Hey everyone and welcome back to Cooking with Corporis, today we’re doing a delicious
dissection, picking apart a poultry pectoralis.
This is a meat only dish so you'll get to piss off your vegan friends and
learn some anatomy. The best use of a Wednesday afternoon I can think of.
Start by putting your specimen in the pot, submerging it in about an inch of water, bring
that bad boy to a boil, then back off for about 15 minutes (plenty of time to subscribe
to Corporis).
Take your specimen out and onto the cutting board.
We’ll cut up some workable cross sections for now.
After letting them cool, you can use your fingers to shred the chicken — and this
is the point of our dissection.
This chicken, as well as pork, beef, and most animals can shred into strands.
Those strands are bundles of muscle fibers.
Its muscles and ours contract thanks to something called the sliding filament model.
Each of those muscle fibers are built of tiny pieces called sarcomeres — sarco for flesh,
mere for part, literally, part of the flesh.
Each sarcomere has parallel, overlapping proteins called filaments that slide past each other
when contracting or relaxing a muscle.
How they slide is a bit more complex, but for now, picture muscle contraction as these
filaments sliding back and forth.
Before we learn how it works, we need to tackle sarcomere anatomy, because it seems overwhelming
at first.
When you’re learning this topic, you’ll probably see a picture like this.
Something along the lines of a macro muscle, then a bundle of muscle fibers
fibers, here's an individual muscle fiber, and then a little myofibril hanging off.
And that’s fine, but to put things in perspective, each of these muscle fibers is only 30
to 100 micrometers wide, which is thinner than a lot of human hair.
And each of these tiny myofibrils is about 1 to 3 micrometers wide
and then each of the sarcomeres, a further division of that
is only 2.2 micrometers long.
Within the sarcomere, we’ve got a bunch of different structures that all line up something
like this.
We can have thousands of these in each muscle cell, but to make things easier on ourselves,
we’ll focus on one section of one sarcomere.
The filaments in the sliding filament model are actin and myosin.
Both of which are long proteins that have some different pieces.
Sometimes actin is called the thin filament and myosin the thick filament.
I remember these because if you look at the sarcomere sideways, you can kinda see an M
in the Myosin strand, so the other one must be Actin.
At the end of each sarcomere is the Z line, or Z disk, whatever you want to call it.
This is formally the border of each sarcomere — and since it’s the Z line, it’s easy
to remember.
Z is the end of the alphabet, and it makes up the end of each sarcomere.
We also have Titin, a massive, spring like protein which goes all the way from the Z
disc to the midpoint of the sarcomere called the M line.
Titin acts like a spring that helps our muscles bounce back into shape after overstretching
them and helps stabilize the myosin filament.
To help regulate actin, we have Nebulin, which gives some structure for the actin filament
to attach to.
This structure lines up with three distinct zones that show up that
scientists see when they look at
sarcomeres under a microscope.
The I zone which extends from myosin to myosin across two different sarcomeres so it only
has actin, the A band which runs the length of the myosin filament but overlaps on some
actin, and the H zone which spans the middle of a sarcomere so it only has myosin.
Now, that can get kind of confusing, so I want you to remember artificial intelligence
and HAM.
There's mostly Actin in the I zone, while the H zone and A band are mostly Myosin, so I remember
this as an AI eating HAM.
Heads up, I made the art from this section into desktop wallpapers that you can download
and study if that’s your jam.
The link is down in the description.
Quick recap, these filaments have to slide past each other in order for muscle to contract.
Because we’re focusing on skeletal muscle, and since we contract skeletal muscle voluntarily,
we have to get a signal from our brain to our muscles to start that contraction.
And after that signal is received a bunch of things change within the sarcomere that get it to
shorten.
When we zoom in, we see that our actin and myosin filaments aren’t straight lines,
but instead have complex 3D shapes.
When you contract your muscle, myosin attaches itself to actin forming something called a
cross bridge.
It’s not a straight bridge, it doesn’t take the shortest route from point A to point
B, it crosses kind of diagonally so it can fling the filament forward.
That grab and pull is called a power stroke.
It’s okay to giggle, it’s a silly name.
This part needs two cofactors to happen: ATP and calcium.
For clarity, this next part is sometimes taught as a list of steps, and it's totally fine to learn
it like that, but I’ve found that understanding /why/ each cofactor is important is more useful
than just memorizing the list.
ATP matters because it provides energy for the contraction.
Before contraction, myosin is actually attached to actin.
If an ATP molecule shows up, myosin will let go of actin.
We’re gonna break that ATP into ADP plus phosphate, which releases energy and gets
that myosin head to tweak itself into the forward position.
Its oar is hovering above the water for the power stroke so to speak.
Then, when the phosphate and ADP actually separate, that lets the myosin head change
shape and stroke forward.
It’s rowing at this point.
If your body had no ATP to use, like, say, when you die, myosin would actually stay attached to
actin and your muscles would be perpetually stiff.
That’s a thing that totally happens, it’s called rigor mortis.
Calcium comes in when we look more closely at actin.
If we zoom in on the filaments, we’ll see molecules on the actin strand called tropomyosin
and troponin.
Tropomyosin is blocking myosin’s attachment site on actin.
And for the sliding filament model to do its thing, we need to move tropomyosin out of
the way.
To do that, we need calcium ions.
Great.
Where do the Calcium ions come from?
They come from the sarcoplasmic reticulum.
If you remember the endoplasmic reticulum, that one organelle you learned once in 7th
grade and never heard of since, this is kind of the muscle cell version of that organelle.
So a bunch of calcium ions come into the muscle cell, and they bind onto troponin, which shifts
tropomyosin out of the way with this kind of pivoting motion.
This exposes the binding site, which gives myosin a spot to grab onto.
Then cross bridging, all that.
Super simply, you need calcium to /let/ the contraction happen, and ATP to /make/ the
contraction happen.
That’s the basic model of the sliding filament theory but there are some unanswered questions.
Like there’s some disagreement about what titin does exactly.
We know it provides stabilization to the myosin filaments and provides some passive force generation.
But according to most recent comprehensive review I could find which was from 2018, it might have
a role in active force generation too.
If it does, I'm gonna have to redo this entire video.
To make things more complicated, we have more information and research on Titin’s role in cardiac muscle contraction
than in skeletal muscle, and that's fine, if you think the cardiac muscle is the only important muscle there is.
Before you go, just wanted to remind you that I made you some study guide material. It is linked
in the dooblydoo.
It is hosted on Patreon but you don’t have to sign up for anything or pay me anything to
get it. It's just there for you.
I’ve also got two playlists that you might like if you’re an anatomy student yourself — I got this one which is all about
the basics of anatomy and this one which is all about muscle stuff.
Have fun, be good, see you next time.