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Muscle Contraction PhysiologyZone Muscular Series with English subtitles   Complain

hello this is Jack from physiology zone

and in this third part on skeletal

muscle we're going to be looking at

muscle contraction so we'll cover two

things in this tutorial the contraction

cycle and therefore the contraction part

of the excitation contraction coupling

that you'll read about in textbooks and

then we're going to finish by looking at

the length tension relationship which is

intimately linked with the contraction

interestingly prior to the mid-1950s it

was a widely held belief that muscles

contracted by folding themselves up and

so they lengthened and shortened by

effectively folding and straightening

process and this was so hard to dispel

because we didn't really have powerful

enough microscopes to actually see what

was actually happening but in 1954 there

were two separate teams of scientists

that unbelievably published a paper on

the same day in the same journal Nature

which proposed a new method on wanting

we had Andrew Huxley and Ralph Nader

Kirk and they used a type of

interference microscope which utilizes

two separate beams of light and in the

second research group we had gene Hanson

and Hugh Huxley who used the electron

microscope to study muscle now

fundamentally what both these teams

showed was the inner contracted and

relaxed state the length of the thick

and thin filaments within a myofibril

remained the same so effectively it was

dispelling that the thick and thin

filaments were folding in anyway and

what was actually happening was that

they were sliding over one another and

this was the responsible factor in

causing contraction the shortening of

our muscles and this fundamental shift

in our understanding of how muscles

contract and relax is known as the

sliding filament theory so that leads us

on to the contraction cycle which

describes the steps by which the

striated muscle so meaning skeletal and

cardiac muscles contract so on screen

you can see a diagram of myosin and

actin on the respective thin and thick


gone over previously so firstly for

clarity let's just go through the

structures that are on screen so here we

have the thin filament with the acting

molecules on them and they have the

myosin binding sites we have troponin

and remember that troponin C is the bit

that we're really concerned with for

contraction and we have the tropomyosin

and remember the troponin tropomyosin

form a complex so we also have the thick

filament and on here we have the myosin

head and tails and we also have proteins

at its base that we've mentioned

previously but they're not particularly

important to detail here and at the top

we also have calcium which you'll

remember from the last tutorial is

released from the sarcoplasmic reticulum

and moves into the sarcoplasm and it's

the movement of the calcium into the

sarcoplasmic which is effectively

represented on here as the white

background that leads to the contraction

cycle beginning and this can be broken

down into five steps so firstly calcium

binds to troponin C and causes a

conformational change that causes

troponin to slide the tropomyosin off of

the binding sites on the actin molecules

secondly we have cross bridge formation

so myosin has adp which is adenosine

diphosphate and P I which is just

meaning an inorganic phosphate that's on

it from a previous contraction cycle so

the the presence of this phosphate group

phosphorylates the myosin head and that

causes a conformational change in its

shape so it attaches to the actin at its

myosin binding sites and thus it forms

our cross bridges next we have the


so this is the bit that causes the

movement and here we get the release of

the ADP and inorganic phosphate from the

myosin head and that causes a another

conformational change so that the the

myosin head actually bends to 45 degrees

and that pulls the actin molecule

towards the center of the sarcomere

which you remember is called the my

the fourth point is that ATP comes and

binds on the myosin heads acting binding

site and it releases the myosin from the

actin and then finally we have ATP

hydrolysis so as well as an ATP binding

site the myosin head also has an ATP

aise enzyme and this hydrolyzes the ATP

to adp and an inorganic phosphate and

that releases the myosin head down and

it puts it into what's sort of a cocked

state so it puts it into a position

where the myosin head is then ready

again to bind to the myosin binding

sites and this process just repeats

itself so long as you have enough ATP

available and the calcium concentration

near the thin filament remains high now

if you pull this out it's easier to see

that what's happening here is that the

myosin is effectively walking its way

along the actin molecule now this occurs

really really fast so there's 500

crossbridges per thick filament which

attach and detach five times a second so

at any one time you've got some myosin

heads that attach to actin and some

generating force others are detached and

others are just ready to begin the

process again so this causes this

walking along the actin molecule pulling

all of that thin filament towards the

center of the sarcomere if you

extrapolate that out to the muscle fiber

you've got lots of sarcomeres lying

parallel to one another in a muscle

fiber so if they all contract the muscle

fiber contracts and obviously we have

many muscle fibers making up an

individual muscle so hence that's why

your muscle contracts so the final bit

is that once the stimulus for the

contraction has ceased then the calcium

moves out of the sarcoplasm and it does

this as follows so there are active

transport pumps on the sarcoplasmic

reticulum and these pumps use ATP which

binds to the pump and is

hydrolyzed to ADP and an inorganic

phosphate and that process causes a

conformational change in the active

transport pumps shape so meaning that

they open once they are open they

literally pump calcium back out of the

sarcoplasm into the sarcoplasmic

reticulum and that returns the low-level

of calcium in the sarcoplasm and as a

quick side note within the sarcoplasmic

reticulum there is a protein that's

called cal sequestering and that binds

up about 20 calcium molecules each and

that's how the sarcoplasmic reticulum

keeps so much calcium ions within it so

if we take this back down to the level

of the thick and thin filaments so we

can see that the reduction in calcium

when it's moved back into the

sarcoplasmic reticulum that causes the

troponin tropomyosin complex to slide

back into the position that it was

resting in originally blocking the

myosin binding sites on actin and thus

preventing further contraction so if you

pull that out to the sarcomere then we

get the relaxation and lengthening of

the actual sarcomeres and intenta T

therefore the muscle fibers going to

lengthen and ultimately our muscle is

going to lengthen and therefore relax

but when a muscle contracts it doesn't

always lengthen and shorten and that's

why I want to talk about now the length

tension relationship the length tension

relationship states that the

forcefulness of the muscle contraction

depends on the length of the sarcomeres

within a muscle before contraction

occurs so just for interest the optimal

length of a sarcomere for maximum muscle

contraction power is about 2 to 2.4

micrometers this is because the overlap

between the actin and myosin molecules

is optimal at this point so there's

enough myosin overlying the actin to

attach and pull it towards the center if

a sarcomere is too stretched then there

is little overlap between the myosin and

actin which therefore means that fewer


Edge's can be formed and that less

tension is developed and equally if a

sarcomere is too short then there is

plenty of overlap between myosin and

actin but the z disks at the end of the

thin filaments crumple the myosin heads

so they can't attach to the actin and

for any of the myosin heads that can

attach to the actin there's just nowhere

to pull the actin because it's blocked

by the z disks so you can effectively

show this process on yourself if you

imagine flexing your wrist that will

decrease the length of the sarcomeres

within the muscle so if you try and make

a fist in the flexed wrist position

you'll find it's very weak if you then

pull your wrist into a neutral position

and make a fist as strong as you can

you'll find it you can produce quite a

lot of force and if you then extend your

wrist all the way as much as you can

that is therefore lengthening the muscle

and therefore lengthening the sarcomeres

you'll find that in that position you're

not as strong as in the neutral position

and all that's showing is that muscle

length is very intimately linked with

the tension that it can develop so

that's everything that I wanted to cover

in this tutorial so just to quickly run

over what we've been through we've

looked at the contraction cycle and seen

how when the calcium arrives it binds to

the troponin and removes that

tropomyosin off of the myosin binding

sites that allows the myosin to flick

over and form its cross bridges we get

the power stroke that pulls the act in

towards the centre of the sarcomere and

then we get ATP that binds and releases

that myosin head and then the ATP a

enzyme then causes hydrolysis of the ATP

molecule forming ADP and inorganic

phosphate and this process keeps

happening so long as there's enough ATP

around and you have enough calcium and

then finally we looked at the length

tension relationship of muscles and we

saw how muscle tension is intimately

linked with the length of the muscle so

thanks for watching this tutorial and

we'll see you in the next one where we

talk about some of the aspects of

metabolism in skeletal muscle

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