Well hello there. You caught me while I was working out.

The 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 for understanding the organ system we use to do all 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 the same molecule your cells use to get all their jobs done: good old Adenosine triphosphate.

Now your muscles maybe your body's 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.

:Intro 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 most of your involuntary processes like pushing food through your digestive track 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, you know, important for chewing your hot pockets, the abductor pollicis brevis, right at the base of your thumb, a.k.a. 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 you make a ballerina out of that.

If you were to peel back my skin and take a look at one of 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 it 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-tendons 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, 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 of this 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 and 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, 'cause after all meat is just muscle. This chicken breast is, or was, the pectoralis major muscle of a chicken.

It connected the bird's sternum or breast bone to the humerus in its wing. And sometimes, I feel like some times chickens have bigger pecs than I do, it's crazy.

When you peel this muscle apart, you see that it's really made of layers of thing 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 I'm talking about starts with prefix "myo-" or "sarco-" from the Greek words for "muscle" or "flesh," respectively. When 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 myosin, which is thicker and studded with these little golf club shaped knobs 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 bottom. 

Now when the muscle cell is at rest, none of these strands are touching one another 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 its 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. 

I mentioned last week that we didn't even have even a passing understanding of the human skeleton until the 1500s, which seems kind of tardy to the party to me. But that's nothing compared to this. We didn't figure out how muscles worked until 1954. 

In 1954, two teams of researchers independently discovered 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 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 discover the muscle-contracting mystery. Until the early 1950s, 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 1950s, we've pretty much learned everything we could about muscle cells 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 length 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 Huxleys, were using another newfangled tool: the electron microsope. 

Using that, they observed that muscle fibers were composed of thick and thin filaments, the myosin and the actin, and they were arranged in such a way that the filaments 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'll remember, creates the energy needed for almost anything your body does. Yes, that goes for muscle movement as well. 

Another thing to remember is that some proteins change shape when they come into contact with certain ions. Like we've seen that with the Sodium-Potassium pump, for instance. Those pumps are proteins that can accept Sodium ions outside of 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 shape changers 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'll drag those actin strands towards 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 thing from happening. 

The first is a set of two proteins wrapped around the actin. They're called tropomyosin and troponin, and together they act as a kind of insulation... and let's just continue our middle school metaphor: they're the, uh, chaperones that protect the actin from groping. 

At this point, each little head on the myosin strand has a wreckage of a spent little ATP molecule on it. That's an ADP and a phosphate. And the energy from that broken ATP is already stored in the head. So yeah, the myosin has a lot of... pent up... frustration. 

Now, while the muscle cell is resting, it's preparing a stock pile 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, every time you create a high concentration gradient, you know it's going to get used. 

So now, we're ready for a muscle contraction to start, but what starts it? Well, stimulus, of course from a neuron. Stimulus are activated by motor neurons, and each sarcomere has a motor neuron nearby. 

When a signal travels down from the neuron to the neuron synapse with the muscle cell, it triggers the release of neurotransmitters which in turn set off another action potential inside the muscle cell.

That action potential continues along the muscle cell's 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 diffuse down the concentration gradient. 

The Calcium ions combine with one of the chaperones, the troponin, which causes the troponin to rotate around the actin and drag the myosin out of the way revealing all of those super hot binding sites on the actin. 

With our chaperones distracted, the myosin... it totally goes to town. It reaches all those little tiny heads along its length to bind up with the actin and the excitement at long awaited precious contact finally released 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're going to have to tear those two proteins apart because each myosin head is really comfortable here snuggling with its beloved actin. 

So, it'll take another passing ATP molecule to attach to the head which breaks off one of the phosphates to release its 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 diffuse 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 being hard at work pumping all the Calcium ions back inside it, storing it up for next time. That lets our chaperones come back. The troponin and the tropomyosin retake their positions around the actin strand, resets the sarcomere for the next impulse to come along. 

Chemistry makes it all possible from blasting your guns to my awesome dance moves. 

Thank you for watching this episode of Crash Course: Biology. 

If you want to go back and look at some stuff, 'cause it was a confusing episode today... Table of Contents!

And thanks to everyone who helped put this together. This one was a doozy, so thanks to our head writer, Blake de Pastino, and of course Amber as always for doing our amazing graphics. 

If you have any questions please leave them below in the comments, or get in touch with us on Facebook or Twitter. We'll endeavor to answer you as will all those extraordinarily helpful people who are not affiliated with us at all but who are quite smart and helpful. So thank you to them, and we'll see you next time.