Muscle Physiology Chapter 12

Front 1

skeletal muscles

Back 1

biceps of the arm – connected to at least two bones; exceptions: connect to facial muscles of the skin, muscles of the larynx for exp are connected to cartilage

Front 2

tendons

Back 2

connect muscles to bones, cords of elastic connective tissue that transmit force from the muscle to the bone

Front 3

Fascicles

Back 3

bundles of individual muscle cells, connective tissue, blood vessels and nerves

Front 4

muscle fibers

Back 4

muscle cells, long & elongated inshape, each runs full length often running diagonally and encased in a sheath of connective tissue. Unlike most cells, which have a single nucleus, muscle fibers have many because each muscle fiber is formed during embryonic life from the fusion of several cells and these nuclei like immediately below the muscle fiber's plasma membrane called the sarcolemma.

Front 5

sarcolemma

Back 5

muscle fiber's plasma membrane

Front 6

sarcoplasm

Back 6

muscle fibers plasma membrane

Front 7

myofibrils

Back 7

rod-like filaments that contain the fiber's contractile machinery. each myofibril is a bundle of overlapping thick & thin filaments made of proteins myosin & actin.

Front 8

sarcoplasmic reticulum

Back 8

saclike membranous network surrounding each myofibrils & close association with T tubules. Functions are: storage of Ca2+ ions & release them into the cytosol when the muscle cell is timulated to contract. The Ca+ ions are released in response to electrical signals that travel from the sarcolemma to the T tubules & serve as chemical messengers that carry these signals to the cell's interior, where the myofibrils are located.

Front 9

Transverse Tubules

Back 9

connected with the sarcolemma & penetrate into the cell's interior.
Plan an important role in activating muscle contractions because they help transmit signals from the sarcolemma to myofibrils, enabling a muscle cell to respond to neural input.

Front 10

Striated muscle

Back 10

skeletal muscle under the microscope (also cardiac muscle has this appearance). Striations in skeletal muscle are due to the orderly arrangement of protein fibers in the myofibrils called thick & thin filaments

Front 11

thick & thin filaments

Back 11

run parallel to muscle cell's long axis.

Front 12

Myofibrils

Back 12

each muscle fiber is full of these! they are contractile proteins that cause a muscle fiber to shorten. They are made of overlapping thickand thin filaments of mysosin and actin

Front 13

Sarcomere

Back 13

each muscle fibril is made of these - they are the fundamental uinit, or monomer of contraction. (they can be seen as the distance between 2 Z-lines

Front 14

Thin Filaments

Back 14

made from a bunch of proteins: actin, troponin, tropomyosin. Actin monomers called G actin (because they are globular protiens) and have a mysoin-binding site. G actin protiens are linked together end to end (like pearls in a necklace) to form strands of F actin (are fibrous protiens). The two are arranged in a double helix to form the actin strands found in thin filaments. Tropomysosin and troponin are regulatory protiens that allow the muscle fibers to start or stop contracting. Tropomysoin (long fibrous molecule|) extends over many actin molecules blocking myosin-binding sites in muscles at rest. Troponin (a complex of three proteins|)1 attaches to the actin strand, 2 binds to tropomyosin, 3 containing a site to which Ca ions can bind reversibly. The binding of Ca to this site triggers muscle contraction by causing troponin to move tropomyosin aside, exposing the myosin-binding sites on the actin molecules.

Front 15

M & Z lines

Back 15

proteins that anchors to the filaments. M lines anchor the thick filaments & Z lines anchor the thin filaments.
Remember M line myosin

Front 16

Thick filaments: what are they made of ? Name the protiens, why important?

Back 16

also part of a sarcomere just like thin filaments. Made of Myosin molecules. a myosin molecule is a dimer made of two long fibrous intertwined protein subunit tails with fat protruding heads similar to golf-clubs called crossbridges. The crossbridges or heads are the buisness end of the myosin molecule because they actively partake in generating a muscles mechanical force. Crossbridges have two binding sites: 1. binds actin monomers on thin filaments,2. ATPase site that has enzymatic activity & hydrolyzes ATP. Additional proteins: Titin - elastic spring-like protein that anchors thick filaments in place (M to Z line), resists stretching.

Front 17

A- band

Back 17

appears dark & is the length of the thick filament soits length won't change as the muscle contracts

Front 18

i band (I)

Back 18

appears light & contain only thin filaments the distance between 2 thick filaments , shortens as muscle contracts

Front 19

H zone

Back 19

distance between 2 thin filaments, gets smaller as muscle contracts

Front 20

name the number of thick vs thin filaments for skeletal muscle & smooth muscle

Back 20

skeletal muscle: 2 thin filaments for every thick filament

cardiac muscle: 8 thin filaments for every thick filament

Front 21

thin filaments

Back 21

run parallel to muscle cell's long axis, 3 proteins: Actin, Tropomyosin, & Troponin. Actin monomers called “G Actin”, 2 G actins make up an F actin.
G Actin has a myosin binding site, generates force on binding regulatory proteins
Regulatory proteins: Tropomyosin & Troponin.
Troponin-3: on attaches the Actin strand,another binds to tropomyosin, third contains the Ca+ binding site in muscles at rest.
Tropomyosin – extends over actin, blocks myosin binding sites when muscle is at rest

Front 22

excitation – contraction coupling

Back 22

sequence of events that links the action potential to the contraction

Front 23

Know all three proteins for thin filaments

Back 23

Actin has long thin fibrous proteins called tropomyosin. Tropomyosin at rest (muscle at rest) notice it covers olive pit holes. Tropomyosin trumps the myosin. If it is over the myosin binding site, myosin cant bind therefore no muscle contraction. Again this is at rest. How do you move the tropomyosin so myosin can bind to actin? Thats where Troponin comes in. Troponin are these little balls that sit on these long filaments of tropomyosin.Filamentous actin with myosin binding sites. At rest tropomyosin (other long filament|) covers binding site on actin. On top of tropomyosin is a protein called troponin. On troponin, it has the binding site for Calcium, because Ca is critical for muscle contraction.

Notice at rest on the filaments tropomyosin is covering up myosin binding sites. In the presence of Calcium (little green balls), Ca will bind to troponin because troponin has the Ca binding site.

Actin: asleep
In presence of Calcium.. awake.. rips the tropomyosin (blankets) off the binding site.
Now binding sites are exposed in a cell... causes muscle contraction. (hyper simplified)
Tons of other proteins involved... Titin holds everything in place.. super stretchy

Front 24

Thick filaments

Back 24

filamentous and globular
Recall a pic of a myosin (globular vs fibrous)
made of one myosin... one of these heads in a straight line with a tail.
Looks like golf clubs. You have too golf clubs and you twist them around in a helix but the two heads are sticking up. 100's of these make up a thick filament and they are always arranged tail to tail with heads up high. Notice how thick and how many, notice the arrangement.
Golf clubs arranged in a spiral. Remember you have tons of myosin and actin that are going to be holding onto each other
On the myosin head you have two sites
1.actin binding sites poke into olive holes of the actin
2.ATP binding site (ATP ase because its an enzymatic site that breaks up ATP)
Because things are going to move here you need energy which is derived from ATP.

Front 25

Sarcomere

Back 25

from Z line to another Z line is called a sarcomere
all thin filaments going in both directions and thick filaments in between. In pics thick filaments look like they are floating in between those thin filaments. Notice titin is in between there and holds those filaments in place. Note Titin can be stretched to 3 times its shape and bounce back again, very elastic protein.

Front 26

What must happen in order for the crossbridge cycle to occur.

Back 26

Calcium must be present so that binding sites are open (not covered by tropomyosin). Ca binds to Ca+ binding site on troponin, pulls away tropomyosin (or moves it aside) off of myosin binding sites on Actin molecules. The yellow ball is ATP. ATP comes into the ATP binding site, cocks its head back. Notice it splits into ADP and inorganic phosphate. It's cocked and ready to go.. got the power of the phosphate.. thats the power stroke. It kicks out the ADP and inorganic phosphate. Your waiting for the next ADP. Remember ATP is binding to ATP ase on the myosin binding site.

Front 27

sliding filament model

Back 27

muscles contract because the thick and thin filaments of the myofibrils slide past each other.

Front 28

What needs to happen for muscle contraction? what is the mechanism that drives this?

Back 28

the mechanism that drives sliding of thick and thin filaments past one anoher is called the crossbridge cycle. Back & forth motion of myosin crossbridges powered by ATP hydrolysis. Cyclic binding and unbinding of crossbridges to thin filaments occurs so that the motion of the crossbridges pulls the thin filaments toward the center of the sarcomere. Back and forth movement of crossbridges occurs when myosin molecules change in conformation. Changes allow heads to change position, alter ability to bind to actin monomers in thin filaments & energy content in myosin molecules. I.E. 1. High energy form: step 5, myosin heads go into this conformation after they hydrolyze ATP, called this because it stores energy released in hydrolytic splitting of ATP. 2. Low energy form - after stored energy is released to drive movement of thin filaments (step 3)

Front 29

Cross bridge cycling: how does this work? this is critical !! must know this:How does it work? who binds to what? What is the timing on this thing?

Back 29

5 steps: Assume Ca has bound to troponin, pulled tropomyosin off of myosin binding sites of the actin 1. Energized (thick) myosin head binds to Actin (thin): ATP bound to ATPase site on myosin head is split by enzymes in the site. ADP+ Pi on thebyosin head increase its affinity for actin (thin), and binding occurs. Binding triggers step 2. Power stroke: first Pi is relaeased (from ATPase site) which gives the myosin head power to pivot against actin moving the thin filament along. ADP is released at the end of this step. Myosin is low energy state and is stuck on actin. 3. Rigor: low E state, actin & myosin are tightly bound. Rigor mortis coninues until enzymes leaked by disintegrating cellular components begin to break down the myofibrils. 4. Unbinding of myosin & actin: ATP enters ATPase site on myosin, makes it change conformation, looses affinity for actin. Myosin detaches from actin. 5. Cocking of the myosin head: As myosin moves all the way back ATP splits into ADP & Pi causing myosin to reach a state of high energy. If Ca is present the cycle will happen again.

Front 30

The CNS controls the skeletal muscle contractions with___?

Back 30

motor neurons

Front 31

Input from motor neurons always has a ____ effect on muscle cells and serves to _____ _____ of those cells

Back 31

excitatory, trigger contraction

Front 32

Explain how muscle cells are like neurons.

Back 32

They are excitable, capable of generating action potentials if their PM's are depolarized to a sufficient degree.

Front 33

In general terms what occurs when a muscle cell receives input from a motor neuron

Back 33

cell depolarizes, firesan action potential that stimulates contraction. The sequence of events that linkds the action potential to the contraction is excitation-contraction coupling

Front 34

Connection between a motor neuron & muscle cell occurs _____.

Back 34

Neuromuscular junction

Front 35

What is the role of neuromuscular junction in Excitation-contraction coupline?

Back 35

Presynaptic motor neuron cell transmits an action potential at the axon terminal.
1. Action potential reaches the terminal baton of a motor neuron.
2. It allows the voltage gated Calcium channels to open.
3. Calcium floods into that neuron.
4. It causes the fusion of synaptic vesicles full of ACh (always ACh) to get dumped into that neuromuscular junction of the synaptic cleft.
5. ACh goes down and it binds to nicotinic cholinergic receptors (ion channels).
They open up and allow Na & K to flow.
Na+ flows faster so Na causes a depolarization in this motor end plate & this depolarization is called an End plate potential. Its a depolarizing graded potential.
This is large enough to cause an action potential.
Once an action potential is initiated in a muscle cell, it propagates through the entire sarcolemma and travels through T tubules, extensions of the sarcolemma, triggering Ca+ release from nearby sarcoplasmic reticulum. Ca+ signals initiation

Front 36

What is the purpose of excitation- contraction coupling?

Back 36

Its a sequence of events that links the action potential to the contraction and basically turns contractions on & off. muscle cells are excitable, can generate action potentials if their PM's depolarize sufficiently enough and this ultimately will stimulate a contraction.

Front 37

What is neuromuscular junction

Back 37

|Its a highly specialized central region where the motor neuron synapses with skeletal muscle fiber

Front 38

Describe some of the specialized structures of the motor neuron ( terminal boutons) and skeletal muscle cell (motor end plate).

Back 38

Terminal boutons are the axon terminals of motor neurons that store ACh. Opposite the terminal boutons is a specialized region of the muscle fiber's plasma membrane called the motor end plate, with invaginations that contain large numbers of nicotinic cholinergic receptors. Note acetylcholinesterase in between these invaginations terminate the excitatory signal, and allows muscle fibers to relax.

Front 39

Describe the functional anatomy of the neuromuscular junction

Back 39

Note axon terminal of motor neuron & portion of PM of skeletal muscle (motor end plate) are specialized at the N-Juxn. Communication at the N juxn: Action potential arrives at the axon ternimal of a motor nueron. 1. voltage-gated Ca cahnnels open & Ca enters the cytosol. 2. The entry of Ca triggers the release of ACh by exocytosis 3. ACh diffuses to and binds to nicotinic cholinergic receptors a the motor end plate, opening cation channels, causing Va to enter the cell. 4. This produces an end-plate potential that generates currents throughout the plasma membrane of the skeletal muscle cell. 5. This causes the membrane to depolarize to threshold which generates an action potential. 6. action potential spreads along skeletal muscle cell membrane, ultimately stimulating contraction. Acetylcholineasterase degrades acetylcholine to produce acetate and choline. 7. choline is actively transported into the terminal bouton 8. here it can be used to make more ACh

Front 40

What happens when a muscle is relaxed? Describe the concentration of Ca in the cytosol, the conformation of proteins in thick and thin filaments

Back 40

Ca+ is low, very little binding between Ca+ & troponin. Troponin is in resting conformation ecause tropomyosin is positioned onthe thin filaments in sucha way that it blocks actin's myosin-binding sites, so crossbrdge cycle cannot occur. Note Pumps in the SR actively transport Ca+ ions from the cytosol into the SR. Ca+ levels in the cytosol are low as a result. These calcium voltage gated channels are normally closed preventing leakage.

Front 41

What happens to cause Ca+ to leak out of the SR. What makes these voltage gated channels unique?

Back 41

As an action potential travels through the T tubules, it causes these channels to open briefly, Ca+ flows out into the cytosol, thus increasing cytosolic Ca concentration. What makes these channels unique is that they are triggered by electrical signals from the T tubules not the membrane of the SR itself.

Front 42

what links the SR membrane with T tubules? why important

Back 42

Protein receptors called Ryanodine receptors bridge the gap between them and function as Ca channels. R-receptors contact T tubule membranes through other proteins called DHP receptors that function as voltage sensors.

Front 43

Describe what happens when an action potential hits the T tubules of the SR

Back 43

Action potl travels thru T tubules, voltage sensors (DHP receptors) react (possibly undergo confrmtl change) by transmitting a signal directly to ryanodine receptors they are in contact with. Signal triggers Ca+ channel pores within the R-receptors to allow Ca2+ to flow out of SR.

Front 44

Upon initial release of Ca+ ions into the SR, what occurs? What role does Ca+ continue to play? How does this affect contraction

Back 44

as the Ca ions enter the cytosol, some of them bind to specific sites on other SR Ca+ channels and cause them to open. The initial release of Ca+ triggers the release of even more Ca from the SR. As Ca+ rises in the cytosol, some binds to one of the three proteins that make up the troponin complex (step 4), causing confmtl change, makes t-myosin shift out of resting position, exposing myosin binding sites on actin monomers. The myosin heads of thick filament are now able to bind to actin, and crossbrdgecycle can begin, ant the myosin contracts.

Front 45

describe the events in excitation-contraction coupling. What happens with the first step (hint neuromuscular junction)?

Back 45

Contraction of a skeletal muscle fiber is initiated and maintained by the arrival of action potentials at the axon terminal of a motor neuron.1.ACh released from terminal of motor neuron, binds to nicotinic cholinergic receptors in the motor end plate (of the skeletal muscle). Binding elicits an EPP (end plate potential), which triggers an action potential in the muscle cell.

Front 46

What is the second & third event that occurs with excitation - contraction coupling?

Back 46

Step 2. Action potential propagates through the sarcolemma and down the T tubules (extensions of the sarcolemma).DHP receptors, proteins in the membrane of T tubules, are voltage sensors that react by changing conformation. This transmits a signal to ryanodien receptors.Ryanodine receptors function bridge the gap between SR & T tubules, but also function as Ca+ channels. This signal from DHP triggers Ryanodine receptors to react releasing Ca+. Step 3 Ca+ flows out of the SR into the cytosol. Some ions will bind to specific sites on other SR Ca+ channels, causing them to open. Thus more Ca+ is released from the SR.

Front 47

What is the 4th event that occurs with excitation - contraction coupling?

Back 47

4. Ca2+ in cytosol binds to troponin, exposing myosin-binding sites. (Ca+ in cytosol binds to one of three proteins that make up troponin. Troponin undergoes conf-change, causing tropomysin to shift from it's normal resting position, exposing myosin binding sites on actin monomers.) Myosin heads of thick filament able to bind to actin, 5. cross bridge cycling can begin & sarcomere contracts.

Front 48

What is the 5th, 6th, & 7th events that occurs with excitation - contraction coupling?

Back 48

5. Crossbridge cycle begins (muscle fiber contracts)!!!
6. Ca2+ actively transported back into lumen of SR followingthe action potential
7. Tropomyosin blocks myosin-binding sites (muscle relaxes)

Front 49

what happens with muscle contraction from neuron to excitation-contraction coupling.

Back 49

1. action potential moves down motor neuron, releases ACh,
2. ACh binds to nicotinic cholinergic receptors. These allow an EPP

Front 50

what do you need to continue cross bridge cycling?

Back 50

Ca2+ must be in cytoplasm for this to continue

Front 51

What always follows an action potential generated in the motor neuron?

Back 51

Note the action potential that occurred in the motor neuron is always followed by an action potential in the muscle cell it innervates.

Front 52

what are T tubules

Back 52

T tubules are pores that go down and around the sarcolemma, and across your muscle fiber.voltage sensitive receptors. They have DHP receptors. DHP receptors change shape in response to the depolarizing effect of an action potential. the fact that you have voltage gated Na/K channels throughout the area and it keeps the action potential moving. As the action potential moves passed these DHP (pink) it makes them change their shape because of the voltage affects the shape of a DHP receptor.

Front 53

Although a motor neuron typically branches andinnervates more than one muscle cell, each muscle fiber receives input from __(4 words)___?

Back 53

only one motor neuron

Front 54

How do EPP's differ from EPSP's

Back 54

EPP - normally sufficient in magnitude to depolarize the muscle fiber to threshold, generating an action potential, thus triggering contraction of the muscle fiber.

Front 55

From start to finish: "can you describe events from the neuromuscular junction - how the events get started in a muscle cell & how it propagates? How that action potential causes a release of Ca+ in the muscle cell? How do Ca+ and cross bridge cycling work.

Back 55

1.action potl moves down motor neuron: terminal boutoun of motor neuron releases ACh.
2.ACh binds to nicotinic cholinergic receptors
3.Nicotinic cholinergic receptors will then open & allow an EPP (end plate potential), which is large enough to cause an action potential
4.action potential will propagate across the sarcolemma (PM of muscle cell), down the T tubules to the DHP receptors – which are the ones that change their shape when an action potential reaches passed them. DHP's (transmembrane proteins that function as sensors) are stuck to ryanodine receptors, so DHP is like one big globular protein. DHP changes shape pulling on ryanodine receptors, opening them up to allow Ca+ to flow in to the sarcoplasm. (not a lot of sarcoplasm in there but it is present.
5.Ca+ floods out of the SR, binds troponin, exposing tropomyosin
6.cross bridge cycling can occur!


Whats cool about the sarcoplasm? Sarcomeres located here

Don't forget: when Ca floods out of the SR, it binds to troponin, pulls away tropomyosin, exposing myosin binding sites (allows cross bridge cycling) with ATP. As long as Ca+ is in the cytoplasm you will have crossbridge cycling.

Front 56

What energy source is used for muscles? what is needed to get this energy? Describe how muscle cell metabolism changes with exercise intensity.

Back 56

Oxygen is needed. Most ATP is supplied by oxidative phosphorylation. 1. 1st few seconds: muscles use own glycogen storage to supply glucose as fuel for ATP production

Front 57

How muscle cells stop contraction:

Back 57

Ca+ re-uptake stops muscle contraction
Calcium ATPases = Ca+ pumps (direct active transport) in SR, will pump Ca+ back into your Sarcoplasmic reticulum.
1. this will pull Ca+ off the troponin
2. which will allow tropomyosin to cover those myosin-binding sites: blocks binding of myosin to actin
3. no more cross bridge cycling

Front 58

How do we get ATP for muscle contraction?

Back 58

1.first dephosphorylate creatine – turn ADP to ATP, instant energy
2.second oxydative phosphorylation -
3.lactic acid fermentation - not enough glucose and/or oxygen (in cytosol, kicks pyruvate to lactate lactic acid fermentation ) faster than oxidative phosphorylation. Doesn't need oxygen. Last resort to get energy. Causes soreness in muscles the following day.

Front 59

Why are we still breathing heavy after exercise?

Back 59

We are still breathing to reverse the lactate (usually we just let it go to our liver), but we want to make enough ATP to re-phosphorylate creatine. Oxygen is needed to make ATP to accomplish this.Amount of time it takes for breathing to return to normal after exercise tells us how in shape we are.

Front 60

How do you get energy if you eat mostly Proteins and fats, not enough carbohydrates:

Back 60

Gluconeogenesis: carried out by the liver
breaks down triglycerides used to make glycerol phophate, then glycerol (intermediate in glycolysis pathway)
lactate: first converted into pyruvate, normal end-product of glycolysis
Amino acids: produced by the breakdown of proteins.

Front 61

Can you draw an isometric contraction graph?

Back 61

Isometric twitch - (iso = same, metric = distance) Same length.
Muscle doesn't shorten, it simply increases its tension.

When muscles contract, sarcomeres are contracting increasing tension, they pull on the Tendons (SEC's) making them longer.
Tendons: series elastic components, SEC's,
Muscle: contractile component, CC

Isometric contraction: No movement, but force is increased to hold on to heavier weight. Muscle stayed the same because its contracting to keep that tension enough to hold this heavy object, but it's pulling and lengthening the tendons.

Notice the action potential and where it hits on this curve: During the latent period!

Can you draw an isometric twitch (contraction) graph?

Front 62

phases of muscle twitch

Back 62

X axis – time milliseconds
Y axis – tension: force generated by your muscle fiber (amount of contractile force to move a bone)
phase I – latent period (small) – time between excitation & contraction; period between neurons synapsing and your muscle cell firing your action potential.
Phase II – contraction phase – Ca+ release is increasing, which causes crossbridge cycling.
Relaxation phase – Ca+ levels are decreasing inside the cell, which decreases crossbridge cycling.

Front 63

Can you draw an isotonic muscle twitch?

Back 63

Isotonic contraction: (iso=same, tonic=tension), same amount of tension
X axis = time
Y axis = force – amount of tension produced in the muscle
Phase I: Latent period
Phase II = contraction phase
then you have flattening = the isotonic part (same tension), as its contracting you have the same amount of tension. It means that over time the tension doesn't change. Your just moving the bones in relation to eachother
Phase III = relaxation phase

Your actually shortening the muscle. Your moving bone against bone, but the shortening of the muscle is allowed by those tendons.
Type of contraction that the tension remains the the same but the muscle shortens. This is the motion we usually associate with muscle shortening, such as bringing an apple to our mouths.

Front 64

Effect of load on tension: (heavy suitcase idea)

Back 64

As the load gets heavier, it takes more tension to shorten that muscle. Tension is increased as weight of load increases.

Front 65

Have you ever picked up an object so heavy that you cannot shorten your arm? What happens with the muscle?

Back 65

- no longer able to isotonically contract, cannot shorten the muscle because it is pulling so hard on the bone
isometric contraction can occur at this point.

- The muscle will not be shortened but you can generate enough tension to move that really heavy load or at least hold the heavy load.

Front 66

What factors actually effect the force a muscle can generate? Whats the neuron doing to the muscle?

Back 66

1.frequency of stimulation by the neuron: neuron controls the muscle.
- the more the neuron fires = the greater the frequency of action potentials the muscle can fire
- the greater the frequency of action potentials = the more Ca+ can be released
- The more Ca+ can be released = the greater tension you can have
2.Fiber diameter: if you have more sarcomeres you can generate more tension
3.Changes in fiber length:
4.Extent of fatigue: how fatigued is your muscle? Can your muscle generate the same amount of force after heavy lifting?

Front 67

Frequency of stimulation: Whats the neuron doing to the muscle?

Back 67

This is what happens at a moment in time to strength of contraction with increasing action potentials.
Treppe = frequency of muscle stimulation where muscle stimulation; only seen in a laboratory; you go through Treppe for a couple of milliseconds before you hit full on contraction of your muscle.
what happens to a twitch with repeated action potentials from the motor neuron.
Pink arrows: action potentials coming from the motor neuron.
Time is on the X , Tension is on the Y axis; look at what the muscle is doing.
You hit with one Stimuli.
What kind of contraction is this showing you? is isometric contraction, tension is changing all the time
(no plauteu, not the same tension, no muscle shortening).
Not much of a latent period. Then you have contraction and relaxation.
After another action potential, notice the tension has gone up. Think Calcium: because you had not sequestered all of the Ca+ back in the SR, you still have some free calcium. So at the next burst of Ca+ comes through, you have a larger amount of Ca+ in the muscle tissue--> and this can generate more cross bridge cycling.
Peak tension continues to rise with each twitch until you reach a platuae, that is the maximum force that your muscle fiber is capable of generating.

Front 68

What is full on contraction of your muscle?

Back 68

Tetanus – full on, sustained contraction of muscle; you will see it if you lift a load or shortening your muscle.
In order to fully contract your muscle, your motor neuron must have a high frequency of firing. It has to fire fast enough to keep releasing Calcium constantly until enough Ca+ has been released to generate that full amount of tension. Once that point has been reached, if your load is light enough, your going to go ahead and shorten your muscle. It has a plateau right there so that has to be an isotonic contraction.

Front 69

The more action potentials = ___

What does this mean as far as generating force.

Back 69

the more force you can generate until you reach titanic force.
Titanic force is the maximum force that that particular muscle fiber can produce - Tetanus.

Front 70

Frequency stimulation: Fiber diameter:

Back 70

basically you don't grow more muscle fibers. Shortly after birth you have all the muscle fibers you are going to have. You can make them bigger by using them.
Repeatedly re-using you muscle → fatiguing it:
Your body will signal it to take in more proteins and make more sarcomeres.
The more sarcomeres you have stacked in there = the more force/tension you can produce on that fiber.

Front 71

Length – tension graph (curve)
what does it show?What does it mean? why would certain lengths be easier. What if it's too contracted to begin with? What if it is pulled apart?

Back 71

shows your muscle has an optimal length that it likes to contract at. For each muscle fiber there is an optimal length at which it can generate the most force due to maximum participation of myosin crossbridges in force generation.
The constant force-generating capacity of a muscle fiber at the peak of the length-tension curve occurs for two reasons: 1. all cross-bridges are overlapped by thin filaments & therefore are capable of generating force. 2. sarcomeres are not short enough to allow thin filaments to come into contact, so interference between them does not occur.

Why easier: because cross bridge cycling, a certain amount of overlap between thick and thin filaments , they can produce the absolute maximum force. More force = easier contraction

If it's too contracted to begin with (already under a lot of force) you will start pushing as you contract, and those thin filaments will overlap a lot. That will start to interfere physically and you will have a much greater decrease in your ability to generate tension because you have interference between your tension producing pieces of your muscle.

As the length of the muscle fiber increases, or is pulled apart, they can produce less force because they don't have full overlapping crossbridging.