MT1

Question 1

4 properties of muscles

Answer 1

1. Contractility: contract forcefully
2. Extensibility: contract from an extended state
3. Excitability: respond to stimulus by producing electric signals
4. Elasticity: recoil to resting length after extension

Question 2

Gross muscle histology (CT, components)

Answer 2

1. Periosteum of bone continues as tendon (dense reg), into muscle fascia surround whole muscle
2. Below fascia, epimysium surrounds all units of muscle fibres (fascicles)
3. Perimysium surrounds each individual fascicle
4. Endomysium surrounds each muscle fibre in the fascicle
5. Arteries, veins, and nerves branch to supply each muscle fibre, each fibre has one motor neuron connection at the synaptic end bulb

Question 3

Muscle fibre histology

Answer 3

1. Nuclei on the sides to prevent interference with electric signal
2. Sarcolemma is the cell membrane
3. Sarcoplasmic reticulum is endoplasmic reticulum storing high amounts of calcium
4. Mitochondria produce ATP required for muscle contraction/relaxation
5. Triad comp of 2 terminal Cisternae (thick inward fold of sarcolemma) and a T-tubule
6. Myofibrils comp of sarcomeres comp of actin and myosin myofilament

Question 4

Muscle fibre characteristics

Answer 4

1. Long, multinuclenated (myoblast fusion), hexagonal (allow dense packing with spaces for nerves and BV b/w), striated (alternating myofibril proteins create bands)
2. Sarcomeres in series makes myofibril, in series and parallel forms muscle fibre

Question 5

Structure of actin myofilaments

Answer 5

1. Thin filament
2. comp of monomer G actin proteins with active site (where myosin binds) bonded together to form F actin
3. tropomyosin wraps around F actin, covering active sites
4. troponin has attachment site for tropomyosin, Ca2+, and to G actin, when Ca2+ binds to troponin, it moves tropomyosin off of actin to expose active sites for myosin binding; work with tropomyosin to reg myosin binding

Question 6

Structure of myosin myofilament

Answer 6

1. thick filament
2. myosin heavy chain coil to form alpha helix rod region, connect to head at hinge
3. myosin light chains off myosin heads, contain ATPase to breakdown ATP for cross-bridge cycling
4. myosin molecules connected together at rod with heads staggered (allow constant binding of actin) to form myosin myofilament

Question 7

1. Z disk
2. I band
3. A band
4. H zone
5. M line
6. arrg of actin and myosin

Answer 7

1. attachment site for actin
2. region comp actin only, next to Z disk
3. actin and myosin overlap
4. myosin only part of sarcomere
5. proteins hold myosin rods together
6. hexagonal arrangement of units of 6 actin around 1 myosin

Question 8

sliding filament model:
1. relaxed muscle
2. partially contracted muscle
3. maximally contracted muscle

Answer 8

A band does not change size
1. I band and H zone are at max length
2. I band and H zone narrow as myosin pulls actin, pulling the Z disks closer
3. I band and H zone disappear as myosin pulled actin strand together so the ends overlap

Question 9

Cross bridge cycle

Answer 9

1. presence of Ca2+ binding to troponin moves tropomyosin to expose actin active sites to myosin
2. ATP broken down by myosin ATPase allow myosin head to enter high E pos, myosin binds to actin forming cross bridge, Pi released
3. power stroke pulls actin closer to the M line, shortening sarcomere, ADP detaches
4. ATP binds to myosin to release it from actin, myosin head enter low E pos, hydrolysis of ATP energizes myosin, repeat from step 2 if enough Ca2+ and ATP

Question 10

1. bare zone
2. characteristic of cross bridges
3. electric properties of muscle cell
4. MAP propagatuon

Answer 10

1. area of myosin with no cross bridge
2. are asynchronous to allow for constant binding of actin for contraction
3. RMP at -85 mV, greater than neuron bc more K+ leak channels, K+ inside/Na+ outside at rest
4. AP (stimulus) causes another AP to be produced in adj sarcolemma, allowing the AP to propagate down the cell

Question 11

Neuromuscular junction
1. overview
2. process

Answer 11

1. where the synaptic end bulb of motor neuron meets the motor end plate of the sarcolemma
2. AP depolarize axon terminal, triggering Ca2+ channels to release Ca2+ into synaptic end bulb, Ca2+ trigger exocytosis of synaptic vesicles to release Ach into the synaptic clef, Ach diffuse across to bind to Na+ channel on motor end plate to depolarize cell

Question 12

excitation-contraction coupling

Answer 12

SR at rest has no Ca2+ permeability
1. MAP reaches triad, CaV1.1 detects change in MP of T-tubule, triggers ryanodine receptors in SR to open and release Ca2+
2. Ca2+ in sarcoplasm bind to troponin to begin cross-bridge cycling

Question 13

Titin
1. overview
2. Role
3. how it works

Answer 13

1. From M-line to Z disk, largest protein, two for each sarcomere
2. Stabilize myosin, spring prevent overstretching, adhesion
3. Compliant proximal Ig near Z disk ext with low F, stiff PEVK ext with high F, N2A connects the two regions, when Ca2+in area, binds to actin; when titin stretches, increase recoil (elastic property) to provide F transmission

Question 14

nebulin
1. overview
2. how it works
3. neublin KO

Answer 14

1. Spans the length of actin to the Z disk
2. Specify actin length to stabilize and maintain struc integrity while it is pulled
3. WT mice show consistent sarcomeres length and increased F in comparison to KO; makes cross bridge more efficient

Question 15

1. cytoskeletal protein
2. sarcomere force transmission
3. costamere force transmission

Answer 15

1. Keep sarcomeres aligned and anchored at M line and Z disks
2. Longitudinal F transfer from Z disks to MTJ when myosin pulls on actin
3. Lateral F transfer between sarcomeres in parallel to ECM (endomysium) to MTJ, continued contraction creates org buckling of the lipid bilayer (festoon)

Question 16

costamere
1. structure
2. function
3. Frog muscle experiment

Answer 16

1. Sub membranous protein complex forming rivets in sarcomere aligned with Z disks, maintain sarcomere length and support lipid bilayer
2. Dystrophin anchors Z disk to DGC (connect to actin), Desmin anchors Z disk to INT (bind sarcolemma to transmit force lat); maintain structural integrity of sarcolemma, bidirectional muscle signalling
3. Isolated muscle fibre shares tendon with other fingers, most force transmitted through single muscle fibre thus lat F greater than long F

Question 17

1. myotendinous junction
2. turnover

Answer 17

1. Transition b/w muscle and tendon, F transmitted from muscle to tendon creates lots of F on tendon
2. Plasticity of muscle and MTJ allow constant remodelling in MTJ by satellite cells when there is dmg

Question 18

1 . satellite cell
2. SC role

Answer 18

1. muscle stem cells, type I & II, normally quiescent, activate to travel to local tissue fuse to myofibril and donate for muscle growth and repair
2. maintain muscle mass by repairing disruption tissue (same number of SC), add in more satellite cells if they need to support new structures permanently

Question 19

Satellite cell:
1. Association with NMJ
2. activation program and assoc markers

Answer 19

1. under basal lamina, above sarcolemma, communicates with other cells, tell NMJ where to repair, move to dmg area to repair
2. Pax 7 indicates satellite cell (always present), to activate, MyoD transcriptional factor turns on, allow cell to proliferate and differentiate, DAPI marks nucleus (always present)

Question 20

1. exercise and satellite cell
2. number of myonuclei
3. hypertrophy

Answer 20

1. muscle dmg increase CK, consistently results in increased satellite cell activation, 6-24 hrs increase after exercise (acute)
2. number of myonuclei and satellite cell associated with muscle size
3. increase number satellite cells with resistance training causes hypertrophy

Question 21

1. regen/repair/remodelling
2. quantify dmg in muscle

Answer 21

1. regen = regrowing tissue after necrosis, repair = maintaining healthy muscle during daily life
2. Z-band streaming, membrane disruption, central nuclei, embryonic MHC expression, inflammatory cell infiltration, satellite cell activation

Question 22

How movement of calcium is reg
1. CSQ
2. Cav1.1/DHPR
3. SERCA

Answer 22

1. CSQ stores great amt Ca2+ in SR to allow high release
2. Cav1.1/DHPR ion channels sense change in voltage during AP, opens ryanodine receptor Ca2+ channels to release Ca2+ into sarcomere for CBC
3. SERCA pumps Ca2+ back into SR, SERCA1a predom in Type II, SERCA2a predom in Type I

Question 23

Caffeine and performance

Answer 23

increase by reducing the threshold for ryanodine receptor activation, allowing Ca2+ to fill the sarcomere faster

Question 24

1. Motor unit def
2. all or none principle
3. innervation ratio

Answer 24

1. motor neuron and all muscle fibres it innervates
2. MAP in MU will contract all muscle fibres in it
3. number of muscle fibres controlled by motor neuron, lower ratio more fine control, higher for large movements

Question 25

1. muscle twitch 2. ryanodine v. SERCA 3. femoral muscle stim

Answer 25

1. contractile response to single MAP, req Ca2+ for both contraction and relaxation 2. ryanodine dump faster than SERCA can uptake, relaxation period longer than contraction period to make up for SERCA slower pace 3. lag phase before contraction bc electric stimulus takes time to reach muscle myofibril

Question 26

1. Twitch 2. Summation

Answer 26

1. Low freq MAP, CA2+ released but not removed during full relaxation b/w stimulation, constant peak in force, next stimulus Ca2+ higher making contraction more efficient 2. increasing freq MAP, incomplete relaxation, force increasing in wave pattern

Question 27

1. tetanus def 2. unfused tetanus 3. fused tetanus

Answer 27

1. response to many MAPs at given freq 2. high freq MAP, partial relaxation, constant peak in force 3. very high freq MAP, no relaxation, force is constant

Question 28

1. recruitment 2. subthreshold 3. threshold 4. submaximal 5. maximal

Answer 28

1. stronger stimulus, greater number of MU, more muscle fibres for high recruitment 2. not strong enough for AP 3. produce MAP, activate all fibres in MU 4. increase number of NU 5. all MU respond

Question 29

Series elastic component 1. Tension and elasticity 2. Components 3. Function 4. Series v. Parallel

Answer 29

1. elasticity is ability to deform and revert to original pos, spreads tension (transfer of pulling force) over longer period 2. Tendon, CB, titin, CT 3. Muscle/tendon complex use tension to pull on bone and muscle’s elastic properties allow greater gen of force due to recoil 3. Series elastic bands attaching end to end at Z disks, parallel sarcolemma and CT around contractile unit

Question 30

SEC: 1. During muscle twitch 2. During tetanic contraction

Answer 30

1. One MAP, short time (~50-100 ms) for CB, no time for force to fully stretch SEC before muscle relaxes (recoils) little force to bone 2. high freq MAP (seconds), constant CB allow time for force to travel to tendon for full stretch of SEC, applying force directly to bone

Question 31

1. Force-Ca2+-Frequency relationship 2. unfused tetanus 3. fused tetanus 4. diminishing returns

Answer 31

1. Higher freq MAP stim lots Ca2+ released from SP, increases CB and force, increases saturation Ca2+ until all active sites have been bound by myosin, force reaches a plateau 2. not enough Ca2+ to allow max CB, relax due to some Ca2+ uptake by SERCA 3. high freq MAP causes constant release of Ca2+, no time for SERCA to uptake --> no relaxation 4. more MAP/sec, less increase of force per MAP

Question 32

1. success of power strokes 2. int v. ext work of muscles

Answer 32

1. always cause contraction, success (joint action) depends on ext force on muscle 2. internal is work by muscle on tendon, external is work by tendon on bone

Question 33

1. concentric v isometric 2. central motor drive

Answer 33

1. always shorten sarcomeres, CON muscle tension overcomes load, muscle shortening, ISO peak tension cannot overcome load, no change in muscle length 2. freq of signal to MU, more MU is CON, less is ECC

Question 34

1. agonist v. antagonist 2. Contraction type and max force

Answer 34

1. agonist under CON to perform action, antagonist ECC opposes force to stabilize 2. strong ECC > ISO > CON; consistent for all joint angles

Question 35

Why ECC strongest: 1. positive braking 2. passive tension of cytoskeleton PRO 3. increased CB 4. passive stretching of titin

Answer 35

1. stretched CB resists ext load by attempting to Powerstroke while it actin is pulled away from M line by ext load, increasing tension 2. proteins resist change to the configuration, resistance increases tension 3. dragging actin away forces detachment and reattachs myosin as it flails, using more heads for stronger resistance, some myosin stuck on, no ATP req 4. winding filament hypothesis: Ca2+ activates titin N2A to bind prox Ig to actin, more tension in PEVK creates more force

Question 36

Why CON are weakest 1. SEC slack 2. sliding filament effect 3. negative braking effect

Answer 36

1. muscle shortening, losing some force to take up SEC when it slacks, less force to muscle 2. as myosin pulls actin fast, other myosin heads do not have opportunity to powerstroke, number of CB decreases, decrease force 3. CB bound to actin during shortening don't have opportunity to detach, creating drag opposing CON force, decrease force

Question 37

why ISO is in between ECC and CON

Answer 37

no sig sliding filaments after initial shortening to take up SEC, muscle force = ext load, CB repeatedly attach and detach from same actin binding site