Hello students, this is going to be a lecture on muscle tension and here we're going to focus on muscle tension at the fiber level. So at the muscle cell. So what is exactly happening to generate tension at within the muscle cell itself. So remember go back to our muscle contraction lecture. This is where we're creating cross bridges. What is generating that tension? So when we talk about a muscle twitch, this is the amount of tension generated by one stimulus, one action potential coming down a motor neuron releasing the specific amount of acetylcholine that is released by that one action potential that generating um that binding to the motor end plate and opening nicotinic receptors and sodium influx in plate potentials and the calcium release that goes with that and then the amount of tension that's generated with that calcium release. So how much tension can we generate with that and so um this is this is the smallest muscle contraction that we can that we can get because it's one single amount. It's not typically visible. And when we when we see this, note that there was a period of time that I was just describing there that we had a stimulus, some sort of stimulus caused this action potential to be propagated and it took a a significant amount of events to get that calcium released and to bind to troponin to move the tropomyosin and allow for those cross bridges to start to happen. So the contraction could be initiated. So remember the latent period is the time it takes from stimulus until muscle contraction begins. So that is the period when all of that those events were happening. We have that action potential traveling down until that calcium causes the removal of tryptoyosin off of the actin and that first crotch bridge can be can occur and we can start generating tension because you can't generate tension until cross bridges can form. And so that is your latent period. And so in generating tension, we're going to get some contraction, but it's going to there's going to be a period of time before that where we don't get any any tension at all. This is our latent period. And then we have a contraction period where with the amount of calcium that we have released, we've got cross bridges happening and we're shortening the muscle more and more and more based on these cross bridges. And then there's a point where we've run out of acetylcholine. Acetyloline is being cleared now. And as acetylcholine is being cleared, there's less acetylcholine, less sodium influx, less calcium being released. And remember in the background, calcium was also being pumped back into cycoplasmic reticulum. So now calcium levels are starting to drop. And as calcium levels drop, more and more um there's less and less calcium within the cell and more and more troponin is now absent of calcium and troponin is going to move tropommy back overactin and so we're going to start to have less and less cross bridges. So now you're going to you're going to have this generation of tension, but then you're going to start to go on the other side where you start to have relaxation and less tension um on the other side of that hill. And so this is that relaxation period. So as acetylcholine is stopped and you start to clear acetyloline and calcium levels drop and tension decreases, this is your relaxation period. So this is the decreasing end tension on that graph of the tension generated from that single action potential. So note that the refractory period in this twitch is um beginning of the latent period up until the start of contraction because you can stimulate all you want during that period, but you're already you've already done the signal and everything's already being carried out. So you can't signal any more than you already have. So you're not going to get any further response during that time. And so this this latent period is um it's pretty short in skeletal muscle but in in cardiac and smooth this latent period is quite long and extended and this requires the muscles to fully relax before the next contraction and this is very important in those muscles and especially cardiac. So this allows for the filling of the heart between contractions and we'll talk about that when we get into the cardiac unit. But the refractory period is very important for the muscle itself. And um in skeletal muscle this period is quite short and this allows us to maintain contraction for a period of time. So I can have sustained contraction and what we call a period of tetanus. So we're going to talk about that. So when we're looking at a graph of this tension generated from a single action potential, this is a generalized graph. So you have your stimulus at at time zero here. And there's a period where we're not generating any tension and all those events that I talked about. So action potential traveling down the motor neuron causing calcium influx at the axon terminal causing acetylcholine release from the syn from the axon terminal. Acetylcholine diffusing across the synapse binding to the nicotinic receptors. Sodium influx in plate potential. Multiple inplate potentials being generated into an action potential. action potential being propagated along the motor in plate and um along the circle lima and then down the T-t tubules that causing the release of calcium calcium binding tropponin troponin moving tropomyosin and then we get myosin binding to actin. Now we start crossbridge that will be the beginning of this rise in tension. So now we can start generating cross bridges because we started to move the the tripy off of that actin and so those sites are open because we've released calcium. So it took all of those events to get to the start of our generation of tension. And so we can continue to generate tension as long as as calcium is present. And so there's a point where a maximal point of tension generated and then at some point this will start to go down. And this goes down because we've stopped releasing acetylcholine. Acetylcholine is done based on the amount. We have our maximum amount of acetylcholine. And now acetyloline levels are starting to decrease. We've stopped releasing acetyloline. Acetyloline is being cleared by acetyloline estration, the synaptic cleft. So acetyloline levels are going down and our action potentials at the circle lima are decreasing. So calcium release is decreasing and calcium levels will now start to decrease because calcium is constantly being pumped back into that cycloplasmic reticulum. And as calcium levels decrease, tension is going to decrease because cross bridges will no longer be possible because when calcium levels decrease, tropponin is now going to move tropomy back over those actin sites. So your cal your cross bridges are going to decrease and this is where your tension decreases and this is your relaxation period. So here on this upswing is tension generated in that muscle twitch and this is your relaxation period. Now understandably if you had not fully relaxed if you still had some tension generated and you stimulated during this period there would be the laten period. Let's say it looks like it's about um 5 milliseconds. So if it if we stimulated here and it was 5 milliseconds right about here, we would start to get more tension generated. And if we generated from this point to this point, we would get about that much additional. So we could add on to this amount of tension and we would come up here. So we would get this amount from this bottom here to this top. Let's say that's X. So, we're going to get whatever this this number is at 60 plus x because we started that's where we started when we when we started generating tension on the other side. If we started up here, we would get more tension. So, it depends on where you stimulate where you get the tension. Now if you stimulate faster, so if I actually create another action potential during the contraction period, I could actually add on to the rising phase here. And so I could generate more tension on this more tension on this side. So I could add to the tension on this side. And you there is a point where you could stimulate the muscle so quickly where you just go exponentially up straight you know as up as fast as you possibly can. Maybe not straight up but at a maximal rate and then you you plateau off at your maximal contraction and this is where you get sustained tetanus. So if you have some amount of relaxation in between, we get something called fu unfused tetanus. And then if you don't have any relaxation in between, you get something called fused tetanus if you're stimulating fast enough. So we're going to talk about that. So tension again varies based on this timing and frequency. So also note that when we started our contraction, where was what was the length of contraction at the start? So if my if my muscle was already maximally contracted, I'm not going to generate much more tension than that because it's already maximally contracted. If my muscle was maximally extended, it's going to be very hard to start to generate tension because my cross bridges are kind of stretched to the max. So, it's going to be very hard to generate tension until I get significant cross bridges and then I can start to generate tension. Well, so where you start with your cross bridges is going to determine how you how much tension you actually get in this in this twitch. And of course then the type of muscle fiber. We talked about that in previous sections um with type one and type two. And we'll talk about this more when we talk about um muscle groups and um our how we recruit muscles and how many we use. But the muscle fibers that we're using, remember if we use type two fibers, they're typically larger. They have more myophibbrals. So you'll be able to generate more tension. And then of course if our motor units are larger, we will generate more tension overall as a whole. So that will affect the amount of tension. When we talk about wave summation, that's what I was alluding to before when I was pointing out that the areas on that graph. This is where we get an increase in tension by the timing of the frequency or the repetitive stimula repetitive stimulation on the amount of tension that we get. So this is a little bit different than summation with neurons. So keep this in mind and separate this out. This is wave summation for tension is different than um summation of graded potentials with neurons. Okay, this is all about tension and the amount of contraction you get. This is in a muscle cell and this is related to the amount of calcium that is present. More calcium, more tension generated, more cross bridges. Okay. So, we can get progressively more if we have more calcium. That's that's it. So, the faster I stimulate, the more calcium is going to be in that space, the more cross bridges I can make. If I wait until calcium is starting to get cleared, I have less calcium. So, I'm not going to be able to generate as much. I can't add on as much tension as I would as if I didn't allow for that relaxation period. And so that's important to understand. So the amount of tension is dependent on the frequency. So we have something called unfused tetanus. This is where we stimulate quickly but not so quickly that we we are are preventing any relaxation. So in this case we're go we're stimulating we're stimulating at a rate where there is some period of relaxation happening in between our stimulation. So there's some sort of relaxation happening before we start our next stimulation. And so um this we get kind of a pulsation of of contraction. And fused tetanus is where you're stimulating so fast that you never have the chance to to get into that relaxation period. So you're maximally throwing out that calcium as much as possible. And so you're contracting at that maximal rate and then you end up with your maximal contraction at the end. And this would be sustained contraction. And ultimately this is going to look like me holding my arm out, right? like I'm I'm in sustained contraction and you get more cross bridges and that's what you see on a graph. They're going to on a on a graph they're going to look look a little bit different. So here notice this first twitch we had a normal you know latent period. You don't see much of it because it's very small. We're not um we haven't blown this up very much. But you have your contraction period. You start relaxation. you stimulate again and then you then you add on the the tension um and you get the same amount of tension to what you still had when you added on and you do the same thing again. You add on at the same rate and you just keep adding to that and you keep adding and you keep adding but you have a period a little short period of relaxation in between your stimulus. So it's it's it's long enough where you get a period of relaxation in between. Here we're stimulating so fast that there is no period of relaxation. So we just com we we completely add on and add on and add on to that tension until we max out. And now we've pretty much plateaued. This is our maximal contraction and tens um or maximal tension that we can generate and then at some point we end and we can relax. And so this is your fused tetanus. This is your unfused tetanus because they haven't come together because there's period of relaxation. So length tension relationship, I kind of alluded to this previously where the start of of your contraction determines how much tension you can generate. Meaning if you are already in a contracted state or in a in a very lengthened state that may um affect the amount of tension you can generate. So there is a an optimal amount of of of contraction to start out at that will give you the maximum amount amount of tension. And so it's usually somewhere in between contraction and extension. And this is due to the overlap of the measin and actin cross bridges. So this is where we're starting. We're already fully contracted. You really can't get much more. So you're not going to get a lot a lot more contraction than you already have because you're already your circumcy shortened. Here we have really good crossover um between the meosin heads and the actin. So when we start to generate contraction, we're going to be able to very quickly pull these um actin toward the midline because we've got good connection with those um the measin heads have good connection with the with the actin. And here, look at the amount of overlap. There's very little overlap between the meosin and the actin. So, at first, it's going to be very hard to get to generate any tension because we have hardly any cross bridges. Now, eventually, like as we're starting to generate tension, we'll get more cross bridges and then when we shorten enough, we'll be in this phase where we can now start generating tension, but we might not have enough stimulus to get past that. So it just depends on how much calcium you have to get past that that point. And so you can see when we're in an extended phase, it's harder to generate tension. This is why if you go to pick up a book with your hand and try this out. So take your phone and try to pick it up with your h with your arm in like an L shape. Pick it, you know, pick it up and then try to pick it up out here with your arm extended. It feels heavier with your arm straight out. And that's why it's harder to generate. You have to generate more force. It's more difficult to hold it in an extended way. And so that's that length tension relationship. So our next lecture is going to be on muscle tension at the organ level. So how do we at at the big muscle itself? So now we're going gross muscle, motor units, recruiting multiple muscle fiber types. How are we going to generate enough strength to get the job done that we need? And not too much and not too little. Like how do we know what to do? And so that's what's g that's what we're going to talk about in the next lecture. I'll see you there.