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- [Voiceover] Now that
calcium that was released

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from the sargoplasmic reticulum,

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well, it's gonna start what's
called a sliding filament.

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The myosin and actin are
gonna slide past each other.

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Thick filaments of myosin
and thin filaments of actin

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are gonna slide past,
causing a contraction.

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A contraction in the muscular sense

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is when the thick filaments, myosin,

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and the thin filaments,
actin, bind together.

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They form what's called a cross-bridge.

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The cross bridge will momentarily
link the two filaments

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until they're being
pulled past each other.

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So up in Figure A,

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you can notice that nothing
is really attached there.

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The thick filaments and thin
filaments aren't attaching.

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But in the presence of calcium,

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go down to Figure B.

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The thick filaments
myosin can actually attach

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to the thin filaments actin.

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This myosin head can
reach out and latch on.

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But it doesn't just latch on,

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it'll start to pull it inward,

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pulling the actin, or thin filaments,

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towards the center of the sarcomere.

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By pulling it towards the center,

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it's becoming shorter.

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So remember, calcium comes from that

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sarcoplasmic reticulum.

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It binds to a structure called troponin.

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Now this troponin is also
attached to something

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called tropomyosin.

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The whole thing just gets
pulled out of the way.

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Calcium actually triggers this movement.

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A myosin binds so it's exposed,

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which means it's time for
the myosin to bind to actin.

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Cross-bridges are formed.

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So the role of calcium
here is to bind troponin.

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Troponin pulls tropomyosin out of the way,

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that allows myosin to bind.

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When myosin binds to actin,

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it forms a cross-bridge.

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The actin filaments are then
pulled towards the center

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of a sarcomere.

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As they're pulled towards a center

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that's shortening the sarcomere.

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If you have dozens of sarcomeres in a row,

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each one being a little bit shorter,

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it all adds up to the
entire muscle movement.

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So what we're looking at here again,

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muscle cell up top,

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can see the thick and thin
filaments in the middle,

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and the bottom.

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The gray are the actin filaments,

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the brown are the myosin.

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But you notice the green.

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The green kind of almost looks like

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life-saving preservers,

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have that little indent,

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perfect for calcium.

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Once calcium binds,

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that causes troponin

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and tropomyosin to move.

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Once it moves, it opens
up the binding sites.

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Myosin actin can now bind.

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The cross-bridges are formed.

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And once those cross-bridges are formed,

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now you can finally
start to move the muscle.

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Now what's really
amazing is all this stuff

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we just talked about,

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from that electrical impulse coming down,

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to when these cross-bridges form

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and start to move the muscle,

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that takes a whopping four milliseconds.

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Man, that's faster than
snapping your fingers.

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Just goes to show how fast and how quickly

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all these can occur.

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You've had signal coming down
from your brain to your muscle

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and it's practically instantaneous.

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OK, traveling at hundreds
of miles per hour.

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So all of this is very quick,

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and very precise.

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Now how do you relax?

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Well, not a trick question.

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I mean how do you relax your muscles?

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You can't just simply say "Muscles relax."

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Doesn't quite work that way.

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What you have to do is
stop any nervous impulse.

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Stop the nerve.

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If the nerve is not sending any signals,

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the contraction ends.

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Once it ends, calcium
is pumped back into that

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sarcoplasmic reticulum.

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It's pulled back in.

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Well, if it's pulled back in,

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that means it's not bound troponin.

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So if the calcium's moved from troponin,

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is there any reason for troponin
to have a different shape?

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No, so it moves back over to
cover the myosin binding sites.

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Once that occurs, are the
myosin heads binding anymore?

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No, so no calcium, no cross-bridge.

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No cross-bridge, no muscular contraction.

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But all this movement requires energy.

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In the case of humans,

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we're talking ATP, adenosine triphosphate.

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That's where your cells
obtain their energy from.

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ATP is an energy molecule
that your body produces.

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You can take carbohydrates
or proteins or lipids,

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and convert them into ATP.

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You need ATP for contraction,

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the muscle can't move without it.

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You need ATP for relaxation:

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again, the muscle can't move without it.

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It can't contract, it can't relax.

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So now here's a question.

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I'm willing to bet everyone's
probably seen road kill

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at some point on the side of the road.

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Now, a lot of times with road kill,

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you have the legs sticking straight out,

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they're rock-solid.

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Well, when they're that stiff,

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why aren't they moving?

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Why don't they just
sag down to the ground?

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It's because of this ATP.

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Rigor mortis is caused
by a lack of energy.

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A dead organism cannot create ATP,

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therefore the muscles cannot relax.

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So the whole idea of rigor mortis

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is based on this principle
of muscles needing ATP.

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Now you can replenish this
ATP, you can make more of it.

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You can use creatine phosphates,

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I've heard creatine
maybe with working out.

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You've have this stored glycogen.

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Glycogen is just a whole
big chain of glucose,

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a lot of carbohydrates.

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You can use aerobic metabolism.

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Now metabolism is just
basically chemical reactions

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in your body.

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Aerobic means you have oxygen.

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So you can take glucose,
you can take fatty acids,

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anything else that really is high-energy.

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You can take these high energy molecules,

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run them through this aerobic process,

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and create energy out of it.

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You can create ATP.

