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.