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Course: Health and medicine > Unit 2
Lesson 7: Heart muscle contractionSympathetic nerves affect myosin activity
Check out how the amount of Myosin that is tugging on your heart can change depending on your activity level! Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.
Want to join the conversation?
- What is the z-disk made of?(7 votes)
- The Z-disc (or Z-line, as he says at) is made up mostly of a protein called alpha-actinin. I got this out of my undergrad textbook (Marieb & Hoehn 2013), but this is not something undergrads are expected to learn. 3:15
I hope this helps.(7 votes)
- doesn't the SA node stimulate the heart to beat at approx. 120 bpm? Yet resting HR is approximately 60 bpm. What is the mechanism in which the Parasympathetic nervous system keep the heart at approx. 60bmp at rest?(1 vote)
- The parasympathetic nervous system slows down the heart rate through the release of acetylcholine by vagal nerve. It hyperpolarizes target cells by opening potassium channels that would require more calcium ions to enter the cells to keep HR at 120 bpm. The calcium release is induced by norepinephrine during sympathetic stimulation (such as stress, anxiety, or exercise). In the absence of such stimulation, the heart rate is at about 60 bpm at rest.(4 votes)
- What happens to the Ca2+ after a muscle contraction? What makes it leave the cell - or go back inside the sarcoplasmic reticulum?(1 vote)
- There is a pump in the membrane of the sarcoplasmic reticulum called the Ca+ ATPase. It uses energy to sequester Calcium back into the Sarcoplasmic reticulum.
As a secondary Calcium transport mechanism, there is also an antiporter in the muscle cell plasma membrane that uses the electrochemical gradient of Na+ (eg: lets sodium flow into the cell) in order to pump calcium out of the cell. This Na+ that flows into the cell must then be extruded back out of the cell using the plasma membrane Na+/K+ ATPase.(4 votes)
- Does adrenaline affect this process in any way?(3 votes)
- The main effect of adrenaline on the heart is increased rate. Norepinephrine (or noradrenaline) is the hormone (neurotransmitter) involved here because it increases force, which is a function of this kind of muscle cell (this is the part in the video atwhere he says: "to be clear, this is a ventricular heart cell"). When you get deeper into it, you have to start learning about corresponding receptor sites and their effects in different parts of the body. 1:10(3 votes)
- Is there a video where Rishi explains what norepinephrine is and how it works with sympathetic nerves?(2 votes)
- Not Rishi, but there's probably a video that will help you in the neurology section:
https://www.khanacademy.org/science/health-and-medicine/nervous-system-and-sensory-infor(1 vote)
- When the Z-Disks are pulled together (), this causes cell contraction, correct? So is this what ultimately causes the muscle that the cells are part of to contract, or I am misunderstanding? 3:27
If this is correct, and Myosin is working more when you are more active (), is this why your heart beats more when you are walking or running rather that sitting? Also, calcium is being used in this process, especially when you are more active; does this mean you need more calcium when you are being active than when you are not? 7:00(1 vote) - In some earlier video there was an explanation that actually Ca2+ that is going to the heart cell throught t-tubules is binding some receptor that will make Ca2+ realesed from sarcoplasmatic reticulum. So I am wondering if the force that pushes heart cell to work (respectively amount of myosin heads binded to actin) is not the same at all situation (active vs nonactive) and what differs is time when cell reach some critical level of Ca2+ that will lead SR to release more Ca2+(1 vote)
- The strength of a muscle contraction (including that of the heart) ultimately depends on the amount of Ca2+ in the cytosol: more calcium exposes more binding sites on actin for myosin, which in turn allows more crossbridge cycling to occur. The autonomic nervous system regulates the heart muscle by modulating the frequency and force of heart muscle contractions.
If you increase the frequency of action potentials, then this will in turn increase the amount of Ca2+ that is released from the SR and will result in increased cardiac output. Therefore, the force of the cardiac muscle is driven chiefly by the neural system but is strongly influenced by hormones. For example, epinephrine increases action potentials which increases heart rate. Thyroid hormones, insulin and glucagon primarily increase the force of myocardial contraction, but glucagon also promotes increased heart rate.
Source: Principles of Human Physiology, Cindy L. Stanfield, 5th edition.(1 vote)
- Are there a certain amount of myosin heads her myosin molecule?(0 votes)
- yes there are a certain amount of myosin heads her myosin molecule(0 votes)
Video transcript
We're going to do a
little comparison. I'm going to draw three
different people here-- or it could be
the same person, I suppose-- in three
different situations. So you've got the first
person just kind of sitting and maybe they're watching a
YouTube video on their laptop. And you've got a
second person who's actually going
for a little walk. Let's see if I can draw
this person walking. And you've got a third person
who's-- let's say this person is actually really active
and they are running. So they are actually in
full stride, running. And maybe they're late
for a test or something. So-- oh, let me actually change
that so their arm does not look broken. So there have
these three people. And they're running and
walking and sitting, right? So you can imagine if you were
to take a look at their heart cells they might be
doing different things. In fact, let's draw
all three's heart cells and show you what
they might be doing. So we've got our heart cell. And in this case I'm actually
going to draw also a nerve. This is going to be
the sympathetic nerve. I'll write an s, for
sympathetic nerve. And the heart cell,
just to be clear, is going to be a
ventricular heart cell. So this is a-- I'll write
ventricular heart cell here. Just so that we know we're not
talking about some pacemaker cell or some other
cell in the heart. This is a ventricular cell. And now, just to remind us
of a couple things we know, this ventricle cell is branched. And it's got two little nuclei. And it's got some receptors
on its surface waiting for, potentially, norepinephrine
from that sympathetic nerve. Right? Now inside of that
heart cell, if we were to dive inside of the heart
cell, you might see some actin. And you'd see that at
the ends of the actin. It's a Z-disk, right? So we've got a Z-disk
with our actin. And I've drawn this
far too close together. Let me actually make a
little bit of space in here. But you get the idea. You've got our actin kind
of like little ropes. And in the middle
you've got our myosin. And our myosin, you
remember, is basically going to have a whole
bunch of myosin heads. And these heads are
going to want to do work. They're going to want
to pull the actin and yank that Z-disk closer
to the middle, right? That's what they want to do. So these myosins are hanging
here, waiting to do work. And their trigger
for work, of course, is going to be calcium
binding the troponin C and pulling tropomyosin
out of the way. So this is our actin and myosin. This is our actin up here. And we've got our
myosin in the middle. And then finally, I'll
draw one last thing and that is the titan. And the titan,
remember, is a protein that basically is
going to attach the myosin to the Z-disk. Remember, our Z-disk is
this thing at the end. This is our Z-disk over here. Let me just kind of
draw it in for us. This right here is our Z-disk. I've been calling it a Z-disk. Sometimes you see Z-line. That's kind of interchangeable. But this is our
Z-disk right here. And it's basically tethered
by those actin ropes, you can think of them as. And we're going
to use those ropes to pull the Z-disks together. So this is basically the set
up and what it looks like. And now I'm actually going
to just take this and cut and paste it a couple of
times so that we can actually use this for our two
other situations. We've got one there. And we can actually do it
again and have it like so. So now you can see our
three situations side by side and our three setups
with our actin, myosin, and our Z-disks. So what would happen
in situation one? Well in situation one
you're just hanging out. You're happy. You're maybe watching something
kind of funny on YouTube. And you don't have
much sympathetic drive. You don't have any
stimulation coming from your sympathetic nerves. You're not running or you're
not frightened, let's say. So you have-- you know, your
normal amount of calcium comes into the cell when
it's time to contract. And so you get a little
bit of calcium in here. Looking over at the other side,
when the calcium comes in, you have a low amount
of calcium, let's say. Because not much is coming
through the channel. You're not activating
that channel in any way. So that calcium, let's say, it
binds here and it binds here. And let's say a little
calcium binds here and here. And when I say binds
remember I mean it binds the troponin
C. Remember that. So the calcium binds there. And what do you get? Well let's draw a little table
on the side of-- this is, let's say, the
proportion-- I'm trying to make sure I
phrase it correctly-- the proportion of myosin
heads that are working. And if you count them
up, if you count up all the little purple heads--
you can do that right now-- you'll see there are 20. So this is the proportion of
myosin heads that are working. And what would you get
for this first situation? Well, at four spots the
calcium has bound, right? And it doesn't bind forever. At some point the
calcium is going to be kind of taken back into
the sarcoplasmic reticulum, or thrown out of the cell. But for the time that
our heart is contracting, for that brief bit of time, how
many myosin heads are working? Well we've got
this guy over here. This guy. And we've got this
guy down here. And we've got this
guy and this guy. So four of them are working. And that means that
16 are not working. So 4 out of 20 are working. So really we've got-- what
does that work out to? 20%. That's equal to 20%
of them are working. So that's not too many. But what's going to happen? Basically these
myosin heads are going to pull-- let me erase
the little arrows, not to confuse you. But basically
these myosin heads, these four that are
working, are going to pull the actin
that way and that way. And this way and this way. And the Z-disks will
come closer together. Let's not be confused
about that point. The Z-disks definitely
will come together. But it's going to take a while. Really it's like
having four-- you can think of it as four of
your friends pulling on a rope. It's not as effective
as having 20, right? So let's go to
situation number two. So in situation
number two, let's say now you're going for a walk. And you're enjoying
the beautiful day. But you're walking, right? And so there's a
little bit of activity. And so let's say your
sympathetics are firing a little bit, a little bit
of a sympathetic drive here. And a little bit of
neurotransmitter gets released. And so this neurotransmitter, we
know, is called norepinephrine. And so a little
bit gets released into that space
between the nerve and the cell, the heart cell. And it binds to, let's
say, one of the receptors. So one of the receptors
is going to fire. And during a muscle contraction
you've got calcium coming in. But because that
receptor fired now you have a little bit
extra calcium coming in. Meaning that channel
has been activated so that it's letting
more calcium in. OK so if more calcium's coming
in-- let's now take a look at our diagram. Now you've got a little bit more
calcium coming in and binding. And I'm just choosing them
by random, in a sense. But let's say these six. And on this side let's
just choose another six. Let's say four up here and
maybe a couple down here are going to bind calcium. So you've got troponin C's
that are binding calcium. And of course that
means that those are the myosin heads
that get to work. And so in total, how many
myosin heads are working? Well now instead
of only four total, we've got-- what is
that-- 12 myosin heads out of 20 working, or 60%. So it's really gone
up considerably. So just as before,
you're going to have the Z-disks getting yanked in. But now the yanking is
going to be much more forceful because you've got
many more myosin heads actually involved in dragging
that Z-disk over. So this is actually
quite interesting because now you can
see that you have, as a result of the
sympathetic drive, more force in your contraction,
your heart contraction. So you can probably guess where
the last one is going to go. Now you're running. You're excited. And let's say, now instead
of just a little bit of transmitter, you've got
tons of neurotransmitter being released, lots and
lots of norepinephrine. In fact, let's say a
little bit over here. And you've got all three
receptors kind of firing, right? Because all that
norepinephrine is allowing lots and lots of
stimulation to the cell. And so with all
this norepinephrine your calcium channels are going
to be really active, right? They're going to be
pouring in calcium. So instead of just a
little bit of calcium, now when you have a
contraction you've got lots of calcium dumping
into the cell, right? And this is, of course,
just during the time when your contracting
or squeezing. So with all this
calcium now it's going to go and bind the
troponin C everywhere it can find the troponin C.
It's going to come and sit basically everywhere. And all these myosin
heads are excited because now they
all get to work. And with this full set
of myosin heads working-- you have 20 out of 20 working. You have 100% of
them doing their job. And as a result you
can see that now you're going to have a huge mechanical
force, enormous forces, yanking those Z-disks
closer together. So in all three
situations you do get the Z-disks coming together. But remember, the period
of time that the calcium is in the heart is finite. Right? It's not like it's
there forever. Because, at some point,
that calcium's going to get, as we said, brought
back out of the cell or into the
sarcoplasmic reticulum. So while it's there, for
those few precious moments that the calcium is
there, you really want your heart to be able to
do as much work as possible. And in this case,
you're actually seeing that here at the
top-- let's actually draw an arrow-- at the top this
side there's really low energy use because not too
many of the myosin heads are actually converting
ATP to ADP plus phosphate. So remember, the myosin
heads that are working-- those are the only ones that
are actually converting ATP to ADP plus phosphate. And the ones that
are not working are of course not doing that. So in this case you can also
see that, in addition to force, the other thing that's less
in this sitting situation is that it's a low-energy state. You're not really
burning any energy. Whereas over here,
when you're running, each one of these myosin
heads is cranking through ATP. It's making lots
and lots of ADP. So it's using lots of energy. It's a high-energy situation. In other words, you're using
up a lot of energy here. And so of course
this makes sense. Right? Because you think, well if
I go for a run of course I'm going to use up energy. Whereas if I'm just sitting I'm
not using much energy at all. And now you can see exactly
why that's the case. Because in the running
situation, all 20 of your myosin heads
are burning through ATP.