so we discussed how calcium is released and what it does once it's released into the sarcoplasm so we're going to discuss a little bit about how contractions happen and this is called the sliding filament theory or a lot of people call it the sliding filament mechanism so we have to remember that when contractions occur it's shortening of the muscle now the sliding filament theory is going to explain to us how this occurs so in this picture we're seeing two sarir on the top we also notice that we have the a band The I band and the hzone labeled remember the a band is the entire length of thick filaments the hzone is just thick filaments and the I band is just thin filaments then we have that area of overlap where we can see that actin and mein overlap each other or Thin and Thick filaments overlap each other so this first picture is a relaxed muscle now I want you to look at this picture and calcium's been released and myosin has attached to actin the head has swiveled and it's moved actin towards the mline when you looking at this picture when actin gets moved towards the mline that means we're taking away some of the are of just thick filament and we're increasing the zone of overlap so we can see that the H Zone the area of just thick filament gets smaller we're also pulling thin filaments towards the mline so the area of just thin filaments the ey band gets smaller but the thick filaments are not moving at all in the sense that they're not getting smaller because all the heads are doing is swiveling back and forth so the thick filaments actually never change position so the a band's going to remain the same so this is just a partially contracted muscle now in a fully contracted muscle what we'll see is that the hzone which is area of just th thick filaments is no longer existent the area of just thin filaments the iband is no longer in existence but the a band is the entire length of thick filaments and that remains intact because the thick filaments don't change their shape they're not losing any area so what this is telling us is that the sliding filament theory states that when muscles contract everything shortens except for thick and thin filaments so in the sliding filament theory the muscle shortens the facles shorten the muscle cell shortens s arir shorten but mein and actin never shorten they just slide past each other so if you're looking at this picture again actin never changes its length it just slides past the thick filaments so we're never changing Acton's length and we're never changing mein's length masin just pulls Acton towards the mline so they slide over each other now how does this occur well if we go back we can talk about the steps leading up to it an action potential will come down the sarcolemma down into the T tubules those T tubules are going to actually come into contact with the terminal systems of the SR on the terminal systs are calcium Gates that when excited will open they get excited from the AP when they open calcium is going to rush from the SR to the sarcoplasm once calcium's in the piroplasm calcium is g to go find its lover which is troponin when calcium binds to troponin troponin changes shapes pulls tropomyosin with it and exposes the mein binding sites this allows mein now to bind to actin so here the mein binding sites are covered because there's no calcium present here calcium's present so troponin moved trip myosin out of the way and now mein can bind to act in once mein binds to Acton this head will swivel and it's going to pull the thin filaments towards the mline the thin filaments never change length neither do the thick the only thing that happens is they slide past each other hence the sliding filament theory or mechanism now for this to happen it's actually going to be a series of repeated steps we call the contraction cycle and for the contraction cycle to occur what we're going to see is a repeated series of steps that pulls thin filaments towards the mline and as they get pulled towards the mline they just slide right past over the thick filaments so Thin and Thick filaments never change length they just slide over each other shortening the sarcomere which shortens the myop fibral which shortens the muscle cell shortens the facies and shortens the muscle everything shortens except for meas and and acting they just slide past each other now the series of steps the contraction cycle is a series of four repeated steps the first step we've already talked about mein cannot bind to actin until we have energy stored in its head for swiveling so the first step is called ATP hydrolysis this is where we're going to take ATP we're going to break it down into ADP and phosphate and we're going to store that energy in the mein head when energy is stored in the mein head it's considered to be a high energy State now once this energy is stored in the head M has the capabilities of flexing or swiveling but until it attaches the actin it doesn't need to flex or swivel so that energy is just store so the first step is break down that ATP as soon as calcium is available able we're going to be able to expose these mein binding sites which leads us to the Second Step mein attaches to act in this step is called crossbridge so ATP is broken down energy stored in the myosin head we have a high energy State head as soon as calcium's available the mein binding sites will open on actin and mein will attach to actin and this is called crossbridge as soon as myosin's attached to actin the mein head will Flex or swivel and what this means is it's pulling actin towards the mline at this point the mein has used the energy in its head and now it's considered a low State molecule so it's low energy but one swivel of aasin head is only going to be a partial contraction so we're going to want to be able to fully contract well to do this we need to re-energize mein's head well the only time myosin is going to let go of actin is if ATP is available so for us to re-energize mein's head it needs to detach from actin and it will only do that if ATP is present now as soon as ATP is attached to mein what do you think mein's going to do if you said break down act ATP you're correct as soon as that ATP molecule is available mein head breaks it down stores the energy in its head now considered to be in a high energy state it will bind to actin it will swivel called the power stroke pulling AC in towards the mline but again maybe not fully contracted yet so it's going to detach again but it will only detach of atps available if ATP is available it's going to break down ATP hence where we get the cycle ATP hydrolysis attachment through cross Bridges Power Stroke basically the head flexes pull acting towards the mline we detach as long as ATP is available we break down the ATP and we start over again as long as we have ATP and we have calcium this process is repetitive it can theoretically go on forever so we know that our muscles don't contract constantly So eventually we know we're going to want to relax now there's one problem for us to relax Max there has to be something we get rid of so are we going to be getting rid of ATP are we going to be getting rid of calcium which is our limiting factor well our limiting factor is going to be calcium that's what we need to get rid of so if we look in this picture right here we see that we have an action potential down the sarcolemma into the T tubules those T tubules are going to communicate with to terminal systemns it's going to cause gates to open calcium rushes out binds to troponin moves tropomyosin out of the way so mein can contract well we need ATP for contraction so what we're learn is that we're also going to need ATP for relaxation we need to get rid of that calcium where did calcium come from calcium came from the SR so we need to put it back in there the problem is calcium is so abundant in the SR it's overcrowding and it's not going to want to go back in there on its own imagine yourself in a classroom with 200 people but outside of the classroom is just wide open spaces if we Tred to stuff another 100 people in that same classroom it would be very uncomfortable so as soon as people started exiting the classroom they wouldn't want to go back in well that's how calcium feels about the SR the SR has so much calcium in it that even when calcium is released there's still tons left so the calcium needs to be put back in there so it needs to go back to an area of high concentration so that's against its concentration gradient so remember diffusion is movement from high to low that's passive we need to do something active we need to shove that calcium back in there so what you'll see is you'll see these little X's these little pin wheel X's are calcium active transport pump now notice it is saying that it is calcium active transport pumps ATP active transport pumps use ATP to work we have to have ATP available to make these pumps Force calcium back into the Sr so ATP cannot be our limiting factor we have to have ATP for not only contraction but also for relaxation now once we get that calcium out of the piroplasm back into the SR our troponin is going to change back to its original shape pulling tropomyosin back over The Binding SES if the meas and binding sites aren't available can meas and bind to actin anymore the answer is no if it can't bind to actin then the muscle will be relaxed so our limiting factor is not as much ATP I mean it's not as much ATP but it's calcium we need to get rid of calcium now because these active transport pumps can only put so much calcium back in without it leaking out too much we have a second way that we hold calcium in the SR so use your imagination a little bit with this picture okay these green structures are your Sr where calcium is stored basically this is the terminal sstn of the SR and we can see that it's budding right up to the T tubules where APS will come down so Action potentials will travel down this T tubule causing gates to open right here these are Gates when the gates open calcium will exit into the sarcoplasm but when we're ready to relax we need to get that calcium back into the SR so to do that we will be using calcium active transport pumps these active transport pumps will be using a to to shove calcium back in but the calcium is going to leak out a little bit so we also will be using a protein called calques I like to think of calques as a magnet basically calsequestrin is a protein that sequesters calcium it helps calcium stay put in the SR so when we want the muscle to relax we actively use energy to shove calcium back into the SR and the calcium is staying put because of the protein Cal sequest so we have a double method once calcium is back into the SR that means troponin no longer has this lover so it's going to change back shapes pulling tropomyosin back over the mein binding sites and mein can no longer bind if mein can't attach the actin then it can't pull in towards the mline causing relaxation