050 Regulating Stroke Volume, Skeletal Muscle Pump and Frank-Starling Mechanism
Here, Leslie discusses how stroke volume can be regulated. Depending on which factors are changed, blood volume entering the heart may increase and in effect increasing heart contraction too. Watch, listen, and learn how this happens.
Transcript of Today’s Episode
Hello and welcome to Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 50, I’m going to talk about regulating stroke volume, the skeletal muscle pump and Frank-Starling mechanism. So, let’s get right into it.
So, we’ve been looking at stroke volume and we’ve been looking at the fact that blood enters into the heart, comes in through the atria and then, into the ventricle and then, it gets pumped out, as you can see here, to the aorta, to the rest of the body, and to the lungs, and so on.
Then, we looked at how to determine the stroke volume, and we said, if we have blood entering into the ventricle, the ventricle is being filled and then, at a certain point, the ventricle contracts shooting that blood out to go to the rest of the body and we have the EDV and the ESV, the end diastolic volume and the end systolic volume, the difference between the two, that’s this difference here, that is the stroke volume (SV).
Looking at the stroke volume, if we want to increase or decrease the stroke volume, we can do it in two ways. We can either change the end diastolic volume or the end systolic volume. I guess, you can say we can do it in three ways. We can do one of those two or we can do both of them. If we adjust those, that’s going to change what the stroke volume is.
So, the question today is, how do we change the end diastolic volume and the end systolic volume?
Now, I want to look at a number of ways to change the end diastolic volume and the end systolic volume thus changing the systolic volume. But, I’m just going to discuss a few of them so that you can kind of get the concept.
The first where we can do that is by increasing the amount of time that we have before the ventricular contraction. So, if we have more time, we have more time for the ventricles to be filled. So, here it is being filled until about 120 mL. If we increase the amount of time that we have, it might go upto a 140 mL before the ventricles can contract. Then, when the ventricles contract, you can see, we have a greater stroke volume. So, just by increasing the amount of time, that can increase the amount of blood entering into the heart which increases the end diastolic volume and we’re going to show a little later how that even decreases the end systolic volume. So, that’s the first way – by having more space between the heart beats. In other words, by having a lower heart rate.
Another way of increasing the end diastolic volume, let me just write that here, is by causing more blood to be sent back to the heart. How do we do that? Well, there are a number of mechanisms. The way I want to talk about is called the Skeletal Muscle Pump.
What that is, it’s a mechanism for increasing what we call, venous return. The difference between arteries and veins, arteries are the vessels that are going away from the heart and veins are the vessels that are returning to the heart. So, arteries take the blood to the muscles and to the organs and the tissues that need the blood and the oxygen that comes with the blood and once those nutrients and the oxygen are used by the organs and so on, the blood returns to the heart via the veins.
What I’m going to do right now is, I’m going to draw a vein. The cool thing about these veins is that in the veins, we have these valves. So, I’m going to draw these valves. The way these valves are constructed is so that, the blood can only flow in one direction. The blood can enter the veins and go in this direction with no problem. But, if you try to go back in the opposite direction, that won’t work because these valves are actually going to stop them.
Now, associated with these veins, we have skeletal muscles. So, this is some skeletal muscle here and this is, I’m just going to draw these strands to show that it’s striated and here, we have more skeletal muscles on this side (forgive my poor drawing skills). Here we have skeletal muscle on this side and skeletal muscle on this side. What this does is, it actually contracts in a way that helps to push the blood in the direction that it needs to go. This is something that happens, for example, when you’re exercising, you want more blood going back to the heart so that it can be pumped to the lungs, pick up more oxygen and then be sent back to the rest of the body.
So, when you’re working out, you’re exercising, the skeletal muscle pumps are doing their work and they’re helping to push that blood so the blood can go faster, more blood can be going to the heart. That is what we call, increasing venous return. We’re increasing the amount of blood that’s returning to the heart via the veins. There are a number of things that regulate this process. But, this is the concept. Skeletal muscle pump increases the amount of blood returning to the vein. That has to do with increasing the end diastolic volume, the EDV.
The other factor that influences stroke volume is the ESV, the end systolic volume. Let’s look at one of the ways where that is controlled.
We’ve looked at muscle contraction and we said that the functional unit of contraction is the sarcomere. This is one sarcomere here. We looked in Episode 041 at how this process happens. When muscle contraction happens, we have this that we call, myosin. This is the myosin filament. The blue here, we call actin. This is “A” for actin and this is “M” for myosin. On the myosin we have myosin heads and those myosin heads associate with the actin and they pull so that, this process can happen where we have the sliding filaments. The filaments slide against each other , the muscle contracts and then the muscle relaxes. This is the exact same process that happens in the heart. If you need a review of this process, you can go back to Episode 041 to check out those details.
Now, the way the structure of this sarcomere is set up, in order for us to have the maximum amount of contraction, we have to have optimum overlap. Here, we have the overlapping between the myosin heads and the actin. In order to get the best, the strongest contraction, we have to have maximum overlap. This is how this works. When the heart gets filled with blood, this stretches out more. So, the end of this sarcomere might be over here because there’s more blood in the heart.
That stretching of the muscle causes an increase in contraction for a number of reasons. Imagine if the end of this actin was over here. There’s an increase distance between these two points so that, it has a farther distance to travel as the sarcomere gets shorter. That’s going to cause a stronger contraction and if you have a stronger contraction, it’s going to send more blood out of the heart, leaving less blood in the heart.
In addition to this, we’ve spoken about how calcium is involved in this process. And, you can check out Episode 043 for more details on this. Calcium ions (Ca2+) are released from the sarcoplasmic reticulum. That binds to troponin which is on here, blocking the binding sites for the myosin head.
When calcium comes, that exposes the binding site so that the myosin heads can bind freely. The stretching of the heart increases the affinity of this troponin for calcium ions. If have an increased the affinity for calcium ions, you’re going to have more myosin heads being able to bind to the binding sites on the actin and that is also going to increase the contraction. This is called the Frank-Starling mechanism. It’s called that because it was named after the two guys who first described that process.
What it says is that, if the heart gets filled with more blood, that is natuarally going to cause a stronger contraction sending more blood out of the heart and increasing the stroke volume even further by decreasing the end systolic volume. We looked at how this happens. You have better overlap and you have a greater affinity for calcium which is going to cause a stronger contraction.
Once again, if you need to understand the details of how calcium is involved in this process, go back into Episode 043 where I go into those details. That’s pretty much it for this video.
As usual, I want to invite you to visit the website at Interactive-Biology.com for more Biology videos and all of the other resources we’re adding there on a regular basis so that we can help make Biology fun. That’s it for this video , and I’ll see you on the next one.