Muscles, Part 1 – Muscle Cells: Crash Course A&P #21

Romeo and Juliet. Helen and Paris. Tristan
and Isolde. These famous star-crossed lovers bring to
mind insatiable longing, forbidden love, and tragic separation. And poets and emo rockers
love them for it. But you know where else you can find a nice
hot romance? Your muscle cells. They’ve got their own famous coupling — a pretty
pair of tiny protein strands called actin and myosin. Romeo and Juliet may have set a chain of tragic
events into motion with their infatuation, but deep down in the cells of your muscles,
the hot protein action between actin and myosin is actually, literally causing all of
your motions. ALL of them. And I don’t just mean voluntary stuff, like
walking down the street, or moving your mouth so you can talk or chew chips. Because your muscles
also support your weight and help fend off gravity. The amazing thing about your complicated,
self-healing, blood-guzzling muscle tissues is that they turn chemical potential energy
into mechanical energy, or movement, simply by doing two things — contracting and relaxing. And that contracting and relaxing is exactly
what’s fueled by the constant coupling and separation of biology’s greatest lovers. Somebody get these proteins a movie contract. You will recall from our early lessons on
tissues that you’re kept alive and moving by three types of muscle tissue: smooth, cardiac,
and skeletal. Your smooth muscle tissue is found in the
walls of all your hollow visceral organs, like your stomach, and airways, and blood
vessels, where it involuntarily and very usefully pushes fluid and other material around by
contracting and relaxing, over and over. Your heart is so important that it gets its
very own muscle tissue type — cardiac muscle, which looks striped, or striated, and also
functions involuntarily to keep your blood pumping without you having to think about
it. But when you hear the word “muscle,” you
probably think of the kind you see on Chris Evans when he first walks out of that machine
in Captain America. And those types — the ones you can see and
feel and flex — are your 640 skeletal muscles. They’re striated like cardiac muscle tissue,
but they’re also mostly voluntary, meaning you have to think about using them and activate
them with your somatic nervous system. Most of them attach to your skeleton, and create movement by
pulling bones in different directions as they contract. Each one of your different skeletal muscles
— like your biceps brachii, or vastus lateralis or gluteus maximus — is technically its own
organ, made up mostly of muscle tissue, but also of connective tissue, blood vessels,
and nerve fibers. And because your muscles are voracious energy
hogs, each one is rigged up with its own personal nerve to stimulate contraction, and its own
artery and vein to keep it well-fed with all the blood, and oxygen, and nutrients it needs
to operate. But to understand those operations, we first
need to get a grip on the anatomy of a skeletal muscle, which involves fibers within fibers,
and lots of layers. Basically, a skeletal muscle is constructed
like a really sturdy piece of rope. Thousands of tiny, parallel threads called
myofibrils squish together to form muscle fibers, which are your actual muscle cells
— cells with mitochondria, multiple nuclei, and a cellular membrane called a sarcolemma. Those muscle fibers then form larger, string-like
bundles called fascicles, which combine to form the larger rope-like muscle organ, like
your biceps brachii. Overall, this bundles-of-bundles configuration
makes muscle tissue fairly sturdy. But considering how much abuse your muscles take when you
do something like pretty simple, like lift a big bag of dog food, it’s no surprise
they need a little help. That’s why every muscle contains a few different
kinds of supportive sheaths of connective tissue — the protective reinforcements to
keep that bulging muscle from bursting. So that is the structure part of the story. But if you want to get into the nitty-gritty
— the down-and-dirty — of how you actually move, well, there are rules. Really, just two main rules, and they have
to do with proteins. And they’re both true for a lot of the proteins
we talk about, whether they’re enzymes or ion channels or receptors or muscle proteins. And these rules are: One. Proteins like to change shape when stuff
binds to them. And two. Changing shapes can allow proteins to bind — or unbind — with
other stuff. So keep those rules in mind, while we see
how a muscle fiber contracts and relaxes. Now, remember those tiny myofibrils that bundle
up to form your muscle fibers? They’re divided lengthwise into segments
called sarcomeres, which contain two even tinier strands of protein — two different
kinds of myofilaments called actin and myosin. And it’s their angsty story of star-crossed love that fuels
every movement your body could possibly dream up. A sarcomere contains both thin filaments,
made up mostly of two light and twisty actin strands, and thick filaments, composed of
thicker, lumpy-looking myosin strands. Each sarcomere is separated by what’s known
as a Z line at either end, which is just a border formed by alternating thin filaments
in a kind of zig zag pattern. A muscle contracting is all about sarcomeres
contracting, bringing those Z-lines closer together. All right, so now comes the romance. When your muscle cells are at rest, your actin & myosin
strands don’t touch, but they really, really want to. Specifically, that club-headed myosin wants
to get all up-close-and-personal with the actin. When this happens — and it will, eventually — it’s called
the sliding filament model of muscle contraction. But in the meantime, like in any good love
story, the pair have some obstacles to overcome. Namely, actin is blocked by a couple of protein
bodyguards — called tropomyosin and troponin — which keep getting in the way. Luckily, these guards can be bought off
with a little ATP and some calcium. I prefer cash and nachos, but whatever. Remember, ATP is kind of like molecular currency.
It contains chemical energy, and your muscles are all about converting chemical energy to
motion, so they’re always hungry for more ATP. Your muscle cells have lots of nuclei, but
some of them also have a lot of mitochondria, whose sole purpose in life is to crank out
ATP. And muscle cells also have their own version
of an endoplasmic reticulum — the cell’s transport and storage system — but in this
case it’s specialized, so it gets a special name: the sarcoplasmic reticulum. Its walls are loaded with calcium pumps — which
use ATP to save up a bunch of calcium ions. And it’s also studded with calcium channels
that are linked to voltage-sensitive proteins in the membrane of the muscle cell. Say I want to move my arm. My brain sends an action potential along the motor
neuron until it synapses with a muscle cell in my arm. The receptors on that muscle cell are ligand-gated
sodium channels, so when the motor neuron releases our old friend acetylcholine into
the synapse, the channels open up, and create a rush of sodium into the cell as a graded
potential, which, if it’s strong enough, causes nearby voltage-gated sodium channels
to open. Now, I want to take a second and point out
here that we’re still talking about an action potential, but not in a neuron. This is happening
in a muscle cell, people. So that action potential zips along a muscle
cell’s membrane, the sarcolemma, which has lots of tubes that run deep inside the cell,
called T-Tubules. When the action potential travels down one
of those tubes, it eventually triggers the voltage-sensitive proteins that are linked to those
calcium channels on the cell’s sarcoplasmic reticulum. When those channels are thrown open, the calcium
stored inside rushes into the rest of the cell, and finally myosin is like, YES! Here
we go! At this point, the myosin is totally stoked,
because the bodyguards that have been frustrating it are in for a big, irresistible distraction. That’s because the protein troponin just
loves to bind with calcium, and remember: When stuff binds to proteins, the proteins
change shape. So the calcium latches on to the troponin
and causes it to pull the other bodyguard protein — the tropomyosin — away from the
sites on the actin strands that the myosin really wants to get its paws on. And suddenly it’s all, “Okay?” “Okay.” But the only myosin heads that can bind to those newly
exposed sites are ones that are ready for action. That is, the ones that have already grabbed
a molecule of ATP that’s been floating around, and broken it down into ADP and the leftover
phosphate. When a myosin head does that, it moves into
an extended position, kinda like a stretched spring — still holding on to the ADP and
phosphate, and still storing the energy that was released when they were broken apart. So after all that, with the myosin primed
for action and the bodyguards out of the way, the myosin finally binds to actin, and it
is beautiful. When they bind, the myosin releases all that
stored energy, and — in the excitement of it all — the myosin changes shape. It pulls
on its precious actin strand, kind of like pulling a rope hand over fist. In the process, it shrinks the whole sarcomere,
and contracts the muscle. That’s the sliding part of the sliding filament
model. Now, with its energy spent, that little head
has no use for the ADP and the phosphate. So they un-bind with it, because — remember
Rule Number Two, changing shape encourages proteins to bind or unbind with stuff. That
unbinding causes a small change in its shape, which lets a fresh ATP binds there in its
place. That binding causes another shape change.
But this time, it causes the myosin to release from the actin, in a tear-jerking scene like some
microscopic re-creation of the finale from Titanic. But fear not! This epic is not quite over! Because this is when the myosin breaks down
its new molecule of ATP into ADP and a phosphate, which moves it into the armed position yet
again, getting it ready for its next rendezvous. And meanwhile, those calcium pumps are working
hard to restock the calcium in the sarcoplasmic reticulum. So they start grabbing the calcium that’s
floating around, causing calcium to unbind from the troponin. When it unbinds, the resulting shape-change
puts the tropomyosin bodyguards back into place. It’s a circle. Or potentially a big Hollywood franchise.
With lots and lots of sequels. It keeps repeating itself many, many times
every moment, while I sit here and talk, and while you sit there and eat and text and take notes,
the whole drama replaying itself over and over. Kind of like you’ll have to play this video
over and over again to get all the little steps of the sliding filament model straightened
out. But hey, some stories get better the more
you hear them. If you do watch this one again, you will re-learn
that your smooth, cardiac, and skeletal muscles create movement by contracting and releasing
in a process called the sliding filament model. You’d also re-learn that your skeletal muscles
are constructed like a rope made of bundles of protein fibers, and that the smallest strands
are your actin and myosin myofilaments. Its their use of calcium and ATP that causes the
binding and unbinding that makes sarcomeres contract and relax. Special thanks to our Headmaster of Learning
Thomas Frank for his support of Crash Course and free education. And thank you to all of
our Patreon patrons who help make Crash Course possible through their monthly contributions.
If you like Crash Course and want to help us keep making great new videos like this
one, you can check out Crash Course is filmed in the Doctor Cheryl
C. Kinney Crash Course Studio. This episode was written by Kathleen Yale, edited by Blake
de Pastino, and our consultant, is Dr. Brandon Jackson. Our director is Nicholas Jenkins,
the editor and script supervisor is Nicole Sweeney, our sound designer is Michael Aranda,
and the graphics team is Thought Café.