okay this video talk about muscle fiber contraction and muscle fibers contracted for coordinated steps it starts with nerve stimulation that leads to the production of an action potential in the sarcolemma this action potential or electrical impulse is propagated or spread along the sarcolemma and then ultimately causes a rise in interest other calcium levels released by the sarcoplasmic reticulum now steps one and two like nerve stimulation and action potential these occur at something called the neuromuscular junction which is the point of communication between nerves and muscle cells now steps three and four are basically those things that link the electrical signal up to contraction and then after step four we get something called excitation contraction coupling where three and four which is the excitation component leads to the production of a contraction which we'll talk about later in this video as well so skeletal muscles are stimulated by somatic motor neurons a somatic motor neuron is basically a nerve cell whose cell body is going to be in the brain or spinal cord but it has a long thread-like extension called an axon that goes away from the brain and spinal cord or central nervous system out towards the skeletal muscle whether it's in your face or neck or somewhere on your trunk or limbs and these axons can divide into many branches as they enter the muscle to stimulate multiple muscle cells or fibers now the axon branches end on a muscle fiber and they form something called the neuromuscular Junction or motor endplate and each muscle fiber has at least one neuromuscular Junction with one motor neuron that way it's able to be stimulated by your nervous system so the axon terminal is the end of the axon or the end of that long filamentous extension of the somatic motor neuron now the axon terminal is separated from the muscle cell by a very very narrow space called the synaptic cleft and within these axon terminals we have basically static vesicles that store a lot of neurotransmitter called acetylcholine and neurotransmitter is a chemical message that's stored in these synaptic vesicles and this specific type of neurotransmitter that your motor neurons use is called acetylcholine acetylcholine is a pretty basic molecule but its purpose is to serve as an electrical or chemical signal that can bridge the electrical signal of a neuron to a muscle now the in foldings of muscle cell membrane the sarcolemma are called junctional folds that contain millions of acetylcholine receptors and these receptors receive the acetylcholine signal as it's released from the synaptic vesicles by the axon terminal in the neuromuscular Junction consists of axon terminals that have synaptic cleft itself and those junctional folds with the acetylcholine receptors on them so they look at in a picture here we can see that filamentous extension called the axon that then branches out and these branches form a point of communication with this muscle cell called the neuromuscular Junction if you zoom in here on the neuromuscular Junction we see it that we have an expanded end of the axon here in gold contains our synaptic vesicles with acetylcholine in it that's a little blue circles I'm sorry with the green circles and you know when the electrical impulse travels down the axon it gets to the end of this nerve terminal axon terminal and the electrical impulse our action potential here shown in kind of this pink or purple line it ultimately triggers the opening of these voltage-gated calcium channels now a voltage-gated channel is one which opens in response to a change in charge or voltage and these voltage-gated calcium channels open when the electrical impulse travels towards the end of the axon here calcium rushes into the cell down its diffusion gradient and then what calcium does is it triggers the eggs of cytosis of these vesicles containing acetylcholine now acetylcholine gets exocytosed into the space here called the synaptic cleft where basically diffuses in this space it has the potential now to bind to receptors on the junctional folds of our muscle cell here remember our muscle cell or motor endplate contains millions of these acetylcholine receptors which can bind with acetyl now these acetylcholine receptors are also called nicotinic receptors and when acetylcholine binds here it's basically a ligand gated ion channel which means that when the ligand or acetylcholine binds this channel it opens up the channel and allows these ions to flow so sodium is able to flow into the muscle cell potassium flows out however there's much more sodium that flows into the muscle cell than potassium that leaves so what happens is we get a lot of this positively charged sodium now rushing into our muscle cell in this little local area of positive charge is one something called the M plate potential an implied potential is a little local area of depolarization or positive charge that has the potential now to put maybe stimulate an action potential or electrical impulse in the muscle cell now to get rid of the stimulus or to get rid of the signal here we have another enzyme called acetylcholinesterase in acetylcholinesterase basically breaks down acetylcholine into you know choline and acetic acid and these are actually recycled by your neurons and then basically made back into acetylcholine but when acetylcholinesterase breaks down ACH these degraded bits can't bind with the receptor so these ligand gated ion channels actually close instead of being open see then you stop getting that currents that may trigger an action potential in the muscle cell so just to summarize of steps step one was action potential goes down the nerve terminal step two is where the voltage-gated calcium channels open up calcium moves down its electrochemical gradient step three was calcium entry causes exocytosis of neurotransmitter containing vesicles step four is when acetylcholine diffuses through synaptic cleft and binds the receptors and the motor endplate step five is when acetylcholine now causes these ligand gated ion channels that open up allowing for sodium to rush into the cell causing implied potential and then step six is basically where acetylcholinesterase can break down the signal acetylcholine into the degraded components like acetic acid and choline and that way you can't you know open up these channels and so that the current stops now we find that is that in the sarcolemma we see there's a separation of charge or polarization which means there's a voltage across the membrane so the inside of the cell is typically more negative with respect to the outside and the action potential is caused by changes in electrical charge distribution across the sarcolemma so it turns out that the generation of an electrical current in the muscle cell occurs in three steps here we have M plate potential which occurs at the neuromuscular Junction and it's due to the current flowing through those leg and gated ion channels or acetylcholine channels or receptors in the steps two and three are parts of the action potential we have depolarization and repolarization now M plate potential is when acetylcholine is released from the motor neuron it binds the receptors in the sarcolemma it causes these chemically gated ion channels to open and allows for sodium to diffuse into the muscle cell or fiber so some potassium diffuses outward but not as much as sodium diffusing inward and this influx of sodium makes the inside of the muscle cell locally right there more positive or less negative omit that's because the charge on sodium is positive so if you're bringing in more positive charges you're gonna make that local area more positive and this results in a local depolarization or a local area of positive charge called M plate potential now if n plate potential is big enough it could stimulate an action potential now these employ potentials are basically a wave of sodium that come through these millions of ligand gated ion channels at the motor endplate and so once the seat of choline binds these channels you get a bunch of sodium now that rushes into the muscle cell and because of diffusion it causes this wave of depolarization or a wave of positively charged sodium that spreads through the inside of the muscle cell now this wave of depolarization moves to the local area of sarcolemma nearby where if it's strong enough it may actually trigger the depolarization phase of an action potential now depolarization phase of action potential is basically when there's enough implied potential to cause these voltage-gated sodium channels to open up now voltage-gated sodium channels open at a more positive voltage in that influx of sodium through then the acetylcholine channels could potentially open up these voltage-gated sodium channels which makes the action potential unstoppable and if this happens then we get action potentials that spread across the sarcolemma from one voltage-gated channel to the next in adjacent areas and it caused that area to depolarize we call this propagation and propagation of the action potential occurs all across the sarcolemma down the T tubules and could potentially cause the opening of calcium I'm sorry the release of calcium from sarcoplasmic reticulum so looking at this diagram again we see that this wave of depolarization or M play potential spreads to a nearby a patch of sarcolemma if it's strong enough we get this little depolarization here to due to sodium it could potentially open up these voltage-gated sodium channels that allow even more sodium to rush in and this is the first phase of what we call an action potential or electrical stimulus now this action potential spreads very fast across the sarcolemma and it propagates by exciting other nearby voltage-gated sodium channels now that the next phase of the action potential it's actually a way for action potentials to be eliminated so you can remove this signal from the cell it's called repolarization and repolarization is a restoration of resting conditions where voltage-gated sodium channels close and instead that increase in positive charge within the muscle cell causes voltage-gated potassium channels to open up potassium actually flows out of the muscle cell down its electrochemical gradient and the removal of positively charged potassium from the muscle cell actually makes the inside of the cell more negative it brings the voltage or charge back down towards a resting or negative state now we call this period of time refractory and it's basically a period where muscle cells can't be stimulated again for a specific amount of time until repolarization is complete and ionic conditions of the resting state are restored by the sodium potassium pumps you find all throughout the membrane of these cells so just to look at these steps and three steps you remember the first phase here is n play potential which is generated due to inflow of sodium from these acetylcholine receptors at the neuromuscular Junction that wave of depolarization or imply potential if it's strong enough could potentially cause these voltage-gated sodium channels to open up allowing an influx of sodium which is the depolarization phase of the action potential these action potentials spread really rapidly and there's two phases of the action potential depolarization which is due to the opening of these voltage-gated sodium channels and then repolarization which is the opening of these voltage-gated potassium channels which allow for potassium to leave the muscle cell thereby making the inside of the cell again more negative back towards a resting state so this is showing the the voltage trace of an action potential like if you can record the voltage changes or electrical changes of a muscle cell over time you'd find that resting voltage is around negative 90 millivolts and that once an action potential occurs these voltage-gated sodium channels open up sodium rushes in the cell makes the inside of the cell more positive due to an entry of positively charged ions here and then near the peak of the action potential voltage-gated sodium channels close and voltage-gated potassium channels now open and that due to an e flux or exit of potassium we see that that makes the voltage inside of our muscle cells more negative because they are removing positive charges in a bet that a flux of potassium brings the voltage back down towards the resting state in this little blip and voltage is the action potential now remember these actually spread very quickly across the muscle cell and it's these little blips and voltage or action potentials that actually trigger sarcoplasmic reticulum to release calcium so we call this excitation contraction coupling and if the events of that transmit action potentials along the sarcolemma that's the excitation phase coupled to the slag of myofilaments in the sarcomere which is the contraction phase now the action potential is propagated or spread along the sarcolemma down the t tubules where voltage sensitive proteins in the tubules simulate calcium release from the sarcoplasmic reticulum that calcium eventually leads to a contraction because it can actually bind with troponin move triple myosin out of the way and allow for the myosin heads to bind to the actin active binding sites now action potentials are brief there about a millisecond some one one thousandth of a second and they end before the contraction is even seen but they spread rapidly and eventually could lead to a contraction so just to summarize of steps member of the action potential gets to the nerve terminal triggers the exits at ptosis of neurotransmitter containing vesicles acetylcholine binds the nicotinic receptors causing an end plate potential that spreads to the nearby patch of sarcolemma if an action potential is generated it spreads down across the sarcolemma down the T tubules and that causes the release of calcium from the sarcoplasmic reticulum now in the sarcoplasm and that calcium can bathe the myofibrils now where calcium can go on over bind with troponin on the thin filaments troponin pulls on tropomyosin in the thin filament and removes the inhibition from those actin binding sites that way the myosin head can actually bind with actin it actually forms a cross bridge it pivots to basically pull the thin filament in a direction towards the M line on the sarcomere so at low interest other calcium triple myosin blocks the active sites on actin and the myosin heads can't attach therefore you can't get a muscle contraction so the muscle fiber or cell stays relaxed voltage voltage sensitive proteins and the t tubules change shape and causes SR to release calcium in the cytosol but at higher interest other calcium concentrations calcium binds to troponin troponin changes shape allowing tripple myosin to move out of the way so that myosin can bind with actin forming a cross bridge and cycling as an issue where basically the myosin heads cycle really rapidly by moving around and basically using the chemical energy in ATP to produce a muscle contraction and when nervous system stimulation ceases calcium is pumped back into the sarcoplasmic reticulum thereby ending the contraction so to summarize these steps remember the action potential travels down the t tubules triggers the opening of these voltage-gated calcium channels laughs for calcium to spread from the sarcoplasmic reticulum down towards the sarcomere were binds with troponin troponin pulls on triple myosin moves trip of my son out of the way allows for the myosin have to bind to form a cross bridge now the four steps of a cross bridge cycle are the first of all cross bridge formation which is a high-energy myosin head bond with actin thin filament now the working or power stroke is when the myosin head pivots and pulls in the thin filament towards M line and then to get cross bridge detachment when a new ATP binds of the myosin head myosin has detached and then recaulk basically through the hydrolysis of ATP into a high energy state which could potentially use in the next cross bridge cycle we find that as actually this is a cycle where you know as long as calcium's bind troponin tropomyosin is out of the way and your active sites are now exposed the myosin head can form an attachment it actually pivots kicking off ADP and inorganic phosphate through that power stroke or contraction and then when a new ATP molecule binds with the mouse and head it that myosin head can unbind and then use the chemical energy in ATP to wreak och back into a high energy state where as long as the active sites are exposed again myosin head combined and the whole thing recycles and repeats now one thing it's important to note is you need ATP for this process to continue and you especially need ATP to get the mouse and head thumb bind so one thing that's interesting here is that in rigor mortis or stiffness after death we see that due to a depletion of ATP the myosin heads can't unbind with from actin instead they stay in the bound or crossbridge state which makes muscles more stiff this is actually what's going to explain the stiffness of muscles after death