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Physiology > Excitation Contraction Coupling (ECC) > Flashcards

Excitation Contraction Coupling (ECC) Flashcards

1
Q

what is myasthenia gravis caused by?

A

autoimmune response to ACh receptors (neuromuscular junction disease) so cannot initiate AP in muscle
-ptosis, weak smile, diploplia, speech slur symptoms: improve with edrophonium chloride (cholinesterase inhibitor to increase ACh at neuromuscular junction)

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2
Q

what is ALS amyotrophic lateral sclerosis a disease of?

A

motor neuron death in spinal cord

  • loss of neuronal AP (reduced excitation)
  • weakness, spasticity, muscle atrophy
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3
Q

what are demyelinating diseases caused by?

A

peripheral nerve disease b/c autoimmune VS myelin

  • impaired neuronal AP propagation (reduced excitation)
  • ascending paralysis, weakness
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4
Q

what is muscular dystrophy a disease of?

A

muscle disease (reduced attachment of muscle to ensheathing membrane)

  • inefficient myofiber contraction, myofiber death (reduced contraction)
  • muscle weakness and atrophy
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5
Q

what is malignant hyperthermia a disease of?

A

sarcomere disease (mutation of ryanodine receptor Ryr1 causing excessive Ca++ release into muscle)

  • triggered by inhaled anesthetics
  • excessive and prolonged myofiber contraction
  • blood CO2 buildup, hyperthermia, circulatory collapse
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6
Q

can skeletal muscle contract in the absence of extraccellular Ca++?

A

yes, b/c Na+ dependent AP triggered by ACh release at neuromuscular junction triggers release of Ca++ from SR inside muscle cell/fiber

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7
Q

dihydropyridine (DHP) receptor

A

L-type Ca++ channel on T-tubule membrane, attached to ryanidine receptors of terminal cisternae
-changes structure with depolarization, to open ryanodine receptor channel gate

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8
Q

ryanodine receptor

A

Ca++ release channel attached to terminal cisternae

  • opened by DHP receptor during depolarization
  • causes Ca++ release into sarcoplasm, triggering sarcomere contraction
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9
Q

ryanodine and nanomolar and micromolar concentrations

A

[nanomolar] - binds to and opens ryanodine receptors

[micromolar] - closes ryanodine receptors

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10
Q

calcium induced calcium release (positive feedback)

A

SR releases Ca++ store rapidly

  • ryanodine receptors open via DHP receptors and presence of cytoplasmmic Ca++
  • this means that small amount of Ca++ released into sarcoplasm triggers adjacent ryanodine receptors (away from triad) to open and release Ca++ in positive feedback motion
  • thus, Ca++ release occurs rapidly along entire length of SR, not just triad
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11
Q

what induces skeletal muscle relaxation?

A

when Ca++ is removed from sarcoplasm by Ca++ exchangers and pumps

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12
Q

mechanisms of Ca++ removal from sarcoplasm (3 types)

A

SERCA - uses ATP hydrolysis to pump Ca++ back into SR to be bound
PMCA - plasma membrane Ca++ ATPase that pumps 1 Ca++ out of the cell per 1 ATP
NCX - Na+ Ca++ exchanger that lets 3 Na+ into cell per 1 Ca++ out of cell

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13
Q

unfused tetanus

A

repetitive stimulation (summation) APs oscillate (hit AP during refractory period, but not soon enough to fuse)

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14
Q

what is the strength of contraction of skeletal muscle graded by? (3 things)

A
  1. rate ccoding, or frequency of stimulation
  2. recruitment of additional motor units
  3. size of motor units stimulated
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15
Q

fused tetanus

A

repetitive stimulation (summation) APs don’t oscillate (hit AP during refractory period soon enough to fuse)

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16
Q

treppe

A

steady increase in tension in successive twitches

  • not summation, b/c tension returns to zero before next twitch
  • occurs b/c Ca++ released from previous twitches excceeds Ca++ reuptake, causing increase in Ca++ concentration, thus increasing X-bridges that form
  • also b/c frequent stimulation “warms up” muscle to increase enzymatic rate
17
Q

what does Ca++ bind to within SR?

A

calreticulin and calsequestrin

18
Q

what is a motor unit made of?

A

one motor neuron and multiple myofibers
-a single neuron will innervate multiple muscle fibers, but a single skeletal muscle fiber is innervated by only one neuron

19
Q

small VS large motor units

A

small: single neuron and as few as 3 muscle fibers (extraoccular), in slow twitch
large: single neuron and 2000+ muscle fibers, in fast twitch
when motor unit activated, all innervated muscle fibers simultaneously stimulated

20
Q

what is the order of small/large motor unit recruitment

A

Size principle - smaller motor units recruited first, then larger ones as more force is required
-fine control possible if recruit only few muscle fibers

21
Q

how long does the energy supplied by ATP last?

A

1-2 seconds

22
Q

how does phosphocreatine make ATP, and how long does its energy last?

A

PCr + ADP –> Cr + ATP

lasts 5-8 seconds

23
Q

how does fermentation of glucose make ATP, and how long does its energy last?

A

glucose –> 2 lactic acid + 2 ATP

lasts 60 seconds (limited by lactic acid formation, not glucose amount)

24
Q

how does oxidative metabolism of glucose make ATP, and how long does its energy last?

A

glucose + 6 O2 –> 6 CO2 + 6 H2O + 30 ATP

lasts 2-4 hours

25
Q

how does oxidative metabolism of fats/CHO/PRO make ATP, and how long does its energy last?

A

FA + O2 –> CO2 + H2O + ATP
AA + O2 –> CO2 + H2O + urea + ATP
lasts many hours

26
Q

muscle pain (burn)

A

due to lactic acid buildup when heavy muscle activity and low O2 cause muscle to reoly on fermentation to make ATP

  • lactic acid accumulates in muscle fiber (burning)
  • in heart = angina
27
Q

what is angina?

A

buildup of lactic acid in cardiac muscle, b/c it is undergoing fermentation due to heavy activity and low O2

28
Q

delayed onset muscle soreness

A

not correlated with lactic acid levels

  • occurs in days following intense muscle use
  • associated with muscle damage, maybe inflammatory response
29
Q

muscle fatigue

A

decline in muscle tension due to muscle use, gradual depletion of SR Ca++ stores, and buildup of lactic acid and inorganic phosphates

  • less maximal tension
  • decreased shortening velocity (Vmax)
  • slower rate of relaxation
  • not due to low ATP
  • may be adaptation to prevent rigor from low ATP level
30
Q

what does low ATP favor?

A

stable actin myosin complexes, high Ca++ levels in sarcoplasm, thus rigor

31
Q

high frequency fatigue

A

accompanies high intensity, short duration exercise

  • due to failure in conduction of AP in T-tubule
  • rapid recovery
32
Q

low frequency fatigue

A

caused by low intensity, long duration exercises

  • due to buildup of lactic acid and phosphates, which may change conformation of muscle PRO
  • recovery is slow

Physiology (60 decks)

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