Phys8-9 W/lab: Skeletal Muscle

Front 1

describe the "hierarcy" of skeletal muscle organization

Back 1

whole muscle>muscle fiber (cell)>myofibrils>contractile filaments>structural proteins

Front 2

Describe each of the following components of the sarcomere: Z line, I band, A band, H zone, M line

Back 2

Z line-boundary of the sarcomere, I band- thin filaments only, A band-thick filaments and overlapping tips of thin filaments, H zone-thick filaments only, M line-center of thick filament, bisects H zone

Front 3

which contracticle proteins are found in the thick filaments

Back 3

myosin only

Front 4

which contractie proteins are found in the think filaments

Back 4

actin, troponin, tropomyosin

Front 5

compare the structures and functions of troponin and tropomyosin

Back 5

both are found in the thin filament and serve as regulatory proteins. troponin is globular and binds calcium, tropomyosin is filamentous

Front 6

describe the structure of an actin filament

Back 6

composed of two helical strands of F-actin and two strands of tropomyosin molecules

Front 7

Describe the skeletal muscle contraction cycle (ignore Ca activation,when is ATP used)

Back 7

begin with myosin attached to actin, ATP binds to myosin head and the complex dissassociates. ATP is hydrolyzed "cocking" the myosin head. The ADP-P myosin head binds a new active site on the actin filament, P is released and the myosin head changes conformation resultingin the power stroke. ADP is released and the myosin head is once again attached to the actin in the attached state.

Front 8

List 3 ways ATP provides energy for skeletal muscle contraction

Back 8

1. Relaxation of cross bridges 2. maintenence of ionic graidents 3. SR Ca pump

Front 9

Describe the structure and funciton of T tubules

Back 9

Invaginations of the sarcolemma into the muscle fiber, they convey the action potential to the center of the cell where they meet with the SR at the triad and trigger Ca release

Front 10

Which neurotransmitter is responsible for skeletal muscle excitation

Back 10

acetylcholine (Ach)

Front 11

What is the cause and sxs of malignant hyperthermia

Back 11

A genetic defect in the SR calcium channels. Under anesthesia, the SR Ca channels fail to close and Ca leaks into the cytoplasm. This triggers muslces contractions and an

Front 12

what is the differnece between an isometric and an isotonic contraction

Back 12

isometric= no change in length, isotonic= constant force

Front 13

compare and contrast fast (II) and slow (I) fibers in terms of size and number of mitochondria

Back 13

fast=larger, few mito; slow=smaller, lots of mito

Front 14

Compare and contrast fast (II) and slow (I) in terms of blood supply and myoglobin content

Back 14

fast=less extensive blood supply, no myoglobin; slow=extensive blood supply, lots of myoglobin

Front 15

Compare the metabolisms of fast (II) and slow (I) twich muscle fibers

Back 15

fast=glycolytic; slow=oxidative

Front 16

which bands of the sarcomere change in length during contraction? Which stay the same

Back 16

The I bands change, the A bands do not (the thin slide over the thick so the I band shortens, the thick do not change in length)

Front 17

Describe how muscle contraction is initiated (what is Ach doing)

Back 17

As the AP travels down the nerve, it triggers the release of Ach. ACH activates Ach gated cation sodium channels resulting in an influx of sodium and a LOCAL depolarization (end plate potential). The local action opens the voltage gated sodium channels initiating an action potential in the membrane. The AP travels down the muscle fiber membrane and through the T tubules where it causes teh SR to release Ca ions. The Ca ions bind troponin and expose the active site on the actin allowing mysoin to bind. This initiates the muscle contraction

Front 18

The length tension diagram demonstrates how the length of the sarcomere relates to the tension generated by the sarcomere. Expalin what is happening at the far right end of the curve (long length, low tension)

Back 18

At this point in the curve th actin has pulled all the way to the end of the myosin so there is no overlap. Cross bridges cannot form so no tension can be gerentaed.

Front 19

The length tension diagram demonstrates how the length of the sarcomere relates to the tension generated by the sarcomere. Expalin what is as you move from right to left along the curve (the length is decreasing and the tension is increasing)

Back 19

As the the sarcomere shorters, the actin and myosin filaments begin to overlap and increasing amounts of cross bridges can be made. This increases the tension in the sarcomere.

Front 20

The length tension diagram demonstrates how the length of the sarcomere relates to the tension generated by the sarcomere. Expalin what is happening as the curve flattens near the center

Back 20

At this point, the actin filament has overlapped all the cross bridges of the myosin filament but has not yet reached the center. No more tension can be generated (because there are no more cross bridges to make) but the sarcomere can continue to shorten because the actin filaments have not yet reached the center of the myosin.

Front 21

The length tension diagram demonstrates how the length of the sarcomere relates to the tension generated by the sarcomere. Expalin what is happening as the tension sharpley decreases near the shortest lengths

Back 21

As the sarcomere continues to shorten, the two actin filaments begin to overlap each other and eventually the two ends of the myosin filaments abut the z lines. with continued contraction, the ends ofhe myosin are crumled and the tension is lost.

Front 22

Why does the length tension curve for a whole muscle differ slightly from that of a single sarcomere

Back 22

The whole muslce has a large amount of connetive tissue and not all of the sarcomeres contract the same amount. The concept of passive tension due to connetice tissue must be considered when determining the L-T curve for an entire muscle

Front 23

How does the active tension a muscle can generate change as the resting length/ passive tension is increased.

Back 23

At "normal" length with appropriate passive tension, the muscle is "primed" to contract with the most tension possible. As the passive tension is increased, the force of active contraction decreases because the muscle is "out of alignment". SImilarly, if passive tension is relieved, the force of contractino decreases. In sum, passive tension is necessary for maximal muscle contraction

Front 24

Why does the velocity of a muscle contraction decrease with increased load?

Back 24

A load on a contracting muscle is a reverse force that opposes the contractile force caused by muscle contraciton. As load increases the net force available to cause velocity of shorteing is reduced

Front 25

What are the sources of ATP for muscle contraction

Back 25

1. phsophocreatine 2. glycogen 3. oxidative metabolism

Front 26

describe quantatative summation

Back 26

The intensity of a muscle contraction can be increased by recruting additional motor units

Front 27

describe frequency summation

Back 27

WIth increasing frequency induvidual contractions begin to overlap each other. When frequency reaches a critial point, sucessive contractions fuse and appear as one smooth contraction, this is called tetanization.

Front 28

what is the cause of rigor mortis

Back 28

After death all the muscles of the body go into a state of contracture because there is no more ATP to cause the separation of cross bridges from the acitn filaments.

Front 29

what affect does curare have on muscle contraction

Back 29

curare blocks the gatin action of acetylcholine on the acetylcholine channels by competing for the receptor site. If the Ach channels can't open, an EPP cannot be generated = no action potential= no contraction

Front 30

describe the concept of saftey factor

Back 30

each impulse that arrives at the NMJ causes about 3x as mucl EEP as need to make an AP, i.e. the stimulus is overkill to ensure that the muscle will be excited

Front 31

Describe myathenia gravis

Back 31

antibodies to Ach receptors block/ destory recepto at postsynaptic NMJ. Channels can't open and weak EPP's are not strong enouch to initiate opening of the voltage gated sodium channels. Can tx with drugs that increase the amount of Ach available (anticholinesterase)

Front 32

Describe the receptors involved with transmitting the action potential from the T tubule to the SR and calcium release

Back 32

The action potential travels down the t-tubule into the SR cisternae. The voltage is sense by dihydropyridine receptors that are linked to calcium release channels (aka ryanodine receptor channels). Activation of DHP receptors triggers the opening of ryanodine receptor chanels in the cisternae which releases calcium into the the sarcoplasm surrounding the myofibrils leading to contraction

Front 33

How is calcium removed from the myofibilar fluid after contraction

Back 33

Ca pump in SR membrane