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Blonde Man: Well, hello there. You caught me while I was working out. Last time I was lifting weights during a Crash Course episode, also the last time I was lifting weights we were talking about how all of this is possible because of cellular respiration. The process our cells use to get and store energy from the food that we eat. Remember that? Good times. As it happens, a lot of what we learned then is also really helpful in understanding the organ system that we use to do our gun blasting and walking and fork and knife operating and parkour and playing Assassin's Creed and you know, like moving around. I'm talking about your muscles, of course, and you wouldn't be able to move them without the help of that same molecule that your cells use to get all their jobs done. Good old adenosine triphosphate. Now, your muscles may be your bodies most obvious moving parts, but as with all things that are truly worth learning about, this system is both way more complex and way more awesome than it first appears. Yeah! Why? Because of chemistry. (music) When you think of muscles your mind usually goes straight to the guns there, but you really have three different types of muscle in your body. You have the cardiac muscle, your heart muscle, which is different from all the sorts of muscle in your body and then you have the smooth muscle, which is responsible for carrying out most of your involuntary processes, like pushing food through your digestive tract and pushing blood through your arteries important stuff there. And then there's the muscles that you're most familiar with, the skeletal muscles. Your gluteus maximus, your masseter, which is important for chewing your hot pockets. The abductor pollicis brevis, right at the base of your thumb, AKA your video game muscles. That's important for the Assassin's Creed. Just some of the 640 skeletal muscles you have. Those muscles, like all of your muscles, are only good at two things. Contracting, to become shorter and relaxing back out to their resting length. That's all muscles do. They contract and they relax. It's pretty amazing that you could make a ballerina out of that. If you were to peel back my skin and take a look at one of my muscles, please don't do that, but if you did, you'd see that it thickens in the middle at what's called the muscle belly and that tapers off on either end into a tendon. Tendons are made of fibrous proteins, mostly collagen that connect the muscle to the bone. Just a side note, ligaments, similar to tendons, but instead they connect bones to other bones. These muscle tendon combos stretch across one or more joints. In this case it stretches across my elbow, so that one bone can move in relation to the other bone. So, I just moved my arm and now I'm moving my mouth and I'm basically moving my whole body right now and the question is, how am I doing this? How am I moving all of these things in all these, sort of, amazing fluid ways? How am I able to do that at all? Unfortunately, it's kind of complicated, but it's wonderful and amazing, so it will be worth it in the end. First, we need to understand the anatomy of a skeletal muscle, which includes many, many layers of long, thin strands. Think of one of your skeletal muscles as a rope. It's made of smaller ropes that are bundled together and then those ropes are made of bundles of thread and those threads are made of tiny, tiny filaments. This structure is what makes meat stringy because after all, meat is just muscle. This chicken breast is or was the pectoralis major muscle of a chicken. It connected the birds sternum, or the breast bone, to the humerus in it's wing and sometimes I feel like chicken's have bigger pecs than I do. It's crazy. When you peel this muscle apart, you see that it's really made up of layers of thin strings. These are muscle fascicles and each fascicle is made up of lots and lots of smaller strands. These we can't see. They're called muscle fibers and these are the actual muscle cells. Now because muscle cells perform such a specialized job, they're not like your run of the mill somatic cells. For starters, they each have multiple nuclei. That's because each muscle cell is actually formed by a bunch of cells somewhat like stem cells called progenitor cells fusing together. Muscle cells are basically just bundles of complex protein strands and since nuclei are essential for the protein making process, muscle cells need lots of nuclei to make all the protein they need. From here on you'll notice by the way, that a lot of the stuff that I'm talking about starts with the prefix myo or sarco, from the Greek words for muscle or flesh respectively. Whenever you see those terms in biology you know you're probably in muscle country. For instance, those protein strands that I just mentioned that make up a muscle cell are called myofibrils and each one is divided lengthwise into segments called sarcomeres. This is where the action happens my friends because it's the sarcomere that will actually do the contracting and relaxing to create the muscle movement. Each muscle cell has tens of thousands of these guys and they all contract together to make you do stuff. And this contracting and relaxing occurs through this really cool and complex interaction between two different kinds of protein strands called myofilaments. One myofilament is the protein actin, which are skinny strands that attach to either one of the two ends of the sarcomere and the other is the myosin, which is thicker and studded with these little golf club shaped nobs along it called heads. Inside a sarcomere these proteins occur in layers with a thick strand of myosin floating between several strands of actin. Just how many strands of actin depends on the muscle we're talking about. In this case, let's just say that there are four. Two sitting on top and two sitting on the bottom. Now, when the muscle cell is at rest none of these strands are touching each other, but they really desperately want to. They're like middle school students at a formal dance. The myosin, in particular, wants nothing more than to reach it's little heads up and do some heavy petting with the actin. The chemical dance that allows this to happen is one of the sexiest things that goes on in your body other than, like, sex. And it's known as the sliding filament model of muscle contraction, which reminds me of an interesting story. (music) I mentioned last week that we didn't really have even a passing understanding of the human skeleton until the 1500's, which seems kind of tarded to the party to me, but that's nothing compared with this. We didn't figure out how muscles worked until 1954. In 1954, two teams of researchers independently discovered that the sliding filament model is how muscles contract and as luck would have it, two of the four scientists who made this discovery were named Huxley. We've already discussed Thomas Henry Huxley, the father of comparative anatomy and Darwin's bulldog. Well, his grandkids were all awesome at something too, like Aldous Huxley, who wrote the novel 'Brave New World' Julian Huxley, who was central to the development of modern evolutionary theory and Andrew Fielding Huxley. Andrew Huxley was a physiologist, who with colleague Rolf Niedergerke set out to solve the muscle contracting mystery until the early 1950's, all we knew was that myofibrils were full of protein strands. At that time, most people thought that these strands simply changed shape and shortened like how a spring recoils after it's been stretched out. And by the 1950's, we'd learned pretty much everything we could about muscle cells by using conventional microscopes. So, Huxley and Niedergerke actually designed and built a new microscope. A tricked out kind of interference microscope, which uses two separate beams of light and with that they found that during contractions, some protein strands kept their lengths the same, while others around them contracted, but at the very same time, British biophysicist Jean Hanson and Hugh Esmor Huxley an American biologist who had no relation to the famous British Huxley's were using another new fangled tool, the electron microscope. Using that, they observed that muscle fiber was composed of thick and thin filaments, the myosin and the actin and that the filaments were arranged in such a way that they could slide across each other to shorten the sarcomere. So, in two separate papers published the same day, in the same journal, two teams proposed that muscle contractions were caused by the movement of one protein over another. I guess, an idea whose time had come. Except it's not that simple. To understand how the sliding filament model works, the first thing to keep in mind is that in addition to needing a bunch of protein, muscle cells need to make lots of ATP. ATP, you remember, creates the energy for almost everything your body does. Yes, that goes for muscle movement as well. Another thing to remember is that some proteins can change shape when they come into contact with certain ions. Like we've seen that with sodium potassium pumps, for instance, those pumps are proteins that can accept sodium ions outside a cell and then they change shape to release them inside a cell and also, suddenly, at the same time they become able to accept potassium ions. These shapes changes are how cells get a lot of the day-to-day job of living done. In a sarcomere it's calcium ions that change the shape of some of the proteins, so that the myosin can finally have its way and grope the actin strands all around it. Then it will drag those actin strands toward each other, causing the sarcomere to contract. But when a muscle cell is at rest there are a couple of things that keep this groping from happening. The first is a set of two proteins wrapped around the actin. They're called tropomyosin and toponin and together they act as a kind of insulation. Let's just continue our middle school metaphor, they're the chaperones. They protect the actin from groping. At this point, each little head on the myosin strand has the wreckage of a spent ATP molecule stuck to it. That's ADP and a phosphate and the energy from that broken ATP is already stored inside the head. So yeah, the myosin has a lot of pent up frustration. Now, while the muscle cell is resting it's preparing a stockpile of calcium ions that it will use as a trigger when it's go-time. This is done by a specialized version of the smooth endoplasmic reticulum called the sarcoplasmic reticulum or SR. It's wrapped around each sarcomere and it's studded with calcium pumps. These pumps are constantly burning up ATP to create a high concentration of calcium inside the SR and, of course, whenever you create a concentration gradient, you know it's gonna get used. So now, we're ready for a muscle contraction to start, but what starts it? Well, stimulus, of course, from a neuron. Muscles are activated by motor neurons and each sarcomere has a motor neuron nearby. When a signal travels down the neuron to the neuron synapse with a muscle cell, it triggers a release of neurotransmitters, which in turn set off another action potential inside the muscle cell. That action potential continues along the muscle cells membrane and then flows inside it along special folds in the membrane called T-tubules. When that signal reaches the SR inside the cell, BINGO! The SR's channels open wide and let all those calcium ions defuse down that concentration gradient. The calcium ions bind with one of the chaperones, the troponin, which causes the troponin to rotate around the actin and drag the tropomyocin out of the way, revealing all of those super hot binding sights on the actin. With our chaperones distracted, the myosin, it totally goes to town. It reaches all of those little tiny heads along it's length to bind up with the actin and the excitement of that long-awaited, precious contact finally releases the energy that came from breaking that ATP molecule. This burst of energy causes the heads to suddenly bend toward the center of the sarcomere, pulling the actin strands together and shrinking the sarcomere. In millions of sarcomeres, in hundreds of thousands of muscle cells, this is what allows me to like, lift my arms. You wouldn't think it would be so complicated. Now, in order for the contraction to stop you gonna have to tear those two proteins apart because each myocin head is really comfortable here snuggling with it's beloved actin, so it will take another passing ATP molecule to attach to the head, which breaks off one of the phosphates to release it's energy as soon as they touch. That energy breaks the myosin's bond with the actin and lowers the head, leaving it alone and frustrated once more. So, it's weird that the energy from the ATP is actually used to make the muscle relax, but in fact, that's why we get rigor mortis. When you're dead, there's no more ATP to make the muscle relax and all the calcium ions defuse out of the sarcoplasmic reticulum causing the muscles to enter their resting state, which is contracted, but you're not dead yet, so let's wrap this up. When the myosin and actin are being separated the sarcoplasmic reticulum is hard at work pumping all of the calcium ions back inside it and storing them up for next time. That let's our chaperones come back, the toponin and the tropomyosin retake their positions around the actin strands, resets the sarcomere for the next impulse to come along. Chemistry makes it all possible from blasting your guns to my awesome dance moves.