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Physiology Week 2 > Excitation Contraction Coupling > Flashcards

Excitation Contraction Coupling Flashcards

1
Q

outline

A
  1. A motor AP travels along a motor neuron to the motor end plate at the NMJ
  2. nerve endings secrete Ach, which acts on local area of the sarcolemma to open numerous Ach gated ion channels
  3. opening of these channels permits sodium ions in, depolarizing the muscle membrane potential, initiating AP that propagates along the muscle fiber membrane
  4. muscle AP propagates down the T tubule into the interior to the triad junction, causes a release of calcium from SR
  5. increased concentration of calcium ions in the sarcoplasm activates sliding filament
  6. calcium pumped back in by Ca-ATPase ion pump
  7. lengthening of the muscle achieved by contraction of an antagonistic muscle
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2
Q

Ach at NMJ

A
  1. neuronal AP travels down axon jumping nodes of ranvier, travels to the terminal button (presynaptic terminal)
  2. neuronal AP depolarizes terminal button and causes voltage gated Ca channels to open, ca in
  3. elevated calcium causes the vesicles of Ach to fuse with the membrane and dump Ach into synaptic cleft
  4. Ach binds to receptors in muscle PM (end plate)
  5. Ach R opens, Na in, depolarizes end plate, changes end plate potential
  6. depolarized end plate causes Na channels to open further down in PM, initiating the muscular AP
  7. AchE inactivates Ach
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3
Q

Myasthenia Gravis

A
  • autoimmune attack on AchR-reduced excitation
  • tire easily/ muscle weakness/ ptosis
  • edrophonium chloride is AchE inhibitor
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4
Q

other disorders of EC coupling

A
  1. motor neuron- ALS
  2. nerve disease-demyelinating-Guillain-Barre
  3. NMJ- myasthenia gravis
  4. Muscle- DMD
  5. sarcomere- malignant hyperthermia
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5
Q

ALS

A
  • amyotrophic lateral sclerosis
  • motor neuron death in spinal cord- reduced excitation
  • loss of neuronal AP
  • weakness, spasticity, muscle atrophy
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6
Q

injury

A
  • axonal damage
  • blocked neuronal AP propagation-reduced excitation
  • paralysis, weakness, often some recovery
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7
Q

Guillan Barre

A
  • AI response against myelin
  • impaired neuronal AP propagation-reduced excitation
  • ascending paralysis, weakness
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8
Q

muscular dystrophy

A
  • reduced attachment of muscle to ensheathing membrane
  • inefficient myofiber contraction/death-reduced contraction
  • muscle weakness and atrophy
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9
Q

malignant hyperthermia

A
  • mutation ind Ryr1 causing excessive calcium release in muscle
  • triggered by inhaled anesthetics
  • excessive and prolonged contraction
  • blood co2 buildup, hyperthermia, circulatory collapse
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10
Q

Na and Ca release

A
  • AP propagated down T tubule
  • opens calcium channels in SR, releasing Ca into sarcoplasm
  • doesnt need extracellular calcium
  • some calcium bound by calsequestrin in SR
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11
Q

Ca release at triad

A
  1. membrane depolarization opens L type Ca channel (DHP receptor) in T tubule
  2. mechanical coupling between the L type channel and the Ca release channel (ryanodine receptor) causes the ryanodine receptor to open-DHP receptor changes shape and pulls on ryanodine and opens its calcium channel gate
  3. Ca exits SR via the ryanodine receptor and activates troponin C
  4. Ca entering the cell via L type channels can also activate the Ryanodine receptor, not essential in skeletal muscle
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12
Q

ryanodine

A
  • plant alkaloid that binds to and opens SR calcium release channels at nanamolar concentration
  • higher concentraction of ryanodine closes the receptors
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13
Q

calcium induced calcium release

A
  • SR releases its calcium rapidly through this process
  • ryanodine receptor stimulated to open by cytoplasmic calcium as well as from movement of the L Ca channel
  • small amt released into cytoplasm triggers adjacent ones, occurs along length of SR, not just at the triad
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14
Q

skeletal muscle relaxatoin

A
  • Na-Ca exchanger and Ca pump in the PM extrude Ca
  • Ca pump sequesters Ca in SR
  • bound in SR by calereticulun and calsequestrin
  • SERCA-SR calcium ATPase-pumps back into SR
  • PM Ca ATPas-PMCA-pumps outside
  • NCX-Na/Ca exchanger-3 NA in 1 Ca out
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15
Q

temporal relation between skeletal AP, calcium, twitch

A
  • AP fast, then Ca, then tension

- twitch duration is directly related to calcium duration- more calcium means more twitch

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16
Q

tetany

A
  • single AP produces muscle twitch
  • high frequency AP produce unfused and then fused tetanus
  • single twitches, temporal summation, unfused tetanus, fused tetanus
  • functional refractory period of AP is shorter than contraction time, high frequency APs cause contractions to summate
  • strength of contraction graded by rate coding (freq of AP) and recruitment of additional motor units
17
Q

treppe

A
  • steady increase in tension in successive twitches
  • not summation because relaxes to 0 in between
  • may be because Ca released from previous twitches exceeds reuptake, increases cross bridges each time
18
Q

motor unit

A
  • 1 motor neuron and all the myofibers it innervates
  • single neuron will innervate multiple myofibers but each myofiber only innervated by 1 neuron
  • large motor units can have 2000 muscle fibers
  • smallest is 3
  • large motor units in fast twitch, small in slow twitch
  • when activated, the innervated muscle fibers simultaneously contract with all or none twitches
  • rate coding and summation can occur if the motor neuron fires AP repetitively
19
Q

recruitment

A
  • large motor units are recruited after small as more force is required
  • when force requirement is low but control high, fewer muscle fibers working gives fine control
  • as more force is needed, the impact of each new motor unit becomes greater
20
Q

ATP for skeletal muscle

A

-1-2 seconds

21
Q

Phosphocreatine in muscle

A
  • Pcr+ADP–>ATP

- 5-8 seconds

22
Q

anaerobic metabolism of glucose

A

Glucose–> 2 lactic acid and ATP

  • limited by lactic acid formation, not glucose amt
  • fast twitch
23
Q

oxidative metabolism of glucose

A

Glucose + 6 o2—>6 co2 + 6 H20+ ~30 ATP

  • 2-4 hours
  • slow twitch and type IIa fast twitch
24
Q

oxidative metabolism of fats, carbs, proteins

A
  • FA + o2—> co2 + h20 + ATP
  • AA +o2—> co2 + h20 + urea + ATP
  • many hours
  • slow twitch and type IIa fast twitch
25
Q

muscle pain

A
  • acute-lactic acid buildup
  • delayed onset-due to muscle damage and IF response
  • glucose—>lactic acid and ATP
26
Q

muscle fatigue

A

-decline in muscle tension as a result of use
1. less maximal tension
2. decreased shortening velocity
3. slower rate of relaxation
Probable causes
1. gradual depletion of SR calcium store
2. buildup of Pi that inhibits release from myosin
3. lactic acid buildup leading to lower pH
TnC lower affinity for Ca at low pH
Myosin release of ADP slower in low pH
4. not caused by ATP depletion
-recovery slow-may protect muscle from damage
-high frequency fatigue from high intensity short duration exercise caused by failure of AP conduction in the T tubule, has fast recovery

Physiology Week 2 (4 decks)

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