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Big Guns: The Muscular System – CrashCourse Biology #31

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.

100 thoughts on “Big Guns: The Muscular System – CrashCourse Biology #31

  1. You have no idea how appreciative I am of this channel. It's helped me go through A&P, Microbio, Bio l and now finally…bio ll 😂 you guys are a godsend

  2. Thank you so much for this awesome episode!!! And the result that I got was also fantastic! The first time I got 100% in my Biology assessment!!! Thanks again for crash course!!! Keep on doing it!!!

  3. I сouldn't be аnу hарpiеr with thе results. I gainеd 12 lbs of musсlе in 4 wееks . Nо Sрррeсial Diеt, No Intense Ехеrсise..

  4. Thank you so much for your videos. They are so much help! I like the way you compare processes of the body with other scenarios.

  5. "Hysterically & Entertainingly Educational!" – Rolling Stones. Just kidding, RS didn't say that… 🙂 But seriously, thank you for taking the time out to share this knowledge, brother."

  6. UCSB biology upperclassman here… currently taking upper division physiology… this video is the perfect review tool; covers just about everything 100x better than the professors can with just slides

  7. I feel that all Anatomy Courses should have tons of videos like this, but also focused at helping students pass practicals, and exams.

    Find professors who put their lectures into video presentations. That will help a ton.

  8. Hello. When I do eccentric workout moves (i.e. hold dumbbells in some position), why is it that I dont simply hold it without pain and suffer? Actin wants to stay with myosin so I dont get it. Thanks in advance

  9. I really enjoy using a crash course in my high school classes, however, I was extremely disappointed with this one. In the future, please avoid sexual references. The references made in this video are not appropriate for young teenagers in the classroom.

  10. I hope you eventually switched arms and performed the same amount of reps to prevent asymmetries lol

  11. Hank thank you hope to meet you in person someday. I learned a lot from all your videos but, I still didn't pass my Anatomy & Physiology test. lol.

  12. I never understand the bits where he talks about ATP and ADP
    Please can someone explain like im 5 aha. 😭😭😭
    Anywaysss GREAT VIDEEOOOOO!!!!

  13. If your muscles contracting is the relaxed form, why does it take more effort and energy to kove around than to sit and do practically nothing?

  14. Can't believe we knew about general relativity and quantum mechanics before we knew how our muscles worked

  15. pleasseeee never grope yourself in the arse on youtube… unless of coure, you're a cute japanese girl lol

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