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kin 131 > musle physiology 1.1 > Flashcards

musle physiology 1.1 Flashcards

1
Q

contraction

A
  • activation of the force generating sites within muscle fibers - the cross bridges
  • does not necessarily mean shortening
  • can be isometric where muscle generating tension while its holding the joint in a steady position
  • or even when lengthening (eccentric - down)
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2
Q

alpha motor neurons

A
  • innervate skeletal muscle fibers
  • located in brain stem or spinal cord and carry out to skeletal muscles
  • are myelinated and have large diamteter axons
  • propagate fast, allowing signals from the CNS to travel to skeletal muscle fibres with minimal delay
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3
Q

motor unit

A

motor neuron + muscle fibers it innervates

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4
Q

how many muscle fibers does a single motor neuron innervated

A

a single motor neuron innervates many muscle fibers, but each muscle fiber is controlled by a branch from only one motor neuron

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5
Q

what happens when AP occurs in motor neuron?

A

all the muscle fibers in its motor unit are stimulated to contract

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6
Q

motor end plate

A

region of the muscle fiber plasma membrane that lies directly under the terminal portion of the axon

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7
Q

neuromuscular junction

A

junction of axon terminal with the motor end plate

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8
Q

events at neuromuscular juntion

A

AP arrives in a motor neuron to axon terminal

  • Ca2+ diffuses into the axon terminal
  • Ach released from vessicles to extracellular cleft to the motor end plate
  • Ach binds to ionotropic reecptors (nicotinic)
  • channel open, Na and K pass down diffusion gradient (Na in K out)
  • depolarization of the motor end plate (end-plate potential) (EPP)
  • Ap propagated over surface of muscle fiber into T-tubules *
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9
Q

magnitude of EPP smaller or larger than that of EPSP

A

Magnitude of EPP much larger bc the neurotransmitter is released over a larger surface area, binding to many more receptors and opening many more ion channels

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10
Q

how many EPP neccesary to depolarize

A

only one is normally more than sufficient to depolarize the plasma membrane to the end-plate membrane to its threshold potential

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11
Q

muscular junction excitatory inhibitory both?

A

all muscular junctions are excitatory in skeletal muscle

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12
Q

acetylcholinesterase

A

enzyme that breaks down Ach
-choline is then transported back into the axon terminals where it is reused in the synthesis of new Ach

-As we breakdown Ach, more Ach will come off the receptors and be broken down. No more Ach bound= ion chanels in the end plate close. Now it returns to its resting potential and can respond to the subsequent arrival of Ach released by another neuron AP

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13
Q

neuromuscular junction

A
  • neuron to motor end plate
  • AP will propagate in both directions
  • Cause an EPP
  • magnitude of EPP is much larger than EPSP
  • 1 EPP sufficient to depolarize
  • All excitatory
  • every AP in a motor neuron produces an AP in each muscle fiber in its motor unit
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14
Q

inhibiting acetylcholinesterase

A
  • organophosphates inhibit acetylcholinesterase
  • in pesticides/nerve gases
  • What happens? Ach is not destroyed, channels remain open-> cannot generate another AP
  • receptors desensitized to Ach
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15
Q

antidote for disruption of neuromuscular signaling

A

pralidoxime (reactivates acetylcholinesterase) and atropine (muscarinic receptor antagonist)

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16
Q

excitation-contraction coupling

A

-the sequence of events by which an action potential in the plasma membrane activate the force-generating mechanisms (muscle contraction)

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17
Q

ap skeletal muscle lasts

A

1-2msec

-is completed BEFORE any signs of mechanical activity begin (MUSCLE CONTRACTION)

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18
Q

mechanical activity

A

follows an AP and last 100msec or more

AP’s are quick, mechanical activity longer

19
Q

electrical activity in plasma membrane

A
  • *does not** directly act upon contractile proteins
  • > increases cytosolic Ca2+ concentration

-when we continue to contract the muscle after the action potential is gone because of the calcium in the cytosol

20
Q

tropomyosin at rest

in ca2+ cross-bridge formation

A
  • composed two intertwined polypeptides
  • partially cover the myosin-binding site on each actin monomer, preventing cross bridges from making contact with actin
21
Q

troponin at rest

A
  • holds tropomyosin in place and covers the myosin binding site on actin
  • are all on the thin filament
22
Q

tropomyosin during contraction

what process allows cross bridges to form?

A
  • moves away from myosin-binding site
  • This process occurs when Ca2+ binds to troponin, resulting in the tropomyosin moving off the myosin binding site, allowing cross bridge formation
  • if more Ca then greater contraction
23
Q

troponin 3 sites

A

I = Inhibitory

T= tropomyosin-binding

C=Ca2+

24
Q

mechanism of cytosolic increase in Ca2+

t-tubule

A
  • extension of plasma membrane
  • several ion channels (Ca2+)
  • devoted to excitation-contraction coupling
  • site for AP propagation
25
Q

mechanism of cytosolic increase in Ca2+

DHP receptor (dihydropyridine)

A
  • on t-tubule
  • acts as a voltage sensor for calcium
26
Q

mechanism of cytosolic increase in Ca2+

ryanodine receptor

A
  • on sarcoplasmic reticulum
  • has squigley line that connects to DHP receptor
  • will let Ca2 out
27
Q

mechanisms of cytosolic DECREASE Ca2+

A
  • need to remove Ca2+ from troponin by lowering Ca2+ concentration in the cytosol to relax
  • using calcium ATPase
28
Q

calcium ATPase (pump)

A
  • pumps calcium ions from cytosol back into the lumen of the sarcoplasmic reticulum
  • requires longer time
  • Ca2+ is released from the reticulum when an AP begins in the t-tubule
  • Ca2+ pump requires ATP

-Ca2+ is exchanged with na+

29
Q

sliding filament mechanism

A

-tension is produced by the sliding of thin along the thick filaments within the sarcomere

  • no change in length of either the thick or thin filaments
  • movement of the cross bridges causes thick and thin filaments to move past each other

A band stays same size, I band gets smaller

30
Q

power stroke

A
  • pulls thin filaments towards center of sarcomere, maximum contraction
  • sarcomere becomes shorter
  • occurs when myosin binds to actin, myosin will then detach and attach to next molecule, happens several times
31
Q

all sarcomeres contract/shorten simulataneously as well as relax simultaneously

A

true

32
Q

A band

A

thick filaments

33
Q

I band

A

thin filaments

34
Q

how many sarcomeres in a muscle

A

20000

35
Q

cross bridge cycle 4 steps - first step

A
  1. attachment of the cross bridge to a thin filament, actin binding→ cytosolic increase in calcium leads to attachment
36
Q

step 2

A
  • movement of the crossbridge, producing tension in the thin filament
  • power stroke occuring

-release of ADP and organic phosphate which produces movement of cross bridge and powerstroke

37
Q

step 3

A
  • detachment of the crossbridge from the thin filament
  • cross bridge dissociation from actin

-using ATP binding to myosin?

38
Q

step 4

A

atp bound to myosin

  • ready for next cycle
  • ATP hydrolysis which energizes cross-bridge
39
Q

rigor mortis

A

atp decreasing in cells, ca leaking out of SR, cant pump it back in and cross bridges are broken, thick and thin cannot be pulled past each other

-gradual stiffening of skeletal muscles that begins after death

40
Q

synaptic junction

A

neuron to neuron

ap will propagate in one direction

causes an EPSP or IPSP
magnitude of EPSP is not as large as EPP

usually need multiple EPSP to reach threshold and initiate an AP

Excitatory or Inhibitory

41
Q

curare (poison blow darts)

A

binds strongly to nicotinic receptors so doesnt allow you to open those channels, ACh cant bind to them, when that happens you cant contract muscles, preventing you from breathing

42
Q

describe the whole process of the mechanism of cytosolic increase in Ca2+ **review this

A

Ap comes through the motor neuron has vesicles with Ach, come to the motor end plates and attach to receptors for sodium and potassium and causes an action potential, calcium ? travels down the t tubules where voltage sensitive calcium DHP receptors activate the ryanodine receptors which let calcium out of the sarcoplasmic reticulum. This increases cytosolic concentration of calcium and leads to more calcium binding to troponin = more cross bridge formation

43
Q

what happens if there is an increase in calcium ?

A

more ca is binding to troponin and more tropomyosins are moving off the myosin binding sites on actin = greater contraction *

kin 131 (27 decks)

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