Download Skeletal muscle contraction and reflexes

Physio Lecture 13 Skeletal muscle contraction
Properties of Muscle- “Little mouse”
• Excitability-electrical response
• Conductivity-electrical excitation spreads
• Contractility- ability to shorten
• Extensibility-stretch-ability
• Elasticity- recoils
Myo and sarco mean muscle
The word muscle means little mouse, and its because when you flex the muscle the ball of muscle
underneath your skin was thought to look like a little mouse. Some properties of muscle include being
excitable, that’s means they can generate an electrical response, there are conductive, that means the
electrical excitation can spread, in other words travel. Next it has contractility, that means it can
shorten, and it has extensibility, in other words you can stretch your muscle. Lastly the muscle has
elastic properties, and that basically means it can recoil back into its original shape. The prefixes “myo”
and “sarco” also means muscle.
3 Classes of Muscle
Based on histological appearance and function
• Skeletal
– striated, voluntary, myofibers
• Cardiac
– striated, involuntary, branched, cardiocytes
• Smooth
– nonstriated, involuntary, fusiform in shape (spindle)
I now want to talk about the three classes of muscle, and these three classes were generated based on
histological appearance and function. Let’s start with a brief overview. Skeletal muscle is striated, in
other words, it looks like it has lines running through an individual muscle cell. Skeletal muscle is also
voluntary, in other words, you have conscious control over your skeletal muscles, well at least most of
them. Skeletal muscle is also multi-nucleated, and when we speak of an individual skeletal cell, we call it
a myofiber. Cardiac muscle is also striated, in other words, it looks like there are lines running through
the cell. It is involuntary; you do not really have conscious control over how your heart muscle beats.
Next, the cardiac muscle appears branched, and I’ll show you an example of that in a little while, and
when we speak of cardiac cells we speak of cardiocytes. Smooth muscle is non-striated, and is
involuntary, and is fusiform in shape, in other words it looks like a spindle.
Lets elaborate a little bit more on cardiac muscle. Shown in the top left picture is a histological
preparation of cardiac muscle. You’ll notice that the cardiac cells appear branched, much like the
freeway system in Orange County. The blue arrow is pointing to a special junction in between individual
cardiocytes, that is called an intercalated disc, and we will talk about its important properties in another
unit. You’ll also notice the big purple ball like structures; those are the nuclei of each individual
cardiocyte. Lastly, I want you to notice that the individual cardiocyte appears to have lines running
through it, in other words, striations. Those striations occur due to the arrangement of myofilaments. I’ll
be talking about the myofilaments, actin and myosin, in a little while.
I’d now like to talk about smooth muscle, just briefly. Smooth muscle is considered involuntary muscle,
and if I asked you where you would find it in the body, I’m sure the intestinal track would come to mind
most quickly. Smooth muscle is fusiform in shape, and if you look at the cartoon drawing in the bottom
right picture, you’ll also notice that they are mononucleated, that means they have one nucleus. You’ll
also notice that they don’t appear to have lines running through the individual muscle cells. In other
words, in a histological preparation, we say they are non-striated. Now does that mean that they lack
contractile fibers? Do they lack myofilaments? No. Look at the top right cartoon drawing now. You’ll
notice that they still have their contractile fibers, but these myofilaments are not arranged in an
organized pattern. And therefore, in a histological preparation, we do not see organized striations.
Lastly, I’d like to briefly highlight skeletal muscle. The class of muscle that is most important for the rest
of our power point. You’ll notice that in this histological preparation there appear to be lines or
striations running through the skeletal muscle cell, or myofiber. These striations are generated due to
the organization of myofilaments, and I’ll talk about the thick and thin myofilaments in a little while.
Next, you’ll notice that an individual skeletal muscle cell, or myofiber, has many nuclei found along the
perimeter of the fiber, in other words skeletal muscle is multi-nucleated. Lastly skeletal muscle is
considered voluntary, in other words you have conscious control over whether it contracts or relaxes.
Most of the skeletal muscle is voluntary; however there are times that you will learn throughout the
class when a skeletal muscle can be considered to be involuntary, like the diaphragm.
Muscle Gross Anatomy
• Origin
• Insertion
• Belly
• Action
– Prime mover
– Antagonist
– Synergist
– Fixator
An origin is an attachment of a muscle that remains relatively fixed during muscular contraction. An
insertion is the moveable part, or attachment of a muscle. When a muscle contracts the insertion moves
towards the origin. The thickest part of a muscle is considered its belly. Actions come in a variety of
terms such as flexion, extension, opposition, abduction, adduction, and the muscle that is primarily
responsible for causing a particular action is called the prime mover. A muscle that helps with that
movement is called the synergist, and a muscle that opposes that motion is called antagonist. For
example, for flexion of the arm you think of your biceps brachii, but if you want to extend your arm the
antagonistic muscle would be your triceps brachii. A fixator is a muscle that helps stabilize a joint
Levels of Muscle Structure
• Fascicles- smaller bundles within the whole muscle
• Fibers- individual cell
• Fibrils- clusters of protein within the cell
• Filaments
• Epimysium- outermost wrapping; continuous with tendon
• Perimysium- packaging around a bundle of fibers (fascicle)
• Endomysium-individual wrapping around a fiber
It’s now time for me to tell you about levels of muscle structure, and I have a cigarette carton analogy.
It’s not the healthiest analogy, I understand that, but it works none the less. Pretend you go to the store
and you buy a carton of cigarettes, you bring that carton home and open the outer cardboard box;
inside you see individual cigarette packs. Now take out a cigarette pack, unwrap the cellophane
wrapper, open the cigarette pack, and pull out an individual cigarette, look at that cigarette and notice
that it is lined with paper, if you cut through the paper, inside the cigarette you would find shreds of
tobacco. Well that analogy actually carries over quite nicely to the levels of muscle structure. If we think
of a whole muscle as our cigarette carton then the lining of our whole muscle is our epimysium, in other
words that would be the cardboard box. Now, if we cut through the epimysium to pull out an individual
cigarette pack, well in our muscle we would essentially be pulling out a fascicle. A Fascicle is a collection
of individual muscle cells, and much like an individual cigarette pack being lined with cellophane
wrapper, a fascicle is wrapped by perimysium. Now, take out an individual cigarette, in our muscle this
would be like taking out an individual muscle fiber cell. If we could cut through this individual muscle
fiber cell, inside we would find clusters of fibrils. This is much like our cigarette and cutting through the
paper and seeing shreds of tobacco inside. An individual muscle fiber cell is wrapped by its sarcolemma,
that basically means its cell membrane, but also layer of connective tissue called endomysium.
Now let’s review and do this again. In this picture starting at the top right, we see a person’s arm with a
deltoid muscle; again think of that as a carton of cigarettes. If we take out an individual pack of
cigarettes from our carton, that would be much like taking out or looking at a muscle fascicle, and a
fascicle is an individual group of muscle cells. Now let’s take out of our fascicle an individual muscle
fiber, again going back to our analogy that would be like taking out an individual cigarette from the
cigarette pack. If we could open up the muscle fiber, and analyze the fibrils inside, going to our analogy,
that’s like opening up an individual cigarette and looking at the tobacco inside. So if we’re looking at the
myofibrils inside a muscle fiber, you’ll notice, according to this picture that there are striations, or a
lined appearance, and I’m going to talk about these myofibrils in more detail in the next few slides.
You’re going to learn that these myofibrils have this appearance due to the arrangement of
myofilaments.
Nuclei along length of muscle fiber come from satellite cells during formation of fiber.
Fibril
•
•
•
•
•
•
Sarcolemma
Sarcoplasm
T (transverse) tubules
Sarcoplasmic reticulum
Terminal cisternae
Triad
Now it’s time for us to go from a large muscle, down to a fascicle, which is a collection of individual
muscle cells wrapped with perimysium. And in this black and white picture, were looking at an individual
muscle cell or myofiber. If we peel away the sarcolemma of this myofiber you’ll see, in the cytoplasm of
this muscle cell, we see many repeating structures called myofibrils. Let’s do this again, “sarco” means
muscle, and “lemma” means plasma membrane. So sarcolemma basically the cell membrane around the
muscle cell. Sarcoplasm means the cytoplasm within a muscle cell. In the cytoplasm, you’ll notice that
we have these repeating rod-like structures called fibrils. Next, I want you to see these yellow structures
shown here in this cartoon. These are called T-tubules, or transverse tubules. These are invaginations of
the sarcolemma. Please note: this is not to say that the sarcolemma has holes punched through it, No,
the integrity of the sarcolemma is still maintained. These are not rips, nor tares, they are merely
extensions of the sarcolemma, that invaginate into the cytoplasm, and you’ll notice the sarcolemma
wraps around each individual myofibril. Why might these T-tubules be very important? Well you’re
going to learn pretty soon that these T-tubules are going to allow an electrical current to travel deep
throughout the cytoplasm, and basically engage every single myofibril. We’ll talk more about that later.
Next I want you to notice that this blue web like structure is called the sarcoplasmic reticulum. I’m sure
that reminds you of an organelle called the endoplasmic reticulum. Well, sarcoplasmic reticulum is
basically the same thing, except inside a muscle cell. In addition to helping with protein synthesis, the
sarcoplasmic reticulum also stores a tremendous amount of calcium within it. And you should already
start to appreciate, that when calcium is released from this organelle a chain of events will happen that
will allow a muscle fiber to contract, or shorten. Next, I want you to notice that the sarcoplasmic
reticulum has these swollen endings, in other words, areas where the sarcoplasmic reticulum looks
larger, and you’ll also notice that these terminal cisternae occur on both ends of a T-tubule. So, terminal
cisternae are the swollen ends of the sarcoplasmic reticulum that are in functional contact with a Ttubule. In fact, this functional contact is very important for the transmittance of the electrical signal, and
I want you to understand that the terminal cisternae on either end of a T-tubule is called a triad. “Tri-”
meaning three: think of it as 3 T’s next to each other: terminal cisternae, T-tubule, and on the other side,
another terminal cisternae.
Ok, we have gone from a large muscle down to a fascicle, remember a fascicle is a collection of
individual muscle cells or fibers surrounded by perimysium. If we now take an individual muscle fiber or
cell, and peel away the sarcolemma, as demonstrated here in the top left picture, underneath the
sarcolemma you’ll notice that we see dark, black, nuclei. Many of them. (Again skeletal muscle is multinucleated.) Inside the cytoplasm, in addition to the nuclei, we see rods of myofibrils. The center portion
of this picture shows an individual myofibril expanded for view. You’ll notice terms like Z-disc, and Hzone, A-band and I-band. I’ll explain what those mean in a little bit. From one Z-disc to another Z-disc
this region is called a sarcomere, and a sarcomere is the individual unit of the muscle cell. In other
words, it’s the functional unit. This is where contraction is going to occur. Now I want you to notice that
we have bands of thick filaments, and these thick filaments are shown as bright red structures. We also
have structures that are called thin filaments, and they are shown here as the light blue structures.
You’ll notice the thin filaments are anchored to the Z-disc. I’m going to explain what these thick and thin
myofilaments are doing in the cell in the next few slides, but right now I would like to talk to you about
their overall arrangement. I want you to pretend that you are in your lab classroom, and I want you to
pretend that you are floating up by the ceiling and looking down at the tables and at the chairs
staggered in between your lab tables. What if there was a giant light shining through the floor of our lab
classroom? Do you agree that the tables in the classroom would obstruct the light from reaching your
eye, and this would create a shadow? Well, the thick filaments in a sarcomere, shown as the red
structures in the bottom picture, do much the same thing when a fibril is viewed under a microscope.
These thick filaments obstruct the light from getting through, and so it creates a shadow like
appearance. Now, the thick filaments create what’s called the A-band, notice that that term is shown
here in the middle picture. How can you remember that the thick filaments create the A-band? (Which
basically is like a shadow when looked at under a microscope) Well what is the second letter in the word
dark? That’s right A, so you’ll now remember that the thick filaments create the dark band, and this is
known as the A-band. Now I want you to think about the individual laboratory chairs that are staggered
on either side of our lab tables. If you look at the bottom picture, and notice the helical or intertwined
light blue lines (the thin filaments) they too are staggered in between the thick filaments. So if you were
looking at the light shining through our lab floor, the spaces where our desk chairs are found would
allow more light to shine through. Now, how are you going to remember that the thin filaments, where
they attach to the Z-disc, and don’t have any overlap with the thick filaments. Constitutes the I-band
shown in the middle picture? What is the second letter in the word light? That’s right I, so where we
have thin filaments only with no overlap with thick filaments, a lot of light would be able to shine
through. So that’s how I want you to remember the I-band. The second letter in the word light
constitutes only thin filaments attached to a Z-disc. Now let me go a step further, let’s pretend were all
seated in our lab classroom, you all are seated in your chairs and you’re writing your notes on your lab
table. Let’s pretend I asked the whole class to slide over to the middle of the classroom. What would be
the easiest thing to do? Move the tables to the center of the classroom? No, they are anchored in place.
Rather, you all would slide, on your wheeled chairs to the center of the classroom, and that is exactly
what the thin filaments are going to do during muscle contraction. The thin filaments are going to glide
across the thick filaments. In other words, the A-band does not change in length, rather the I-bands will
shorten and even disappear when a muscle is fully contracted. We will go through this process again,
and again, and again…
Filaments
• Thick-myosin
– ATP
– ATPase
• Thin- actin
– Binding site for myosin
– Troponin (Tn)-3 subunits
– Tropomyosin (Tm)- two strands
I now want to spend more time on myofilaments. It is the arrangement of myofilaments, within a
myofibril, within a myofiber, that causes the myofiber to look striated. Let’s start with the thick
filament. Thick filaments are composed of many individual myosin molecules. If you look at the bottom
picture, a myosin molecule looks like a mutated golf club, in other words it looks like it has a long rod
with a single club head, but has mutated to create another club head. So, I like to think of this myosin
molecule as a double headed golf club. On the head of this myosin molecule is a unique enzyme called
ATPase. ATPase, the name tells you what it’s going to do, it is an enzyme that will cleave ATP (Adenosine
Triphosphate). And when it cleaves ATP, it will release an Inorganic phosphate group and ADP, or
Adenosine Diphosphate. Through this action a tremendous amount of energy will be released, and it is
this energy that is going to allow the myosin heads to ratchet or pull the thin filaments across them.
We’ll go through this again. Now I want to focus on thin filaments, shown as the light blue intertwined
strands. Thin filaments actually are created by multiple different molecules. I’m going to talk about
actin, I’m going to talk about troponin, and I’m going to talk about tropomyosin. All three of these
molecules will create a thin filament, if you only have one of them you do not have a full complete thin
filament. You need actin intertwined, you need troponin and you need tropomyosin. You’re going to
learn that tropomyosin and troponin act as regulatory units. In other words they are going to cover the
actin filaments so that the myosin heads cannot bind or engage with them. If the troponin and
tropomyosin (regulatory units) are removed this will expose actin and then the myosin head will be able
to bind with actin and slide the thin filaments towards the center of the sarcomere. That, in a nut shell,
covers contraction.
The sarcomere- functional unit of skeletal muscle
F-actin
 double-stranded helix
 composed of polymerized G-actin
 myosin heads bind to active sites
Tropomyosin


covers active sites
prevents interaction with myosin
Troponin

binds actin
 binds tropomyosin
 binds Ca2+
I now want to continue our discussion on the sarcomere. The far right picture shows one individual
sarcomere bounded by two Z-discs, and you’ll notice that there are thick and thin filaments
interdigitated between each other. I’d like to talk first about the thin filaments. Shown at the end of this
arrow are globular subunits of actin protein, and these globular subunits can link together to form a
filamentous actin molecule shown here at the end of this arrow. You’ll notice that it’s a double stranded
intertwined filamentous actin molecule. Even with this long F-actin filament we still do not have all the
thin filaments put together. Additionally we need troponin and tropomyosin. Troponin is a protein that
binds both actin and tropomyosin. Additionally it binds to Ca+, and this will be an important part of
muscle contraction, which I’ll discuss later. Tropomyosin covers the active sites of actin, the filamentous
actin, then this prevents the interaction with the myosin heads. I now want to talk about myosin. Here is
an individual myosin molecule at the end of this arrow, and when we have a lot of myosin molecules
interacting with each other, with their heads radiating out, then we’ll have a myosin filament, and I’ll
show you this in a little bit. The second arrow is showing an individual myosin molecule. You’ll notice it’s
made of two heavy chains and two light chains, and associated with the head chains are the light
groups. The head of the myosin molecule contains an ATPase enzyme, basically this means that it will
allow ATP to be cleaved and the result will be that the energy released will allow the myosin molecules
to basically ratchet the heads back and forth. I’ll talk more about this later. So let me say it again, you’ll
now notice this third arrow. When we have many myosin molecules associated together with their
heads radiating outward in all directions now we have a thick filament.
Motor Unit: A collection of muscle fibers innervated by a single motor neuron
• All fibers are same type (fast or
Slow) in a given motor unit
• Motor units overlap, which provides
Coordination
• A fiber has a single neuron; a single neuron can innervate many fibers.
• Recruitment of motor units necessary for strong muscle contraction
•
I have taken you through the gross anatomy of a muscle, we have gone from the whole muscle
itself down to collections of muscle fibers called fascicles, to the individual muscle cell called a
fiber, to the long strands of proteins called fibrils, down to the myofilaments that compose a
sarcomere. Now I want to back up and show you this picture in the center of the slide. You’ll
notice that there is a transverse section through the spinal cord, and leaving the spinal cord are
two individual motor neurons. Neurons that innervate muscle are called motor neurons. You’ll
notice that these two motor neurons are innervating individual muscle cells that belong to a
larger muscle. A motor unit is a collection of muscle fibers innervated by a single motor neuron,
and the muscle fibers within this motor unit are generally of the same type. That is, either fast
or slow, and I’ll be discussing motor fiber types in a little bit. Motor units overlap which provides
coordination and we need recruitment of motor units in order to generate a strong muscle
contraction. In other words, if you were to pick up a piece of paper using your biceps brachii to
flex your forearm to pick up that piece of paper, you would likely only use a few motor units in
order to stimulate contraction in a few muscle cells. But, if you needed to pick up ten bricks,
let’s say, you would need to recruit many more motor units in the biceps brachii muscle. I want
to reiterate that a single muscle cell has only one neuron communicating to it, but a single
neuron can innervate many fibers. How can you think about this? Well, let’s pretend that I am
single neuron, and I am communicating to you all, my class. You are individual muscle cells, you
have only one teacher speaking to you, communicating to you, but I communicate to many
individual muscle cells, and that is basically a motor unit. Shown again, let’s pretend these green
and blue muscle fibers compose a whole entire muscle. We would expect more than one motor
unit, in fact shown here is a single motor neuron communicating with three individual muscle
fibers. A second motor neuron communicates with the remaining muscle fibers, if we wanted
only a gentle contraction, probably only the first neuron would stimulate those first three
muscle fibers, but if we needed a very strong contraction, then both motor units would likely
stimulate their muscle fibers to generate a strong muscle contraction.
The Motor neuron – vesicle formation
•
Synaptic vesicles: are formed from budding Golgi and are
Transported to the terminal by axoplasm “streaming”
(~300,000 per terminal)
• Acetylcholine (ACh) is formed in the cytoplasm and is
Transported into the vesicles (~10,000 per)
Terminal bouton
“Synaptic terminus”
Will synapse with motor end plate to create a NMJ
I now would like to talk about the motor neuron itself; this picture represents a single neuronal cell that
innervates muscle. In other words, it is a motor neuron. On the left side of the picture you see the soma,
or the cell body. You’ll notice in the soma, or cell body, that there is a filled in blue circle, and this
represents the nucleus, where gene transcription occurs. You’ll also notice that next to the nucleus are
several oval shaped structures, this represents the endoplasmic reticulum and Golgi apparatus. You’ll
also notice several circle shapes emerging from the Golgi apparatus, this represents the synaptic
vesicles. On the right side of the picture you see the terminal bouton, also sometimes called the synaptic
terminus, filled with many vesicles and the red dots represent Acetylcholine (ACh). Now let me tell you
what happens…Synaptic vesicles bud off of the Golgi apparatus and transfer down to the terminal
bouton by “axoplasm” streaming. Once in the terminal bouton, Acetylcholine molecules,
neurotransmitter, are packaged within the synaptic vesicles. When an appropriate signal comes through
the neuron, the synaptic vesicles will actually fuse with the terminal bouton membrane shown right
now. Once this fusion occurs, the Acetylcholine can now diffuse into the synaptic cleft. The
Acetylcholine is the chemical trigger that can bind to a receptor on a downstream cell.
Neuromuscular Transmission
• Specialized synapse between a motor neuron and a
Muscle fiber
•
Occurs at a structure on the muscle fiber called the motor
End plate (usually only one per fiber)
Let’s stop and review. Here we see a picture of a motor neuron communicating with a single muscle
cell. This functional contact is called a neuromuscular junction or (NMJ). A neuromuscular junction
consists of five things: The neural cell membrane, the synaptic vesicles within the terminal bouton of
the neuron, the synaptic cleft, the muscle cell membrane, and the receptors within the muscle cell
membrane. It is this contact that allows a neuron to release a chemical signal, or neurotransmitter, on
the muscle cell membrane. The part of the muscle cell that is in contact with the neuron is called the
motor end plate. A motor end plate consists of the muscle cell membrane, plus the Acetylcholine
receptors expressed there.
Neuromuscular Junction (NMJ)
Synaptic trough: invagination in the motor endplate membrane
• Synaptic cleft:
 20-30 nm wide
 contains large quantities of acetylcholinesterase (AChE)
•
Subneural clefts:
 increase the surface area of the post-synaptic membrane
 Ach gated channels at tops
 Voltage gated Na+ channel in bottom half
Here is a picture of a neuromuscular junction. We see the yellow terminal bouton, or synaptic terminus,
communicating with the motor end plate. Where the motor endplate invaginates is called the synaptic
trough. The space between the terminal bouton of the neuron, and the muscle cell membrane is called
the synaptic cleft. And you can see that subneural clefts within the motor end plate are simply more
invaginations of the muscle cell membrane. Their purpose is to increase the surface area of the motor
end plate- this means more space to express the Ach receptors. At the top of the subneural clefts we
would find Ach ligand operated receptors and at the bottom of the subneural clefts we would find
voltage operated sodium channels.
ACh Release - details
•
ACh receptors located at top of subneural cleft.
• Mostly nicotinic but muscarinic ACh receptors are there, too!
•
Voltage gated Na+ channels in bottom half of subneural cleft.
Let’s do it again…this picture is showing you an up close version of a motor neuron communicating with
a single muscle cell. The yellow motor neuron is releasing Acetylcholine into the synaptic cleft. The
Acetylcholine is depicted here as blue dots. The Acetylcholine diffuses across the synaptic cleft to bind
to Acetylcholine receptors found embedded within the muscle cell membrane. You’ll notice that the
muscle cell membrane has many smaller invaginations called subneural clefts. At the top of the
subneural cleft you would find Acetylcholine receptors. The types of Acetylcholine receptors found here
are mostly nicotinic, but there are a few muscarinic Acetylcholine receptors too. The difference between
these two receptors will be covered extensively during lecture. When Acetylcholine is released by the
motor neuron it diffuses across the synaptic cleft and binds to Acetylcholine receptors found embedded
in the muscle cell membrane. This leads to a gated channel being opened and this now permits Na+ to
enter the muscle cell. As Na+ enters the muscle cell the membrane potential in this muscle cell will
begin to rise. When the membrane potential rises enough this will trigger voltage gated Na+ channels to
also open. When voltage gated Na+ channels open, then more Na+ is allowed to enter the muscle cell.
Let’s go over this again, this time focusing only on the synaptic terminus of a motor neuron. Shown here
in blue is an outline drawing of the terminal bouton of a motor neuron. The green circles represent
synaptic vesicles filled with Ach. As an action potential travels down the axon, this causes the synaptic
vesicles to fuse with the neuron cell membrane. The synaptic vesicles then exocytose the Ach into the
synaptic cleft and the Ach can now diffuse across the neuromuscular junction to bind to Ach receptors
on the muscle cell.
Now it’s time to review the triad. Remember in our previous ppt segment I described a triad as a Ttubule, the invagination of the cell membrane, surrounded by the swollen ends of the sarcoplasmic
reticulum. These swollen ends are called terminal cisternae. Connecting the surface of the muscle cell
membrane with the terminal cisternae is a voltage sensor. When the action potential spreads down the
T-tubule, this will trigger the opening of voltage operated calcium channels on the surface of the
terminal cisternae. The end result will be calcium leaving the sarcoplasmic reticulum to enter the
sarcoplasm. This phase of muscle contraction is called Excitation-Contraction coupling.
Now it’s time to review the triad. Remember in our previous ppt segment I described a triad as a Ttubule, the invagination of the cell membrane, surrounded by the swollen ends of the sarcoplasmic
reticulum. These swollen ends are called terminal cisternae. Connecting the surface of the muscle cell
membrane with the terminal cisternae is a voltage sensor. When the action potential spreads down the
T-tubule, this will trigger the opening of voltage operated calcium channels on the surface of the
terminal cisternae. The end result will be calcium leaving the sarcoplasmic reticulum to enter the
sarcoplasm. This phase of muscle contraction is called Excitation-Contraction coupling.
In this picture, you see a T-tubule. On the right side you see a terminal cisternae attached to the ttubule by voltage sensors. The green box structure above the terminal cisternae represents a
sarcomere. The green lines representing the thin filaments and the black bar representing the thick
filament. So, let’s view excitation contraction coupling. First, an action potential travels down the Ttubule (this means that the voltage operated sodium channels are opening and the inside of the cell is
becoming less negative. This triggers the opening of calcium voltage operated channels on the Terminal
cisternae, the calcium inside is released and the calcium can now lead to the thin filaments sliding across
the thick filament (see the sarcomere shorten). Meanwhile, a Calcium-ATPase is using active transport
to pump the cytosolic calcium back into the Sarcoplasmic reticulum to terminate contraction (see the
sarcomere relax).
Perhaps you need to go through the events again. Shown here is a single muscle cell with 6 myofibrils
inside. On the right side of the picture you see 2 transverse tubules surrounded by the terminal
cisternae of the sarcoplasmic reticulum.
First let’s cover the excitation phase of muscle contraction- a motor neuron will release acetylcholine
into the synaptic cleft of the neuromuscular junction. The Ach diffuses to Ach receptors expressed on
the muscle cell membrane at the top of subneural clefts. Binding of Ach opens these ligand operated
channels, and sodium diffuses into the cell and the influx of positive charges means the inside of the cell
becomes less negative. This causes voltage operated sodium channels at the bottom of a subneural
cleft to open, furthering the influx of sodium and leading to an action potential. This action potential
sweeps down T-tubules. As it does so, this triggers voltage operated calcium channels on the surface of
the terminal cisternae to open—this marks the beginning of the excitation contraction phase. As
calcium channels open, the calcium levels within the cytoplasm rise and will lead to the final phase of
muscle contraction.
Let’s do it again, but now add on the contraction phase in more detail. First let’s cover the excitation
phase of muscle contraction- a motor neuron will release acetylcholine into the synaptic cleft of the
neuromuscular junction. The Ach diffuses to Ach receptors expressed on the muscle cell membrane at
the top of subneural clefts. Binding of Ach opens these ligand operated channels, and sodium diffuses
into the cell and the influx of positive charges means the inside of the cell becomes less negative. This
causes voltage operated sodium channels at the bottom of a subneural cleft to open, furthering the
influx of sodium and leading to an action potential. This action potential sweeps down T-tubules. As it
does so, this triggers voltage operated calcium channels on the surface of the terminal cisternae to
open—this marks the beginning of the excitation contraction phase. As calcium channels open, the
calcium levels within the cytoplasm rise and will lead to the final phase of muscle contraction.
The calcium within the cytoplasm can now bind to troponin—you’ll remember that this protein is part of
the thin filament and binds to both actin and tropomyosin. When troponin binds calcium, this causes a
conformational change in tropomyosin so that it can no longer block actin’s binding sites. A myosin
head is already cocked in a high energy conformation so that when actin is exposed, it swings its heads
up and binds to actin. The heads of myosin now swivel and pull the thin filaments across the thick
filament. This is called the ‘power stroke.” At the end of the power stroke, a new ATP molecule binds to
myosin and myosin detaches from actin. The myosin ATPase will cleave the ATP and the energy
released will cause the myosin head to re-cock (much like setting up a catapult to hurl a large boulder).
This cycle of cocking, binding, power-stroke, slumping and re-cocking occurs over and over as long as the
neuron continues to excite the muscle cell, and calcium is in the cytoplasm to keep tropomyosin off
actin. As the thin filaments are pulled toward the center of the sarcomere, the I bands narrow and may
even disappear.
You will do this story over again in our next segment, and you will also see a video on skeletal muscle
contraction during lab.
I would like to go over the steps of contraction. Again, when the sarcoplasmic reticulum releases
calcium, the calcium diffuses and binds with troponin. When troponin binds calcium, this causes a
conformational change in tropomyosin so that it can no longer block actin’s binding sites for myosin
cross-bridges. Let’s start at step four on the left of this picture. The myosin heads are already cocked in
a high energy conformation so that when actin is exposed, it swings its heads up and binds to actin—
shown in step one. The heads of myosin now swivel and pull the thin filaments across the thick
filament. This is called the ‘power stroke” shown in step 2. At the end of the powerstroke, the myosin
heads bind a new ATP and as they do so, they detach or “slump”, shown in step three. The myosin
ATPase will cleave the ATP and the energy released will cause the myosin head to re-cock. This cycle of
cocking, binding, power-stroke, slumping and re-cocking occurs over and over as long as the neuron
continues to excite the muscle cell, and calcium is in the cytoplasm to keep tropomyosin off actin. As
the thin filaments are pulled toward the center of the sarcomere (called the M line), the I bands narrow
and may even disappear.
You will do this story over again in our next segment, and you will also see a video on skeletal muscle
contraction during lab.
On the previous slide, you viewed a close up picture of the thin and thick filaments and their interactions
during contraction. This slide is showing you what the sarcomere is doing during contraction. The
shortening of the sarcomere shown at the bottom of this slide is due to the sliding action of
interdigitating actin and myosin filaments.
Looked at the relaxed sarcomere first: notice the length of the A band. The A band consists of the thick
filaments plus a portion of the thin filaments, where they overlap. The I band consists only of thin
filaments that are found on either side of the Z-disk. The H zone consists of only the thick filamentsnotice NO interdigitating thin filaments are found here.
In the contracted state, the thin filaments have been pulled toward the center of the sarcomere, and the
I bands have narrowed and the H zone has almost disappeared.
Muscle Relaxation
• Removal of Ach by AChE
• Electrical impulse from neuron must cease
• Calcium must be removed by pumps
– Active process vs. channel (passive)
In order to relax the muscle and have the muscle return to its original length, the acetylcholine in the
synaptic cleft must be destroyed by acetylcholine esterase. Additionally, the neuron that released the
acetylcholine needs to stop firing action potentials and stop releasing the acetylcholine. Next, the
calcium in the cytoplasm of the muscle cell must be re-sequestered within the sarcoplasmic reticulum.
This requires the calcium ATPase- a protein pump in the sarcoplasmic reticulum that uses ATP in order
to move calcium from the cytosol into the S.R.
 There are two primary categories of muscle fiber types: slow red or fast white. First notice that
if we triggered a slow red muscle fiber to contract, no matter how many times we stimulated it,
it would maintain the same force in contraction over time. In contrast, shown here in blue, if we
stimulated fast white muscle fibers, over time the white muscle fibers would fatigue and
generate a less forceful contraction—shown here as a decline in contraction force. Slow red
fibers are also called “oxidative” because they rely on oxidative phosphorylation to generate
most of their ATP. In order to do this, they must have many mitochondria, have a rich blood
supply (capillary density), and a lot of myoglobin. Myoglobin is a protein within muscle fibers
that binds and stores oxygen. Plus, these fibers tend to be small in diameter and have slow
cross-bridge cycling.
 In contrast, fast, white fibers are called glycolytic. They are usually large in diameter because
these cells have accumulated a lot of cytoplasmic proteins involved in glycolysis. They also lack
robust myoglobin, capillary beds and mitochondria. Because glycolysis doesn’t generate a lot of
ATP, this means that over time, the muscle cells will loose their ability to sustain a forceful
contraction.
In animals the relative proportions of fibres that are type I can be altered by exercise regimes. There is
little evidence of this in man.
Lets summarize the difference between fast, glycolytic, white fibers and slow, oxidative, red fibers. First
lets address their fiber size, slow red fibers are smaller in diameter, and fast white are larger in
diameter. Slow red fibers are called oxidative fibers because they primarily generate ATP through a
process that is aerobic. In other words they use oxidative phosphorylation. In order to do this, they must
have a continuous supply of oxygen. There blood supply is very robust and they also have a high amount
of myoglobin, the protein within a muscle cell that can bind and store oxygen. Fast white
fibers,however, are considered anaerobic. They generate ATP through an anaerobic process called
glycolysis. They, therefore, have a less robust blood supply and a lower amount of myoglobin. The rate
at which the myosin ATPase, found on the myosin heads cycles between a cocking and recocking state,
also varies between the two muscle fiber types. Fast white means that this rate of cycling occurs very
quickly compared to the slow red fiber type. Examples of these types of fibers can be found in your own
body, the muscle right now in your erector spinae muscle group are primarily of the slow oxidative, red
fiber type. They can sustain a long contraction over time, keeping you seated in your chair. However, I’m
sure you have experienced during an exam, perhaps when you are writing an essay, times when the
muscles in your hands became fatigued. Perhaps you put down your pencil and shaked out your hand a
bit. Your intrinsic hand muscles, in fact, are composed of primarily fast white glycolytic fibers. A new
study has suggest that when a gene called PGC-1beta was expressed in mouse muscle, the muscle fibers
were converted to an intermediate type. Fast fibers that are resistant to fatigue are sometimes called
intermediate. These mice ran 25% longer and covered 45% more distance on a treadmill compared to
litter mates that did not express this gene.
Students often ask how our muscles use energy sources when they are exercised. OK, let’s play: let’s say
you have just stepped onto the treadmill at the gym. You start to run. There is a finite amount of ATP in
your muscle cells. As you exercise, you quickly consume it. As you use the ATP already in the cell to
cycle your myosin heads, there is an enzyme called creating phosphatase that takes creatine phosphate
and removes the phosphate group and transfers the phosphate group to ADP to create new ATP.
However, the activity level of this enzyme only lasts a few seconds. You are still running….now what will
you use to generate ATP? Next in line is the breakdown of glucose already in your muscle cell. Glucose
can be anaerobically metabolised which generates very little ATP or aerobically metabolized. If you are
running fast, and not breathing well, your glucose stores will be metabolized anaerobically and this
means small amounts of ATP are generated and lactic acid will be created. The lactic acid causes your
muscles to fatigue and you will also feel discomfort or soreness as the levels build. You will ultimately
stop running. However, if you are breathing well, the oxygen levels will allow you to metabolize glucose,
fatty acids, and even amino acids delivered to your muscle cells via the blood stream. Aerobic
respiration means you are able to fully oxidize these metabolites and generate ATP.
So in summary, as you run, you use your creatine phosphate supplies first, then your muscle glucose and
glycogen stores- these supplies can last for up to 20-30 minutes, and then you switch to fatty acid
oxidation for ATP. It takes about 30-40 minutes of exercise at about 40-80% intensity to start to burn
fat.
In your physioEx skeletal muscle physiology lab, you will experiment with force summation. In other
words, you will learn the ways muscle cell fibers can summate their contractions to generate a more
forceful contraction. There are two ways of doing this: 1) More motor units can be recruited.
Remember, a motor unit is a single motor neuron and the individual muscle cells it innervates. A whole
muscle has many motor units. Lets pretend you are picking up a piece of paper- how many motor units
would contract in the biceps brachii muscle? Now, lets say you are going to pick up 10 bricks, now how
many motor units would be contracted? The answer is many more! This means that more muscle fibers
are shortening and overall the entire muscle is generating a more forceful contraction.
The other way a whole muscle can generate a more vigorous contraction is if the muscle cell is
stimulated repeatedly. With every stimulus, more calcium is dumped into the cytoplasm. More calcium
means more removal of tropomyosin’s inhibition on actin and more interaction of myosin with actin.
More interaction or power-stroking with actin, means more contraction. It also means, the Calcium
ATPase will take longer to remove the calcium from the cytosol to re-sequester it in the sarcoplasmic
reticulum. Eventually, these contractions will lead to fused tetany, that means the whole muscle can
not shorten any more…it has reached its maximum contraction.
Let’s go over the frequency summation again. In red, you see cytoplasmic calcium levels. In black you
see the force generated by the muscle. In green, you see an action potential generated in the skeletal
muscle. With every Action potential, more calcium is dumped into the cytoplasm. More calcium means
more removal of tropomyosin’s inhibition on actin and more interaction of myosin with actin. More
interaction or power-stroking with actin, means more contraction. It also means, the Calcium ATPase
will take longer to remove the calcium from the cytosol to re-sequester it in the sarcoplasmic reticulum.
If another action potential arrives before the calcium has been re-sequestered, then that means even
more calcium is now in the cytosol and more contraction results. Eventually, these contractions will
lead to fused tetany, that means the whole muscle can not shorten any more…it has reached its
maximum contraction.
Students often ask how they can get more muscle mass. When you go to the gym, your increase in
muscle mass occurs due to hypertrophy. This means that the number of myofibrils and myofilaments
increases. So, the girth of existing muscle cells increases. As we age, there is less opportunity for
hyperplasia. This means that muscle cells undergo mitosis to generate new daughter cells. The
immature cells that can divide to generate new muscle cells are called myoblasts. Again, as we age, the
number of myoblasts decline. The evidence that endurance training can stimulate myoblasts to divide
and generate new muscles cells is not robust, but there are some articles out there that describes this
event. I had a friend in graduate school who was studying myoblast activity, and she was able to show
that in young mice that suffered muscle injury their myoblasts could generate new muscle tissue, but
this declined as the mouse aged, due to a decline in myoblast cells.
It’s sad, but if you don’t use it, you will lose it—at least when it comes to muscle mass. You can train at
the gym and gain nice muscle tone, but if you stop training, your muscle mass will atrophy through loss
of myofibrils and myofilaments in as little as 2 weeks. If you really choose to live a sedentary lifestyle,
the number of muscle fibers may decline and you already learned from the previous slide how difficult it
is to gain those fibers back, through myoblast activity.
The next few slides are a review of the CNS and PNS. First, remember that the CNS is composed of only
brain and spinal cord. Any nerve or neuron cell body found outside the brain or spinal cord, is
considered part of the peripheral nervous system. The spinal cord is really a “go-between” the brain
and the peripheral nervous system. It’s job is to conduct or relay sensory information from the body to
the brain. Additionally, it sends messages from the brain to the body. What are these messages, how
are they conveyed? Through action potentials In this segment, you will also learn about spinal reflexesthis basically means that sensory information from the body is quickly replied with an outgoing message,
or action potential, that originated from the spinal cord. In other words, the brain really didn’t initiate
the action potential.
In this picture you see a cross section through the spinal cord. The blue axons in the picture are the
axons that are attached to neuron cell bodies located in a dorsal root ganglion. These axons transmit
action potentials toward the CNS and are therefore called “afferent” or sensory action potentials. The
red axons in the picture came from neuron cell bodies in the ventral horn of the spinal cord gray matter.
These carry action potentials away from the CNS to effector cells and so they are called efferent or
motor action potentials. Remember in class, I spoke about the effector cells of the body as: smooth
muscle, cardiac muscle, skeletal muscle, glands, and now we add on adipose tissue. In this picture, we
see our efferent axon, or fiber, terminating on skeletal muscle. So, this neuron is called a motor neuron.
Now look at the right side of the picture. Notice where the blue and the red axons are bundled together
in a nerve. Nerves are a collection of axons OUTSIDE of the CNS. We say spinal nerves are “mixed”
because they contain both afferent or sensory, and efferent, or motor, axons. What then would be the
axons within the CNS shown here in purple? These bundles of axons within the CNS are called tracts.
Find the structure labeled sensory ganglion on the right side of the screen. This is really called the
“dorsal root ganglion.” A collection of cell bodies outside of the CNS is called a ganglion. A collection of
cell bodies within the CNS is called a nucleus (or nuclei for plural).
Is this material new to you? It shouldn’t be! If it is, I recommend you read the nervous system
supplements that are uploaded on Blackboard for you. Read them, and as always, come to your
instructor during office hours for help.
Now lets review two important parts of the cerebral cortex. Remind your self that the cerebral cortex is
a thin outer layer of neurons. Within the cerebral cortex, we often find neurons that perform similar
jobs. For example: Shown here in blue is the precentral gyrus. The neurons found within this gyrus
create the primary motor cortex. This means this part of the brain is responsible for generating the
initial command for voluntary movement. In the brown area, you see it labeled as the post central
gyrus. The neurons found here create the primary somatosensory cortex. The neurons here are
important for interpreting action potentials into perceived stimuli. What do I mean by that? Let’s play.
Pretend I have used a bone saw to cut off your calvaria, I place that in front of you on the table. Now I
cut through your meninges and your brain is now exposed to me. If I were to take an electrode and
apply an electrical current to one area of your primary somatosensory cortex, I might stimulate some
neurons there and you would report to me the sensation of cold. If I touch another area, you may have
the sensation of a paper cut on your right pinky. That reminds me to tell you, that if I were stimulating
your left primary somatosensory cortex, you would perceive a sensation on your right side of the
body…that is what is meant by contralateral. Similarly, if I were to stimulate the right side of your
primary motor cortex, you might all of a sudden pucker your lips. If I touch another spot, you might
make a fist.
The picture here of the primary motor cortex with pictures of the body drawn next to it is called a
homunculus– it basically means that we have mapped the body parts that correspond to the neurons
within the motor cortex. So, If I touched the lateral side of your primary motor cortex, your face would
likely twitch or move in some way. This same type of body mapping or homunculus has also been done
for the primary somatosensory cortex. The bigger the picture, the more neurons dedicated to serving
that part of the body. For the primary somatosensory cortex, how big do you predict the picture for the
tongue would be? What about your hand? What about your face? What about your back? In order to
answer these questions, ask yourself how sensitive these body parts are. The more sensitive they are,
the bigger the picture for that part on the homunculus.
The spinal nerves are part of the peripheral nervous system, but it is important to remind you that you
also have 12 cranial nerves. These nerves are also peripheral nervous system. CNI is the olfactory nerve
and is sensory only for smell. CNII is the optic nerve and is also sensory only for vision. CN III is called
the oculomotor nerve and is a mixed nerve: it is motor or efferent for 4 skeletal muscles that control
eye movement: medial rectus, inferior oblique, inferior rectus, and superior rectus. It also has
involuntary effector fibers that control the intrinsic muscle near your iris called the ciliary muscle in your
eye. You will learn more about this nerve during your autonomic nervous system lecture. Cranial nerve
4 is called the trochlear nerve and it is a motor/efferent nerve and stimulates the superior obliqueanother extrinsic eye muscle. CN 5 is called the trigeminal nerve and this is a mixed nerve: that means
it has sensory fibers, and motor fibers. Cranial nerve 5 allows you to sense pain or touch on your face
and in your mouth and teeth for example, and controls most muscles of mastication (your chewing
muscles). Cranial nerve 6 is called the abducens nerve and is a motor nerve that controls movement of
the extrinsic eye muscle called the lateral rectus. Cranial nerve 7 is called the facial nerve and is also
mixed: sensory for taste, motor for controlling your facial muscles and the stapedius in the middle ear
(no, you don’t need to know the stapedius for your exam), and it is also the nerve responsible for
releasing salivary secretions from the submandibular and sublingual glands, and also controls your tear
release from your lacrimal gland. CN 8 is purely sensory and is called the vestibulocochlear nerve and
helps with transmitting information on sound waves and orientation of your body in your environment,
in other words your position. CN 9 is called the glossopharyngeal nerve and is also a mixed nerve: it has
motor fibers innervating some swallowing muscles in your throat, it has some involuntary efferent fibers
that innervate your parotid gland and this leads to more salivary secretions, and it also has a sensory
component for taste. Cranial nerve 10 is called the vagus. It, too, is mixed: it has both sensory, motor
and involuntary motor fibers in this very important nerve. It will be talked about extensively during your
autonomic nervous system. CN 10 is the only cranial nerve that extends from your brain all the way to
your thoracic and abdominal cavities! Cranial nerve 11 is called the accessory nerve and it is only
somatic motor- it innervates your sternocleidomastoid muscle and trapezius. Lastly, the hypoglossal
nerve is CN 12 and is motor only as it stimulates the muscles that move the tongue.
Reflexes are rapid, automatic, involuntary reactions of muscles or glands to a stimulus. All reflexes have
similar properties:
1) A stimulus is required to initiate a response to sensory input
2) A rapid response requires that few neurons be involved, and synaptic delay be minimal.
3) An automatic response occurs the same way every time
4) An involuntary response requires no intent or pre-awareness of the reflex activity. Thus, reflexes are
usually not suppressed. Awareness of this stimulus occurs after the reflex action has been completed- in
time to correct or avoid a potentially dangerous situation.
There are five components to a reflex arc, shown at the top part of this picture:
1) Shows you that a stimulus activates a receptor, sensory receptors respond to external and internal
stimuli, such as temperature, pressure, or tactile changes.
2) A nerve impulse travels through sensory neuron to the CNS. Sensory neurons conduct impulses from
the receptor into the spinal chord.
3) You see integration, in other words the information from the nerve impulse is processed in the
integration center by interneuron's. More complex reflexes may use a number of interneuron's within
the CNS to integrate and process incoming sensory information, and transmit information to the motor
neuron. The simplest reflexes do not involve interneuron's rather the sensory neuron synapses directly
on a motor neuron in the anterior grey horn of the spinal chord. I will show you an example of this type
of synapse.
4) A motor neuron transmits a nerve impulse to the effector. The motor neuron transmits a nerve
impulse through the anterior route and spinal nerve to the peripheral effector organ.
5) An effector responds to the nerve impulse from the motor neuron. An effector is a peripheral target
organ that responds to the stimulus from the motor neuron. This response is intended to counter-act or
remove the original stimulus.
Reflex arcs may be ipsilateral or contralateral. A reflex arc is termed ipsilateral when both the receptor
and the effector organs of the reflex are on the same side of the spinal chord. For example an ipsilateral
effect occurs when the muscles in your left arm contract to pull your left hand away from a hot object. A
reflex arc is contralateral when the sensory impulses from a receptor organ cross over through the
spinal chord to activate effector organs in the opposite limb. For example, contralateral effect occurs
when you step on a sharp object with your left foot and then contract the muscles in your right leg to
maintain balance as you withdraw your left leg from the damaging object. Reflexes may also be
monosynaptic or polysynaptic. A monosynaptic reflex is the simplest of all reflexes. The sensory axons
synapse directly on the motor neurons whose axons project the effector. Interneuron's are not involved
in processing this reflex. Polysynaptic reflexes have more complex neural pathways that exhibit a
number of synapses involving interneuron's within the reflex arc. Because this reflex arc has more
components, there is a more prolonged delay between the stimulus and response.
The stretch reflex is a monosynaptic reflex that monitors and regulates skeletal muscle length. Stretch in
a muscle is monitored by a stretch receptor called a muscle spindle. When a stimulus results in the
stretching of a muscle, that muscle reflexively contracts. The patellar, or knee jerk reflex, is a
monosynaptic reflex, that is an example of a stretch reflex. The stimulus, or the tap on the patellar
tendon, initiates the contraction of the quadriceps femoris muscle, and leads to extension of the knee
joint.
Shown here is a picture of a muscle spindle found intertwined among the skeletal muscle cells. I also
invite you to watch the video on the patellar reflex. What I want you to now know is that reflexes can be
an important diagnostic tool. Clinicians use them to test specific muscle groups and specific spinal
nerves or segments of the spinal chord. Although some variation in reflexes is normal, a consistently
abnormal response mat indicate damage to the nervous system or muscles. A reflex response may be
normal, hypoactive, or hyperactive. The term hypoactive reflex means that a reflex response is
diminished or absent. A hypoactive reflex may indicate damage to a segment of the spinal chord, or it
may suggest muscle disease or damage to the neuromuscular junction. A hyperactive reflex refers to an
abnormally strong response, it may indicate damage somewhere in either that brain or the spinal chord
especially if it is accompanied by clonus, rhythmic oscillations between flexion and extension when the
muscle reflex is tested
A withdraw, or flexor reflex is a polysynaptic reflex arc that is initiated by a painful stimulus such as
touching something very hot or someone forcefully grabbing your arm. Stimulation of a receptor organ
causes the transmission of sensory information to the spinal chord. Interneuron’s receive the sensory
information and stimulate motor neurons to direct flexor muscles to contract in response.
Simultaneously, antagonistic muscles are inhibited so that the traumatized body part maybe quickly
withdrawn from the harmful stimulation. On the right side of this screen you see the crossed extensor
variety.Sometimes that painful stimulus elicits a flexor reflex in the effected limb and an extensor reflex
in the opposite limb. This serves to push the body away from the stimulus, also to shift the weight to the
opposite limb
The golgi tendon reflex, prevents skeletal muscles from tensing excessively. Golgi tendon organs are
nerve endings that are located within tendons near a muscle tendon junction shown here. As a muscle
contracts its associated tendon stretches resulting in increased tension in the tendon and activation of
the golgi tendon organ. Nerve impulses in the golgi tendon organ signal interneurons in the spinal chord,
which in turn inhibit the actions of the motor neurons. When the motor neurons are inhibited the
associated muscle is allowed to relax, this protecting the muscle and tendon from excessive tension
damage