11.4 + 11.5

Front 1

major phases of muscular contraction

Back 1

1. excitation
2. excitation contraction coupling
3. contration
4. relaxation

Front 2

excitation

Back 2

the process in which action potentials in the nerve fiber lead to action potentials in the muscle fiber
1. nerve signal arrives at synaptic knob and stimulates voltage gated calcium channels to open
2. Enterance of calcium stimulates exocytosis of synaptic vesciles, releasing ACh into the synaptic cleft
1AP releases 60 SV, releasing 10,000 ACh molecules
3. ACh diffuses across synaptic cleft and bins to receptor proteins in sarcolemma
4. receptors are ligand gated ion channels
2 ACh molecules bind to open the channel, which allows sodium to diffuse in and potassium out.
voltage goes from -90 to +75mV, then back down near RMP
end plate potential
5. areas of sarcolemma next to motor end plate have voltage gated ion channels that open in response to end plate potential. this allows the flow of sodium and potassium creating more action potentials

Front 3

excitation-contraction coupling

Back 3

links the action potentials on the sarcolemma to activation of myofilaments, so they can contract
1. wave of action potentials spreads from end plates in all directions. Reaches T-tubules and travels down them into the sarcoplasm
2. action potentials open voltage gated ion channels in the t-tubules, which are linked to calcium channels in the terminal cisternae of the SR. Channels in the SR open as well allowing calcium to diffuse out ot the SR, into the cytosol
3. calcium binds to the troponin of the thin filaments
4. TT complex changes shape, sinking deeper into the groove of the actin, exposing the active sites.

Front 4

contraction (sliding filament theory)

Back 4

muscle fiber develops tension and may shorten
1. ATP bound to the myosin head is hydrolyzed by myosin ATPase, into ADP and P. this releases energy and activates the myosin head by putting it in its cocked position (recovery stroke)
2. cocked myosin head binds to exposed active site on actin forming a cross bridge
3. myosin releases ADP and P, causing it to flex into bent, low energy position (powerstroke) remains bound until it binds to a new ATP
4. Binding of new ATP breaks the cross bridge. It can now hydorlize this ATP and reckock (recovery stroke) so it can produce another power stroke

Front 5

relaxation

Back 5

*after work is done, the muscle fiber can relax and return to resting length
1. Nerve signals stop reaching the NMJ, so synaptic vesciles are no longer released
2. AChE breaks down ACh as it dissociats from receptors.the synaptic knob reabsorbs these peices for recycling
3. active transport pumps in the SR begine to pump calcium out of the cytosol back into cisternae, where it binds to calsequestrin, which stores it
4. calcium ions disociate from troponin, and are pumped back into the SR
5. Tropomyosin moves back into position, blocking the active sites
**relaxation alone doesnt return a muscle to its resting length

Front 6

end plate potential

Back 6

rapid fluctuation in membrane voltage at the motor end plate

Front 7

myosin ATPase

Back 7

an ezyme in the myosin head that hydrolizes ATP into ADP and P, providing the energy for a recovery stroke

Front 8

cross bridge

Back 8

formed when myosin head binds to actins active site

Front 9

power stroke

Back 9

myosin head releases ADP and P, causing its head to flex into bent, low energy position

Front 10

recovery stroke

Back 10

myosin head hydrolizes ATP to cock into high energy position

Front 11

length tension relationship

Back 11

the amount of tension generated by a muscle, and the force of its contraction depends on how streched or contracted the muscle is before it was stiumlated

Front 12

overly contracted muscle at rest

Back 12

thick filaments to close to z disc, so thick filaments bump them when contracted, causing only a weak contracion

Front 13

overly streched muscle contraction

Back 13

not enough overlap between thick and thin filaments, so not as many crossbridges can be formed, causing a weak contraction

Front 14

muscle tone

Back 14

the CNS continuously moniters and adjusts the length of resting muscles, maintaining a partial contraction
*keeps them at optimum length and makes muscles ready for action

Front 15

myogram

Back 15

a chart of timing and strength of a muscle twitch

*time of stimulation, latent period, contraction phase, relaxation phase

Front 16

threshold

Back 16

the minimum voltage needed to generate an action potential in the muscle fiber
*the voltage need to open calcium channels into the cytosol to stimulate contraction

Front 17

twitch

Back 17

at threshold or higher voltage, a stimulus causes a quick cycle of contraction and relaxation

Front 18

latent period

Back 18

the delay between the onset of stimulus and onset of contraction
*the time it takes for the excitation, excitation contraction coupling, and tension for grow in muscle
*the tension formed in the latent period is called internal tension

Front 19

internal tension

Back 19

tension created during the latent period

Front 20

contraction phase

Back 20

the muscle begins to produce external tension and move a resisting object or load
*very short phase because SR quickly reabsorbs Ca before muscle can develop maximum force
quicker than relaxation

Front 21

external tension

Back 21

tension created during the contraction phase

Front 22

relaxation phase

Back 22

SR reabsorbs Ca ions quickly, Ca levels drop, so myosin heads release the thin filaments and muscle tension declines
slower than contraction

Front 23

What affects the contraction strength of a muscle twitch?

Back 23

stimulation frequency (more=stronger)
concentration of Ca in sarcoplasm
how stretched a muscle is before stimulation
temperature of the muscle (warm=stronger)
pH (lower pH=weaker contraction)
hydration of muscle
voltage

Front 24

higher volatage stimulus

Back 24

higher voltages excite more nerve fibers in the motor nerve, causing more motor units to contract
stronger twitches

Front 25

recruitment (multiple motor unit)

Back 25

process of brining in more motor units for a contraction

Front 26

stimulation frequency

Back 26

greater frequency causes greater contraction
-less that 10 stim/s - identical twitches that recover
-10-20 stim/s- muscles reecover, but each twitch generates more tension than the previous (treppe)
-20-40 stim/s - new stimulis arrives before previous twitch is over. so stregth grows for each stimuli (termporal summation, wave summation)(incomplete tetanus)
- 40-50 stim/s- muscle has no time to relax at all. twitches fuse into a smooth prolonged contraction called complete fused tetanus

Front 27

treppe

Back 27

increasing tension with repetitive stimulation
(staircase phenomenon)
*SR doesnt have time to aborb all the Ca from cytosol
10-20 stim/s
more Ca= stronger twitches

Front 28

temporal (wave) summation

Back 28

stimuli arive so close together that it arrives before the previous twitch is over
*each twitch causes greater tension

Front 29

incomplete tetanus

Back 29

20-40 stim/sec produces a state of sustained fluttering contraction

Front 30

complete (fused tenanus)

Back 30

40-50 stim/s causes the musle to not be able to relax at all between stimulus. twitches fuse into a smooth, prolonged ocntraction

Front 31

smoothness in muscle contraction

Back 31

due to the fact that when one motor unit relaxes, another takes over, so muscle doesnt lose tension

Front 32

isometric tension

Back 32

tension is created, but the muscle creates no external movement
contraction with no change in length

Front 33

isotonic tension

Back 33

contraction with a change in length but no change in tension

Front 34

two types of isotonic contraction

Back 34

concentric contraction
eccentric contraction

Front 35

concentric contraction

Back 35

a muscle shortens as it maintains tension

Front 36

eccentric contraction

Back 36

a muscle lengthens as it maintains tension
(negative rep)