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  • 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 the same molecule that your cells use to get all their jobs done.

  • Good old adenosine triphosphate.

  • Now, your muscles may be 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.

  • 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 other

  • sorts of muscle in your body.

  • And then you have 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.

  • And your 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 can 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 then 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 are 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 of these 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 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 bird's sternum or breastbone to the humerus

  • in its wing, and sometimes I feel like chickens have

  • bigger pecs than I do.

  • This is 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 much 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 start with the prefixes myo- and 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 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 the 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

  • 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 really 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 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 the time, most people thought that these strands

  • simply changed shape and shortened,

  • like how a spring recoils after its been stretched out.

  • And by the '50s, 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 an interference microscope,

  • which uses two separate beams of light.

  • And with that, they found that during contraction,

  • 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 Huxleys,

  • were using another new-fangled tool, the electron microscope.

  • Using that, they observed that muscle fiber

  • was composed of those 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,

  • the 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 the 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 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 toward each other,

  • causing the sarcomere to contract.

  • But when the 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 troponin,

  • and together they act as a kind of insulation.

  • Let's just continue our middle school metaphor.

  • They're the chaperones that 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 an 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.

  • 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's synapse

  • with the 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 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 the calcium ions

  • diffuse down that concentration gradient.

  • The calcium ions bind with one of the chaperones to the troponin

  • which causes the troponin to rotate around the actin

  • and drag the tropomyosin 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 of those little tiny heads along its 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're gonna have to tear those two proteins apart.

  • Because each myosin head is really comfortable here,

  • snuggling with its beloved actin.

  • 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 enter their resting state...which is contracted.

  • But, you're not dead yet, so let's wrap this up.

  • While 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 lets our chaperones come back,

  • the troponin and tropomyosin retake their positions

  • around the actin strands, and 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,

  • because 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 down below

  • in the comments, or get in touch with us on Facebook or Twitter.

  • We will endeavor to answer you, as will all of those

  • extraordinarily helpful people who are not affiliated with us at all,

  • but are quite smart and helpful.

  • So thank you to them.

  • And we'll see you next time.

Well hello there!

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ビッグガン:筋肉系 - クラッシュコース生物学 #31 (Big Guns: The Muscular System - CrashCourse Biology #31)

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    Chi-feng Liu に公開 2021 年 01 月 14 日
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