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Exercise Physiology > MT1 > Flashcards

MT1 Flashcards

1
Q

4 properties of muscles

A
  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
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2
Q

Gross muscle histology (CT, components)

A
  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
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3
Q

Muscle fibre histology

A
  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
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4
Q

Muscle fibre characteristics

A
  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
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5
Q

Structure of actin myofilaments

A
  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
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6
Q

Structure of myosin myofilament

A
  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
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7
Q
  1. Z disk
  2. I band
  3. A band
  4. H zone
  5. M line
  6. arrg of actin and myosin
A
  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
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8
Q

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

A

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

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9
Q

Cross bridge cycle

A
  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
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10
Q
  1. bare zone
  2. characteristic of cross bridges
  3. electric properties of muscle cell
  4. MAP propagatuon
A
  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
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11
Q

Neuromuscular junction
1. overview
2. process

A
  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
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12
Q

excitation-contraction coupling

A

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

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13
Q

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

A
  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
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14
Q

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

A
  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
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15
Q
  1. cytoskeletal protein
  2. sarcomere force transmission
  3. costamere force transmission
A
  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)
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16
Q

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

A
  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
17
Q
  1. myotendinous junction
  2. turnover
A
  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
18
Q

1 . satellite cell
2. SC role

A
  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
19
Q

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

A
  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)
20
Q
  1. exercise and satellite cell
  2. number of myonuclei
  3. hypertrophy
A
  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
21
Q
  1. regen/repair/remodelling
  2. quantify dmg in muscle
A
  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
22
Q

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

A
  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
23
Q

Caffeine and performance

A

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

24
Q
  1. Motor unit def
  2. all or none principle
  3. innervation ratio
A
  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
25
Q
  1. muscle twitch
  2. ryanodine v. SERCA
  3. femoral muscle stim
A
  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
26
Q
  1. Twitch
  2. Summation
A
  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
27
Q
  1. tetanus def
  2. unfused tetanus
  3. fused tetanus
A
  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
28
Q
  1. recruitment
  2. subthreshold
  3. threshold
  4. submaximal
  5. maximal
A
  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
29
Q

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

A
  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
  4. Series elastic bands attaching end to end at Z disks, parallel sarcolemma and CT around contractile unit
30
Q

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

A
  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
31
Q
  1. Force-Ca2+-Frequency relationship
  2. unfused tetanus
  3. fused tetanus
  4. diminishing returns
A
  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
32
Q
  1. success of power strokes
  2. int v. ext work of muscles
A
  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
33
Q
  1. concentric v isometric
  2. central motor drive
A
  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
34
Q
  1. agonist v. antagonist
  2. Contraction type and max force
A
  1. agonist under CON to perform action, antagonist ECC opposes force to stabilize
  2. strong ECC > ISO > CON; consistent for all joint angles
35
Q

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

A
  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
36
Q

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

A
  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
37
Q

why ISO is in between ECC and CON

A

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

Exercise Physiology (3 decks)

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