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muscles Flashcards

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1
Q

events at NMJ

A
  1. AP propagates down presynaptic neuron
  2. depolarization opens voltage-gated Ca channels
  3. Ca entry triggers ACh exocytosis
  4. ACh diffuses across synaptic cleft & binds w/ receptors in motor end-plate
  5. binding opens cation channels ➞ Na enters & depolarizes end plate (EPP)
  6. depolarizing current flows downstream to other voltage-gated Na channels (AP) in PM
  7. ACh in synaptic cleft is degraded by ACh-esterase
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2
Q

tendons

A
  • attaches muscle to bone & contracts
  • shock absorption
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3
Q

myofibril anatomy

A
  • 1 myosin filament is surrounded by 6 actin filaments
  • 1 actin filament is surrounded by 3 myosin filaments

myosin = thick filaments

  • thick bands of sarcomeres
  • cytoskeleton protein made of a long tail & a globular head
  • actin-binding site & myosin ATP-ase site on head
  • 5x larger than actin

actin = thin filaments

  • light band of sarcomeres
  • 3 proteins arranged to form double helical strand
    1. actin
    2. tropomyosin = threads that swirl around actin helix that blocks myosin-binding sites
    3. troponin
      1. troponin I = inhibitory ➔ binds to actin
      2. troponin T binds to tropomyosin
      3. troponin C binds to Ca
  • 7:1 actin to troponin complex ratio

sarcomeres = contractile units of myofibers from Z line to Z line

  • Z line = boundaries & site where actin filaments attach
  • A band = actin & myosin overlap
  • I band = actin only
  • H band = myosin only ➞ lighter area in center of A band where actin does not reach
  • M line = line in middle of H zone (& A zone) where myosin filaments join
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4
Q

myofibril physiology

A
  • myosin heads form cross-bridge with actin
    • heads form cross bridges with 6 surrounding myosin ATPase sites on actin
    • 6:1 actin to myosin
    • myosin ATPase provides ATP for cross-bridges via ATP hydrolysis (Mg-dependent)
  • troponin C binds Ca
  • troponin I binds to actin in a way the holds tropomyosin in place, blocking the myosin-binding site
  • troponin C binds to Ca, which changes the configuration of troponin I, which changes the configuration of troponin T, which changes the configuration of tropomyosin to so it no longer blocks the myosin binding site & cross-bridges can attach
  • sarcomeres shorten during cross-bridge activity
    • Z-lines come closer together
    • H bands shorten
    • I bands shorten
    • A bands maintain same width
    • indiv actin & myosin filaments maintain constant length ➞ only relative position changes
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5
Q

general cross-bridge activity

A
  1. binding: energized myosin heads bind to myosin-binding site on actin
  2. power stroke: myosin heads bend, pulling actin filament & releasing ADP + Pi
  3. detachment: ATP attaches to myosin & myosin detaches ➔ actin & myosin return to original position
  4. binding: cross-bridge binds to more distal actin mol & cycle repeats
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6
Q

role of Ca in initiating cross bridge

A
  1. AP spreads down T-Tubules & transmits AP from sarcolemma to interior of myofiber
  2. depolarization in T tubules activates dihydropyridine receptors
  3. changes Ca permeability in foot proteins (ryanodine receptors) = Ca release channels
  4. Ca released into cytosol to bind to troponin C
  • when myofiber is relaxed: actin-binding site is covered by troponin-tropomyosin complex
  • when muscle fiber is excited: Ca binds to troponin C ➞ causes sequence of conformational changes that pulls troponin-tropomyosin complex aside to expose binding site
    Ca stimulates conformational changes in troponin C
    • troponin C changes structure ➔ troponin I changs structure ➔ tropomyosin changes structure & frees myosin-binding site
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7
Q

sarcoplasmic reticulum

A

modified ER composed of interconnected tubules where Ca is actively transported & stored

  • separate segments of SR are wrapped around each A band & each I band
  • lateral sacs = enlarged regions of SR at the end of each A & I band on both sides of T-tubules that store Ca
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8
Q

lateral sacs

A

enlarged regions of SR at the end of each A & I band on both sides of T-tubules that store Ca

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9
Q

transverse (T) Tubule

A

perpendicular continuous extension of sarcolemma at each A band-I band junction ➔ transmits AP from sarcolemma to interior of myofiber

  • dihydropyridine receptor = voltage-gated receptor protein in T tubule membrane
    • activated by depolarization in T-tubules
    • open foot proteins in adjacent lateral sacs that release Ca
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10
Q

foot proteins

A

Ca release channels in lateral sacs of SE

  • aka ryanodine receptors
  • triggered by dihydropyridine receptor
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11
Q

dihydropyridine receptor

A

voltage-gated receptor protein in T tubule membrane

  • activated by depolarization in T-tubules ➔ open foot proteins in adjacent lateral sacs
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12
Q

ATP movement in contraction

A
  1. split by myosin ATPase ➔ stores energy in cross bridge
  2. when Ca is excited it moves the troponin-tropomyosin complex
  3. ADP + Pi released by power stroke of cross bridge
  4. cross-bridge detaches & ATP binds to myosin
  5. cycle repeats
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13
Q

motor unit

A

1 motor neuron & all fibers it innervates

  1. 1 motor neuron innervates multiple muscle fibers but each muscle fiber is only supplied by 1 motor neuron
  2. all muscle fibers contract when motor neuron is activated
  3. motor neuron is distributed evenly throughout muscle ➔ even contraction
  • # of muscle fibers/unit per muscle
  • precise, delicate movements = ↓
  • powerful, coarse movements = ↑
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14
Q

motor unit recruitment

A

↑ # of motor units contraction

  • less for weaker, more for stronger
  • results in large incremental increases in whole-muscle tension
  • ↑ motor units ≠ same degree of fine control
  • asynchronous recruitment can delay or prevent fatigue
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15
Q

muscle tension

A

extended contraction

  • depends on # of motor units recruited & tension developed my each contracting fiber
  • influenced by:
    • frequency of stimulation
    • length of fiber at onset
    • extent of fatigue
    • thickness of fiber
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16
Q

tetanus

A
  • smooth sustained contraction of maximal strength
  • fiber is stimulated so rapidly ➞ no chance to relax between stimuli
  • much stronger contraction than twitch
17
Q

length-tension relationship

A
  • tension depends on fiber length at onset of contraction
  • optimal muscle length (lo) ➞ can develop maximal tension
    • most myosin-actin binding
    • max # of cross bridges & actin molecules that can interact
    • too shortened ➔ actin overlap = ↑ myosin-actin binding
    • too stretched ➔ no interaction
18
Q

muscle metabolism

A

ATP = energy store for powerstroke & active transport of Ca

  1. creatine phosphate hydrolysis energy + ADP ➔ ATP
    • small reserve of ↑ energy photphate for ATP synthesis
    • immediate ➞ 1st source
    • can supply ATP for <1 minute
  2. oxidative phosphorylation: aerobic metabolism of glucose & fatty acids
    • slowest
    • produces most ATP
    • requires O2
    • good for light-moderate exercise
    • supports aerobic or endurance exercise
  3. glycolysis: anaerobic metabolism of glucose
19
Q

excitation-contraction coupling

A

when thick & thin filaments in a sarcomere slide past each other

20
Q

twitch summation

A

↑ tension of accompanying repetitive stimulation of muscle fiber

  • 2 twichtes from AP close together in time add together to produce even greater tension
  • possible b/c AP much faster than a resting twitch ➔ is over before twitch is beginning so 2nd AP adds on
  • no summation of AP b/c of refractory period, but whole AP cycle can repeat before twitch starts
  • must have enough cytosolic Ca$^2$$^+$ to keep supplying cross-bridges
21
Q

muscle fatigue

A

when an exercising muscle can no longer respond to stimulation w/ the same strength of contractions

  • no glycogen reserves & ↑levels of Pi (ATP was broken down already ∴ not available for use)
  • recovery: replenish muscle glycogen & creatine phosphate following intense activity
  • neuromuscular fatigue = inability of NMJ to synthesize ACh fast enough to sustain chemical transmission of AP from motor axon to muscle cell
  • central fatigue = when CNS cannot adequately activate motor neurons
  • excess post-exercise oxygen consumption (EPOC) = need for elevated O2 uptake during recovery
22
Q

skeletal muscle types

A

slow oxidative (type I)

  • slow contraction
  • relies on oxidative phosphorylation ➞ dependent on O
  • high in:
    • mitochondria (site of oxidative phosphorylation)
    • myoglobin (binds & carries oxygen)
    • blood supply (carries myoglobin/O2)

fast oxidative (type IIa)

  • fast contraction
  • relies on oxidative phosphorylation ➞ dependent on O
  • high in:
    • mitochondria (site of oxidative phosphorylation)
    • myoglobin (binds & carries oxygen)
    • blood supply (carries myoglobin/O2)

fast glycolytic (type IIx)

23
Q

fast oxidative (type IIa) muscle fibers

A
  • myosin-ATPase activity: high
  • speed of contraction: fast
  • resistance to fatigue: intermediate
  • oxidative phosphorylation capacity: high
  • mitochondria: many
  • capillaries: many
  • myoglobin content: high
  • color of fiber: red
  • glycogen content: intermediate
24
Q

slow oxidative (type I) muscle fibers

A
  • myosin-ATPase activity: low
  • speed of contraction: slow
  • resistance to fatigue: high
  • oxidative phosphorylation capacity: high
  • mitochondria: many
  • capillaries: many
  • myoglobin content: high
  • color of fiber: red
  • glycogen content: low
25
Q

fast glycolytic (type IIx) muscle fibers

A
  • myosin-ATPase activity: high
  • speed of contraction: fast
  • resistance to fatigue: low
  • oxidative phosphorylation capacity: low
  • mitochondria: few
  • capillaries: few
  • myoglobin content: low
  • color of fiber: white
  • glycogen content:high
26
Q

neuromuscular fatigue

A

inability of NMJ to synthesize ACh fast enough to sustain chemical transmission of AP from motor axon to muscle cell

27
Q

central fatigue

A

when CNS cannot adequately activate motor neurons

28
Q

smooth muscle

A
  • long thick myosin filaments
  • contain intermediate filaments for structural support
  • thin actin filaments that contain tropomyosin but no troponin
    • calmodulin instead of troponin (very similar)
    • both bind to 4 Ca
    • calmodulin also binds to 200+ other mol (troponin only actin & Ca)
  • no sarcomere ➞ dense bodies that act as anchors instead
  • no T-tubule organization in sarcolemma
  • SR not well developed ➞ primary Ca source = ECF
  • 10-15:1 thin:thick filaments oriented diagonally
  • contraction of filament lattice causes cell shortening & expanding
29
Q

smooth muscle excitation-contraction coupling

A
  • smooth muscle myosin can only interact w/ actin when phosphorylated
  • during excitation: Ca acts as intracellular messenger that causes phosphorylation of myosin
    1. self or neuronal excitation leads to Ca entry from extracellular space through voltage-gated channels
    2. entry triggers release of more Ca from SR ➔ Ca from SR + ECF
    3. binds w/ calmodulin = intracellular protein similar to troponin
    4. Ca-calmodulin complex activates myosin kinase which phosphorylates myosin
    • kinase phosphorylates proteins
    • phosphorylation = key for myosin to bind to actin
  1. phosphorylated myosin binds to actin to form activated cross-bridges
  2. removal of Ca ➞ myosin dephosphorylation ➞ dissociation from actin
  3. gap-junctions rapidly propagate excitation to all coupled-cells in network
  4. contraction strength depends on cytosolic [Ca]
30
Q

types of smooth muscle

A
  1. multi-unit smooth muscle cells are activated by neural input (neurogenic)
  • walls of large vessels
  • large airways to lungs
  • muscles of the eye that adjust lens
  • iris of eye
  • base of hair follicles (goosebumps)
  1. single-unit smooth muscle cells capable of generating pacemaker activity that are coupled to a functional syncytium by gap junctions
  • walls of GI, reprod tract, urinary tract, small vessels
31
Q

smooth muscle innervation by autonomic postganglionic nerve terminals

A
  • no motor unit recruitment ➞ all cells connected by gap junctions
  • diff nerve fibers can influence 1 SM cell can be b/c of gap junction coupling between cells
  • neural input does not directly initiate contraction ➞ can modify rate & strength
32
Q

forms of self-excitation in smooth muscle

A
  1. pacemaker potential = gradual depolarization until reaches threshold
  2. slow-wave potential = alternating depolarizing & hyperpolarizing swigs in MP

NPB 101 (13 decks)

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