now that we're familiar with the basic anatomy of a human skeletal muscle fiber and we've also seen what happens at the neuromuscular Junction we can see what happens within the muscle fiber once it's stimulated so let's go back to our inside our sarcomere where we can see a thick filament made up of our myosin molecules our thin filaments made up of actin they're wound around by the tropomyosin the tropomyosin as we know is held in place by the troponin molecule we know that the myosin heads will want to interact with the actin but of course during the resting state the muscle was not active and so the troponin is holding the tropomyosin gate closed so that the active sites on the actin are covered and therefore these myosin hands cannot interact with them so here once again our purple tropomyosin gate is covering the active sites and it's being held in place by the troponin so what happens when we have an action potential well we've seen the events of the neuromuscular Junction we have our action potential propagates down our motor neuron it releases acetylcholine at the neuromuscular Junction here the siedel choline diffuses across the synaptic cleft open sodium channels on the motor endplate of the sarcolemma causing the rapid influx of sodium and this is what's going to initiate the action potential within the muscle fiber so that action potential will be propagated along the sarcolemma and as it propagates along the sarcolemma that action potential will be brought deep into the interior of the cell by the transverse tubules also news the t tubules which are basically indentions of the sarcolemma or that excitable membrane into the cell and we know that the transverse tool is have a nice arrangement with our sarcoplasmic reticulum so that they are making these junctions called triads around a transverse tubules so we have our terminal cisternae here at which we know Artful kau calcium is the key as we know so what does the action potential do once it's propagated across the membrane and then down into two cell well it's going to cause the release of calcium from the terminal cisternae and as we've noted the terminal cisternae are located strategically over our zones of overlap in our Sarco mirror which is underneath here so if we zoom in a little bit and look at the events within the sarcomere between the thick and thin filaments once that calcium is released from the sarcoplasmic reticulum what's going to happen is that the calcium will come and bind with the troponin molecule and that's like unlocking it so here we have our tropomyosin molecule that is covering our actin filaments right here so that our myosin heads cannot interact with it the troponin is like the lock that's holding the gate in place but if since calcium comes in and diseases out of the sarcoplasmic reticulum into the sarcoplasm then what happens is calcium can now bind with this thing and it acts with a key as a key and the troponin is then like a lock and so it changes its shape and now the tropomyosin can rotate and look at what happens here the tropomyosin has now rotated into a different position and now we can see the active sites on the globular actin here so now we see our active sites revealed and now we see that our myosin hands can interact with it so what they do they form cross bridges and then we'll form a cross bridge and they will grab onto this thing and then they will pivot just like a ratchet and pivot towards the mine and that will pull this these actin filaments towards the in line in this case it's pulling in this direction so it's going to pull the actin filament in this direction and then it's going to release it and it's going to start the cycle all over again and as long as we have calcium bound to troponin and the active sites are revealed then these myosin heads will continue the cycle of cross bridging releasing and cocking itself back out for use again now here's another important thing that we need to notice adenosine triphosphate is our high energy molecule and this is very important without ATP without calcium we cannot make this cross bridge cycle so we cannot have this sliding of the actin over the - and if there's no calcium that there's no ATP because obviously we need the calcium to act as the key to keep the troponin unlocked as it were and the tropomyosin gate rolled open so the active sites are revealed so calcium is key for that ATP is the energy molecule it allows all this to happen so in order to get into this content ready position the myosin hands have to break ATP so they use it as an enzyme or they actually are the enzyme the myosin hands are the enzyme and they use ATP to into the ready position and when they do this then they are ready to grab on to the active sites on their reveal so when it breaks the ATP if you remember ATP is adenosine triphosphate so it's a nucleotide with 3 phosphates attached and the third phosphate is the high-energy phosphate that when you break that bond heõs the energy so what happens is these myosin heads will take that ATP and they will break it and what they're left with is adenosine diphosphate that's adenosine with two phosphate groups still attached and this lone phosphate group that they broke off for the energy now notice that they hold on to this and so they're still holding on to it after they've ratcheted themselves out into the ready position and so what happens is during the resting state they're already ready to go so before the muscles that were stimulated they myosin heads are in the cocked and ready position because in the previous contraction cycle they bound ATP and they broke it and then they ratcheted back out or caught themselves into the ready but once the tropomyosin covers the active sites well then they're not going to interact with it but they're ready to go for the next contraction cycle so when the muscle is stimulated again and the active sites on actin are revealed and they can interact with it notice they still have the adenosine diphosphate and phosphate bound to it once they have made the cross bridge with the actin now they have to pivot and to do that they have to drop the ADP and phosphate so when they pivot they drop the ADP and phosphate but now they're actually stuck to the active sites and they can't let go until ATP binds with them so adenosine triphosphate must bind with the myosin heads in order to get them to let go of the active sites now once the ATP is bound within the myosin head can let go but notice it's still in the pivoted forward position so therefore the myosin heads will break that ATP to Ratchet back out into the ready and cut position and so that is the cycle of cross project and how the myosin heads will interact with the active sites on the actin filament and so long as the active sites are uncovered so long as we have calcium and adenosine triphosphate present in the muscle then this cycle of cross bridging will continue and as long as the cyclocross bridging continues then the muscle fiber will shorten because we have these myosin heads basically pulling on these actin filaments and of course that is like bringing this Z lines closer to the m1 so if we were to say that this room was a sarcomere and my body is the in line and my arms are like acting like myosin filaments and my hands are the hands and grabbing on to active that's coming from the wall and I'm doing this and doing this over and over and over again basically picking up the actin filament rationing it for each time that's going to draw the line at the walls or the Z lines closer to the end line and that's what's going to cause the shortening of the Sur communication so that's exactly what we see here we see that the interaction between the myosin thick filaments and the actin filaments and the fact that the myosin is pulling the actin filaments towards the in line that's bringing the Z lines closer to the in line and that is shortening the sarcomere and that is how a muscle contracts