- [Voiceover] We kind of looked
at the first half of this graph,
the follicular phase,
and we kind of understood
that the follicular phase
is all about stimulating growth
of the follicles in the ovaries
to eventually cause the ovulation of an egg.
This stimulation of the follicles
comes from the release of various hormones,
FSH, LH, estrogen,
and so on.
The second half, after ovulation,
is called the luteal phase.
It's called the luteal phase
because it's about the development
of this yellow structure here,
called the corpus luteum.
So let's talk about it.
Here, after ovulation,
we have an egg that's been expelled from the follicle.
We therefore have the remainder of the follicle.
At this point, luteinzing hormone, LH, is really high.
Together, LH and FSH are going to
induce the old follicle here
to turn into a structure called the corpus luteum.
That just means "yellow body" in Latin.
It's actually a bit yellowy
because of some yellow pigments it has in it.
Remember the follicle was what released estrogen
from its granulosa cells.
Since this is not a follicle anymore,
it greatly reduces the amount of estrogen it makes,
and it actually begins to mass-produce progesterone.
Just to clarify, though: it still does make some estrogen.
It's just not really its primary product.
Progesterone is.
So that's why you see this dip in estrogen here,
and this almost uptick in progesterone that gets produced.
Let's think about this for a second.
We've ovulated, so there's a chance
our egg could get fertilized by a sperm.
Once it gets fertilized,
it's going to need a place to hang out and grow.
It's going to have to implant
into the lining of the uterus called the endometrium.
What would be really helpful right about now
is if we had a nice, vascular, hospitable uterine lining
that our fertilized egg could implant into
to support gestation of our new embryo.
By the way, at this stage of implantation,
our embryo is actually called a blastocyst.
I'll just write that down over here.
So in comes progesterone.
Let's just look at the word for a second.
"Pro," meaning "for,"
and "gest," referring to gestation.
This last part just kind of clues you in
that it's a hormone.
So progesterone is a pro-gestation hormone.
It's what mainly stimulates the uterine lining
to prepare for implantation and gestation
during this phase called the secretory phase.
In this secretory phase,
progesterone does a few things.
It increases blood flow to the endometrium
by stimulating the development of special arteries
in the endometrium called spiral arteries.
You can see them here in red.
These spiral arteries allow the embryo
to eventually have good access to nutrients
from the mother's blood stream.
Progesterone also increases uterine secretions
from special glands in the endometrium.
These secretions are important
for nourishment of the embryo.
Finally, progesterone actually reduces the contractility
of the muscles of the uterus.
Remember, the uterus has
a lot of smooth muscle in its walls.
The progesterone actually reduces
the contractility of those muscles
so that the growing embryo doesn't really get too disturbed
and doesn't get expelled out of the mother's body
too early by those muscles contracting.
Since we really want
that nice, hospitable environment for gestation,
the corpus luteum produces
lots and lots and lots of progesterone.
By the way, there's still a reasonable amount
of estrogen kicking around,
and it's really both the little bit of estrogen
plus the lots and lots and lots of progesterone
that helps to ready the endometrium for pregnancy.
The corpus luteum's hormones
are doing other things, too, though.
The progesterone and the little bit of estrogen
produced by the corpus luteum,
they're going to suppress the FSH and LH production
by the anterior pituitary,
by that process of negative feedback.
So you can see their levels dipping pretty low here.
On top of the estrogen and progesterone
negatively feeding back on FSH and LH release,
the corpus luteum is also producing inhibin.
You can see the amount of inhibin peak here
when the corpus luteum reaches around its maximum size.
That inhibin actively inhibits FSH release
from the anterior pituitary.
Unfortunately for the corpus luteum,
it kind of needs FSH and LH to survive.
Since they're being suppressed
by the corpus luteum's own hormone release,
the corpus luteum starts to atrophy.
It starts to wither away and die off.
When it dies off, progesterone and estrogen levels drop.
And when progesterone and estrogen begin to drop,
two things happen.
The first thing is
that the end of the luteal phase is triggered.
You can see, we've reached the end of the graph here.
Basically, we've triggered the end of the luteal phase,
but the start of the next follicular phase.
At this point, menstruation begins to occur
and the endometrial lining that has built itself up
and prepared itself for implantation starts to shed,
and it'll be lost through the vaginal canal
in what we commonly call the menstrual period,
or menses.
Notice that that sort of takes place
at the beginning of each reproductive cycle.
Generally speaking, menstruation is a sign
that pregnancy has not occurred.
This period can last anywhere from two to seven days.
FYI, women lose usually around 40 milliliters of blood
per menstrual phase.
The second thing that happens
when estrogen and progesterone levels drop
is that they stop exerting their negative feedback effects
on FSH and LH release from the anterior pituitary.
So the FSH and LH levels begin to go back up again.
This increasing FSH then goes on
to stimulate more follicular development in the ovaries
to start the whole cycle all over again
over the course of another 28 days.
Now, what I told you about the corpus luteum
withering away and dying
is only actually true when no pregnancy is occurring.
That's the case in most reproductive cycles,
and that's why I covered that first.
But it's important to know
that things are a little different
if pregnancy does occur
and a fertilized egg is indeed implanted
into the endometrium.
We said that the corpus luteum's
estrogen and progesterone release
suppresses FSH and LH,
and suppression of FSH and LH, in turn,
cause the corpus luteum to atrophy, right?
That's because the corpus luteum
needs luteinizing hormone to survive.
Well, when a blastocyst implants into the endometrium
and gets established there,
the resulting embryo that develops from the blastocyst
starts to produce a special hormone
called human chorionic gonadotropin,
or HCG.
This HCG is structurally really, really similar
to luteinizing hormone,
so much so that levels of HCG produced by the embryo
are enough to keep the corpus luteum alive.
Because remember, we said that the corpus luteum
relies on LH to stay alive.
So now with the corpus luteum remaining alive,
it can continue to produce that estrogen and progesterone
that's necessary to maintain the endometrial lining
and keep it nice and supportive of the pregnancy.
There's a couple implications of this.
First, because the HCG production
is unique to the embryo,
most pregnancy tests work
by checking for the presence of HCG in the blood
or in the urine.
Second, the corpus luteum doesn't produce progesterone
for the entirety of the pregnancy.
It does most of the progesterone production
for about the first two to three months,
and after that,
a joint organ of exchange
shared between the mother and the fetus,
called the placenta,
that starts to take over
as the major producer of progesterone.
Third, the corpus luteum being rescued,
or kept alive, means that its continued hormone release
maintains that endometrial lining.
So the lining isn't lost in menstruation.
It's kept in order to support the pregnancy.
Just to recap:
if no pregnancy occurs,
then the corpus luteum withers away
and the reproductive cycle just continues to repeat itself
for about 28 daily.
And if pregnancy does occur,
the implanted embryo starts to produce HCG,
which rescues the corpus luteum from atrophying
and the endometrium is thus maintained.
No menstruation happens
because you're not losing the endometrium
and the reproductive cycle is put on hold
for the duration of the pregnancy.