I feel like I haven’t spent nearly enough
time lately talking to you about all the stupid and dangerous things that you can do to your
own body, so let’s talk about doping. You probably have heard of this thanks to
Lance Armstrong, who secretly messed with his own blood so that he could illicitly win
the Tour de France seven times in a row. You might be dimly familiar with the fact
that doping isn’t like shooting steroids, but it is still cheating, even though, like,
why is it cheating? And how does it work? And is it even possible to make your blood
better at being blood? In other words, how can some people treat -- or
mistreat -- their own blood like it’s some sort of drug? Short answer: Because your blood is incredibly
powerful stuff. And its power rests largely in your erythrocytes,
or red blood cells. They’re the most abundant cell type in your blood, accounting for nearly
45 percent of its volume. Every time you take a breath, they pick up
oxygen in your lungs and distribute it through your body, and then grab carbon dioxide, and
bring it back to the lungs where it can be exhaled. The main mission of erythrocytes is to keep
your body fed with oxygen, so your muscles can do their thing, and your brain can continue to
think and feel and boss around your various parts. But you don’t want to mess around with your red
blood cells because erythrocytes are weird characters. They go places that other cells won’t. They
purge themselves of their most precious inner belongings, preferring instead to live as
hollow shells. Because of the crushing demands of their job,
they don’t live very long. And just like with your blood pressure, too much of these
good things can turn bad quickly. So the erythrocyte must be respected. It is
not for doping. Or for dopes. Despite their prominent role in some international
sports scandals, your red blood cells are fairly simple and unassuming little cells. They’ve got a distinct biconcave shape -- which
just means that they’re concave on both sides -- making them look kinda like a breath
mint… a tiny, bloody breath mint. And while they have a plasma membrane, they
don’t have a nucleus and don’t have most of the parts other cells do. So they’re basically just glorified, protein-filled
phospholipid-bilayer sacks. But they’re still another great example of that harmony
between form and function. For one thing, that biconcave shape gives them a
large surface area that’s ideal for gas exchange. It also makes them flexible, able to change
shape as they squeeze through tiny capillaries with diameters smaller than the cell itself. Of course, all that squeezing and twisting
is hard on a cell’s membrane, and that, combined with their general lack of organelles
to help repair the membrane, means these cells don’t live very long, surviving on average
only 120 days. But they sure work hard while they’re alive. And their work is mostly in gathering and
transporting oxygen. They’re able to do this because, if you don’t count their water
content, red blood cells are 97 percent hemoglobin -- a molecule that easily binds to, and releases,
oxygen. It’s like an oxygen sponge. Every hemoglobin molecule is really made of
eight different component molecules -- four are a red pigment called heme, and four are
a protein called, you guessed it, globin. Each globin is a globular polypeptide chain
-- hence its name -- and proteins, you’ll probably remember, like to bind to stuff. So each globin has its own personal ring-shaped
heme molecule, and in the center of that heme is an iron atom, kinda like a cherry on top
of a protein-and-pigment sundae. It’s that iron in the center of the heme
that makes our blood red. Incidentally, not all animals have red blood,
because not all animals use hemoglobin to move oxygen. For example, most mollusks like
squids and snails have blue blood, because it contains hemocyanin, a copper-rich protein-pigment
that turns blue when exposed to oxygen. But, iron is what we’re stuck with, and
I have to say it’s great at its job, because each iron can bind with one whole oxygen molecule. And that oxygen really adds up. Since you have four iron atoms in every molecule
of hemoglobin and every red blood cell contains something like 250 million hemoglobin molecules
that means each one of your tiny, floppy red-breath-mints can grab about a BILLION molecules of oxygen. Exactly how they transfer oxygen and carbon
dioxide from your tissue cells is something that we’ll get into when we talk about the
respiratory system. But if you’re wondering why all this hemoglobin
can’t simply skip the red blood cell rigamarole and just run around naked in your blood, it’s
because free-range hemoglobin would actually thicken the blood, making it so viscous that
it would impede blood flow. This also happens to play a part in blood doping,
which -- stick with me -- I will explain in a bit. So what does the brief but glorious four-month
life of an erythrocyte look like? Well, remember when I said a red blood cell doesn’t have
a nucleus? And maybe you thought, hey wait a second, how can it even be a cell without
a nucleus, or DNA? First of all, nice catch. But actually, erythrocytes do start off with
a nucleus and DNA, they just get rid of them, because their entire purpose for existing
is to schlep around hemoglobin and oxygen, and they want the extra room. The whole process of forming blood cells,
called hematopoiesis, happens in your red bone marrow, which is mostly made of reticular
connective tissue that’s snuggled up to special capillaries called blood sinusoids. In short, the process begins with a hemocytoblast
-- or a specialized stem cell -- which soon differentiates into an early erythroblast.
Then, it starts making a whole bunch of ribosomes, the organelles that manufacture proteins. And in this case, the ribosomes start cooking
up tons of hemoglobin, as the cell transforms into a late-stage erythroblast. When it’s got enough hemoglobin, it suddenly
jettisons most of its organelles, which causes the cell walls to collapse a little, giving
it its biconcave bloody breath-mint shape. Now you’re left with a reticulocyte, which
is pretty much just an early erythrocyte that still has a little group of ribosomes left,
called a reticulum. So far, this whole journey so far has taken
about fifteen days. When the reticulocyte is finally bursting
with hemoglobin, then it leaves the marrow and enters the bloodstream, and a couple of
days later, when the last ribosomes have degraded, you’ve officially got yourself a mature
red blood cell. And that cell travels around your body, doing
its job for a few months before it gets old or damaged and needs to be replaced. Now, maintaining the balance between production
and destruction of these cells is crucial. Too many will make the blood too
viscous and difficult to pump, and too few leads to oxygen deprivation, or hypoxia. The process of maintaining the right levels
of red blood cells is regulated by a special hormone called erythropoietin, or EPO. It’s
produced mostly in the kidneys, but also in the liver, and is constantly circulating in
the blood. If you’re anemic, or hiking at a high altitude,
or hemorrhaging blood, or experiencing anything else that creates a drop in your blood oxygen
levels, certain cells in your kidney will notice, and take action. And they can do that, because they traffick
in a signaling molecule called hypoxia-inducible factor, which monitors your blood’s levels
of oxygen. The way that this works is pretty cool. These
special kidney cells need oxygen in order to break down that signaling molecule, so
if oxygen levels in the blood are low, they can’t turn the signal off. This means that
the signal keeps going, which triggers the release of more and more EPO, which stimulates
your red bone marrow to pump out more red blood cells to carry around more oxygen. As oxygen levels in your blood increase, the
signal is degraded, and EPO production slows. And EPO is a key player in blood doping too,
but we’re gonna have to wait a minute before we get there, because I first want to get
back to the fate of your hard-working erythrocytes. So if you’re generating about two million
new blood cells every second, you also have to dispose of about the same number of dead
ones to maintain the balance, right? When these cells get old, they turn rigid,
and their hemoglobins starts to fall apart. As they get stiffer, they can end up getting
stuck in capillaries in your brain or heart, which would not be good. Luckily, you have certain channels to corral
these dying cells, especially around the spleen, which some anatomists call “the red blood
cell graveyard.” So these tired old cells get trapped and then
basically ambushed by big macrophage white blood cells in the spleen, liver, and bone
marrow, which break them down and recycle their various components. The globin proteins are broken down into their
basic components -- amino acids -- which go back into the blood to be used by other cells
for making more proteins. Iron from the heme group is separated and
either bound to proteins and stored in the liver, or put right back into a new hemoglobin
molecule. And the heme gets turned into bilirubin, a yellowish pigment that goes to the liver
where it’s added to the bile that it secretes into the intestine and eventually leaves the
body in your poop. Now that you know how your erythrocytes function
naturally, it’s easier to see how they can be messed with -- often with bad results. You can dope your blood in a few different
ways, but the most common technique is to inject natural or synthetic EPO hormone to
boost your red blood cell production. It’s also possible to draw and store some
of your own blood, and then transfuse it back into your body after your body has recovered
from the blood loss, effectively raising your volume of red blood cells. The logic, if you can call it that, is that
more red blood cells equals more oxygen being carried to your muscles, and therefore better
physical performance. Now, the extra oxygen can’t change your actual
muscle strength, but the added aerobic capacity does reduce muscle fatigue and enhance endurance,
by allowing your muscles to work harder for longer. And it can provide enough of an extra edge
to win a race, like, say, the Tour de France. Seven times. But not only is it banned in athletic competitions,
blood doping is also dangerous. Because, remember, a red blood cell count
that’s too high thickens the blood, and that actually makes it harder for the heart
to pump blood around the body. In addition to defeating the purpose of enhancing the
blood’s effectiveness, this can lead to blood clots, and strokes, and heart failure.
So, no thank you. Plus, cheating sucks. But today you learned about the structure
and function of your erythrocytes, and of hemoglobin, which they use to carry oxygen.
We also went through the formation and life cycle of a red blood cell, and studied how
their levels are regulated by EPO and their signalling molecules. Finally, we learned
how doping the blood is a recipe for disaster and for finding yourself on Oprah and apologizing to
everyone you know and losing all of your yellow jerseys. Thanks to all of our Patreon patrons who help
make Crash Course possible for themselves and for everyone for free with their monthly
contributions. If you like Crash Course and want to help us keep making videos like this
one, you can go to patreon.com/crashcourse. This episode was filmed in the Doctor Cheryl
C. Kinney Crash Course Studio, it was written by Kathleen Yale, the script was edited by
Blake de Pastino, and our consultant is Dr. Brandon Jackson. It was directed and edited
by Nicole Sweeney; our sound designer is Michael Aranda, and the graphics team is Thought Cafe.
