 We are not talking about action potentials. We're talking now about the actual cardiac muscle cell contraction, like the physical shortening of the cardiac muscle cell. How does that happen? We know, I'm going to write that down, cardiac muscle cell contraction. I want to draw you a picture of a cardiac muscle cell, just to remind you of what are we talking about? I'm going to start us off with an auto-rhythmic cell. This is an auto-rhythmic cardiac muscle cell. Remember, only 1% of all cardiac muscle cells are auto-rhythmic. The rest of them are contractile. But auto-rhythmic cells generate their own action potentials, and we already have the mechanism for that. We already know that the whole leaky channels, the funny channels are awesome. They change the membrane potential. They automatically and periodically generate action potentials because they change leakiness, and the action potential gets generated. And then the action potential travels through what? Remember, remember, guys, travels through the intercalated disc of the cardiac muscle tissue, and the intercalated discs, remember, are just structural things that staple cardiac muscle cells together, but they have gap junctions inside. So the action potential is generated by my friend, the auto-rhythmic cell, and it's generated automatically, but as soon as it is generated, that action potential travels down the cell membrane through the gap junction and into who? Into a contractile cell. Remember that contractile cells, they're just connected to the auto-rhythmic cells through these intercalated discs. Contractile cells, I mean, we can draw them into all sorts of things. They actually are branching cells, remember that, so we can have another one attached to something else down here. That's awesome. We're going to attach it to someone else down here, but since this is a contractile cell, we're going to visualize our, so that's just a giant intercalated disc where we actually are then attaching to another cardiac muscle cell and so on and so forth. We're going to throw in a nucleus just for the heck of it. We'll throw in a nucleus over here just for the heck of it. Here comes my action potential. It passed through, it comes down the membrane. Now, the action potential is going to do something. In fact, I'm going to undo that and have it do something right about her. Guess what? Cardiac muscle cells just like skeletal muscle cells, actually have t-tubules in them, and I'm going to have to make my t-tubule red to make sure that you know, what am I drawing here? I'm drawing a t-tubule, and I'm drawing it this way so that you know it's just like in the cardiac muscle cell how it was like this invagination of the cell membrane of the myofiber that carried the action potential down inside. It's exactly the same thing. It's a little bit wider, it's a little bit crazier, but that's okay. It carries the action potential down. So this is my t-tubule, which is similar to what you would see in the skeletal muscle. If you had to guess, what are you going to guess is going to happen when the action potential travels down the t-tubule? Are you correct that you're going to guess? That's so cool. Are you going to guess that my sarcoplasmic reticulum, which is found inside the cardiac muscle cell, the sarcoplasmic reticulum does have calcium inside, but guess what else? There are specific channels, this is a slightly different mechanism. There are channels inside the t-tubule that allow extracellular calcium to rush in through the channel. Okay, I'm going to lay this all out for you and do a play-by-play in a second. The extracellular calcium, this is different than a skeletal muscle contraction. In skeletal muscle contraction, all the calcium that we're dealing with travels from inside the sarcoplasmic reticulum. In cardiac muscle contraction, when the action potential travels down the t-tubule, the voltage-gated calcium channels let calcium in from the extracellular fluid, extracellular out here. In comes the calcium. The calcium gates in the sarcoplasmic reticulum are different. They need calcium to bind in order to let the calcium out. Did you follow that? Okay, let's do a play-by-play and see if we can figure out how this happens. And if I write it down for you, it'll make it a little bit more clear. So the very first thing that happens is my action potential generated by the otterhythmic cell travels down the cell membrane through intercalated discs into contractile cells. That's how the action potential arrives. Does the action potential get generated by the nervous system? No, no, no. It is not. It gets generated by the otterhythmic cell. The action potential travels down. It arrives in the contractile cell. The action potential then travels down the t-tubules, down the t-tubules in the contractile cell. This is step two. Do you see how I've drawn the action potential traveling down? Action potential causes voltage gated. What kind of channels? Calcium channels in the t-tubule. Open, open, open, open, and calcium comes in. It rushes in calcium from the wear, from the extracellular fluid. That's where the calcium came from and it comes rushing in. Four, whoa, that must have been three right here. They travel down. Three allowed the voltage gated t-tubules to open and the calcium rushes in. Four is going to take place over here with a new channel. This time, calcium in the intracellular fluid, now, because it rushed in, it was in the extracellular fluid, it rushed in through the t-tubules and now we've got this flood of calcium in the intracellular fluid. This calcium causes calcium channels in the sarcoplasmic reticulum to open calcium floods out. Now, think about this. You have two sources of calcium coming from the cardiac muscle cell. You have calcium entering the cell through the t-tubules and you have calcium entering the cell through the sarcoplasmic reticulum. These are two different ways that we can get the calcium in. Once the calcium is in, the calcium is going to do exactly the same thing it does in the skeletal muscle because what is the sarcoplasmic reticulum surrounding? If we were to do a little peek-a-boo and look underneath here, we would see myofibrils. Remember, myofibrils were just my overlapping filaments, thick and thin filaments in little sarcomere setup, we just have these long layers of sarcomeres and then it's just the exact same like whatever overlapping process, sliding filament theory as we saw in the skeletal muscle. The calcium binds to troponin, troponin moves tropomyosin, tropomyosin reveals the myosin binding site, myosin binding site on actin. Actin is now able to bind to myosin and once myosin and actin connect, the power stroke of myosin takes place. Holy Kamoles, then we have a shortening of our fibers. The key that is different, and let's just like put a little woof-woof out there, the key that is different is where our calcium comes from. These two steps make it different. We have a little bit of regulation for where calcium comes from. Now, who cares? Why? Why did we do that? Well, we care because the next characteristic of cardiac muscle tissue is that not every contraction is the same and that's because of where our calcium comes from. Let's go figure out more.