitim wrote:
mertdawg wrote:
So, what I am not clear on is this: My old textbooks show a sarcomere as being at least several actin/myosin chains thick. Is this correct?
A sarcomere has actin and myosin in it, I think the typical sarcomere is made up of 3 myosin with 8 actin. The actin are connected to the ends of the sarcomere and when they slide towards each other they pull the ends of sarcomere toward each other, thus shortening it. The length of the myosin is essentially the minimal length the sarcomere can get. Of note is that the actin and myosin do not actually change length, they slide against one another, hence the Sliding Filament Theory.
[/quote]
Thanks, I remember all this stuff now, except I didn’t realize that the sarcomere was 3 and 8. I do see how they fit together though. I also realize that the illustrations and explanations in “graduate level” kinesiology books suck. There is some interesting stuff there that I probably will understand better 10+ years later. I may actually be teaching highshool anatomy next year after 10 years of chemistry, so I may really get to learn it.