047 Action Potentials and Contraction in Cardiac Muscle Cells
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Transcript of Today’s Episode
Hello and welcome to another episode of Interactive-Biology TV where were making Biology fun. My name is Leslie Samuel and in this episode, Episode 47, I’m going to be talking about action potentials and contraction in cardiac muscle cells. So, let’s get right into it.
I’m looking at the heart. We’ve looked at a number of things related to the heart. In the previous episode, we spoke about the SA node, which is what we see here, number one and, we spoke about the AV node, which is this part here, number two, and we spoke about these Purkinje fibers. I’m just going to write PF for now. So, this is the AV node, the SA node and the Purkinje fibers. You can go back to the previous episode to learn more about those, in case you’re not sure what they do; in case you’re not sure how they function.
There are a number of things that I want you to know here. We said that the SA node functions as the pacemaker. There’s an important feature about the heart muscle cells that you need to be aware of. That is the fact that these cells are all electrically connected. So, all of the muscle cells in the ventricle are electrically connected, all of the muscle cells in the atria are also electrically connected.
What that means is that if one of the cells in the ventricle gets stimulated, that signal is going to travel to all of the other cells in the ventricle. Not only that, but, if the SA node starts a signal, that signal is going to spread. This is why we get the heart contracting in response to the signal that’s generated by the SA node. Then, when it reaches the AV node and it spreads via the Purkinje fibers, that signal spreads to all of the muscle cells in the ventricles, causing the ventricles to contract.
There are some other important details that you need to know. When the signal is generated in the SA node and it spreads to the atria, the conduction velocity is one meter per second (1 m/s). So, the signal spreads at a speed of 1 m/s here. At the AV node, it slows down to where it’s somewhere around 0.04m/s. Then, in the Purkinje fibers, it speeds up significantly, and we get a conduction velocity of 5 m/s.
So, what this means is that we have a signal that starts here and spreads throughout the atria relatively quickly at 1 m/s but then, it slows down at the atrioventricular node to 0.04 m/s. So, there’s a delay here, and then, after it passes the atrioventricular node, that signal spreads rapidly to the ventricles. Now, why do we want this? As we mentioned before, the blood first goes to the atria and then, the atria contracts, sending the blood from the atria to the ventricles.
You don’t want the atria and the ventricles contracting at the same time. That would cause problems. You want the ventricles to get filled with the blood from the atria first and then, you want the ventricles to contract sending all that blood to the rest of the body and to the lungs. So, that’s how that works and that is why it’s good that we have this slowing down at the atrioventricular node.
We have a stimulus that comes from the AV node or the SA node and that spreads to the muscle cells. In response to that, what’s going to happen is that the membrane potential of the cardiac muscle cells is all of a sudden going to depolarize very quickly. So, we have that initial depolarization. When the muscle cells depolarize, as with skeletal muscles, we’re going to have calcium being released from the sarcoplasmic reticulum. For a refresher of how that works, you can go back to Episode 42 where I talked about calcium release and how that causes muscle contraction.
Once the calcium is released from the sarcoplasmic reticulum, that’s going to prevent the repolarization that normally happens rather quickly. With a normal neuron, the action potential lasts less than a millisecond. However, in cardiac muscle cells, we have calcium that’s being released that slows down the repolarization process and we get a phase that’s referred to as the ‘plateau.’ The membrane potential does not repolarize as quickly. Then, at a certain point, calcium gets pumped back into the sarcoplasmic reticulum, potassium also leaves as usual, and we get the repolarization of the cardiac muscle cells.
As you can see, the time scale that we have here shows that this action potential can last as much as 300 milliseconds as opposed to the one millisecond or less than one millisecond that we get with a neuron. That’s because of the calcium released. That’s because of this plateau phase.
Let’s see what that does for muscle contraction. Yes, we’re going to have a depolarization but then, we’re going to have the calcium released and that is going to cause the muscle cells to contract just like I showed in Episode 42. Once again, you can always go back at Episode 42 to revisit that concept.
This is what we’re going to do. I’m going to plot the tension in the cardiac muscle cells. So, we’re looking at the cardiac muscle and here, nothing is happening. But, as soon as calcium starts being released, that’s going to cause the muscle cells to contract. This is what’s going to happen. This is the tension and then, once calcium starts being pumped back into the sarcoplasmic reticulum, the muscle cell is going to relax and go back to its resting state.
So, we have the action potential lasting significantly longer than we’ve seen before, because of the calcium that’s released from the sarcoplasmic reticulum and that calcium then causes the muscle cells to contract and we get this tension in the muscle cells.
That’s all I’m going to cover in this video. As usual, you can head back to the website at Interactive-Biology.com for more Biology videos and for more resources that we’re adding there on a regular basis. So, stay tuned. This is Leslie Samuel. That’s it for this video and I’ll see you on the next one.