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PSL300 > Week 13 - muscle > Flashcards

Week 13 - muscle Flashcards

1
Q

classification of muscles

A

skeletal muscle, smooth muscle, cardiac muscle

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2
Q

what is skeletal muscle activated by

A

somatic nervous system

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3
Q

motor unit

A

1 motor neuron and all the muscle fibers it innervates. A muscle may have many motor units of different types; muscle fibers in a motor unit are all of the same type

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4
Q

neuro-muscular junction NMJ

A

Synpase between a motor neuron and muscle fiber

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5
Q

contractile filaments in skeletal muscle

A

sarcomeres; striated
they have a well-developed sarcoplasmic reticulum

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6
Q

muscle

A

group of fascicles
muscle fibers extend the length of muscle from tendon to tendon

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7
Q

what is muscle fiber made up of

A

myofibrils, sarcolemma, t-tubule system, sarcoplasmic reticulum

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8
Q

T-tubule system

A

Invaginations of sarcolemma into muscle fiber
It allows the spread of action potential

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9
Q

sarcolemma

A

plasma membrane

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10
Q

sarcoplasmic reticulum

A

intracellular organelle, Ca2+ storage

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11
Q

3 broad categories of muscle fibers

A
  1. Slow twitch oxidative ; red muscle
  2. Fast twitch oxidative-glycolytic ; red muscle
  3. Fast twitch glycolytic ; white muscle
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11
Q

how muscle fibers of a motor unit contract

A

they all contract together
muscle contraction begins with small motor units being activated first

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12
Q

what do the smoothness and precision of movement depend on?

A

Number and timing of motor units that are activated

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13
Q

slow twitch oxidative fibers

A

slowly contracting
many mitochondria
oxidative metabolism
small diameter
important in posture

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14
Q

fast twitch oxidative - glycolytic

A

faster contracting
moderate amount of mitochondria
glycolytic metabolism but becomes oxidative with endurance training
Used for standing and walking
medium diameter

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15
Q

fast twitch - glycolytic

A

fast twitch time
produce large amounts of tension
rapid fatigue
low mitochondria
its the least used but used in jumping, quick fine movements
large diameter

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16
Q

small diamater motor neurons

A

innervate slow oxidative fibers, more easily excited

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17
Q

large diameter motor neurons

A

innervate fast glycolytic fibers, less easily excited

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18
Q

Anatomy of neuromuscular junction

A

Terminal bouton = axon terminal (motor neuron)
Motor end plate = specialized muscle membrane at junction

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19
Q

properties of NMJ

A

all motor neurons release acetylcholine
all synapses are excitatory

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20
Q

what does activation of motor neurons depend on

A

summation of EPSPs and IPSPs

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21
Q

communication at NMJ - how does Ach bind to nicotinic receptors

A
  1. Action potential arrives at terminal bouton
  2. Voltage-gated calcium channels open
  3. Calcium enters the cell triggering the release of Ach
  4. Ach diffuses across cleft and binds to nicotinic receptors on motor end plate
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22
Q

communication at NMJ- what happens after Ach binds to nicotinic receptors

A
  1. Ach binding triggers opening of channels for small cations (Na and K)
  2. Net movement of positive charge, causes depolarization
  3. causes action potential in muscle cell
  4. action potential spreads through muscle causing contraction
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23
Q

how is the brain protected from toxins in the body

A

blood brain barrier

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24
Q

what is exposed to circulating toxins

A

peripheral tissues including muscles

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25
Q

toxins that block NMJ

A

nicotinic receptor blocker
exocytosis blocker
Ach-esterase inhibition

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26
Q

nicotinic receptor blocker

A

poison dart (curare)
curariform drugs

it prevents opening of the cation channels, in the end plate. hard to generate AP. sometimes its used to relax muscles for medical examinations.

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27
Q

exocytosis blocker

A

botox

botulin poisoning - type of food poisoning and prevents release of vesicles from terminals of motor axon.
End plate not depolarized - no AP
When botox applied to face, it relaxes facial muscles, getting rid of wrinkles

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28
Q

Ach esterase inhibition

A

Ach esterase is responsible for the break down of Ach. Constant depol occurs – paralysis – depolarization block occurs s Na+ channels in vicinity are kept inactivated

nerve gases, pesticides

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29
Q

cross bridge cycle

A

how muscles generate force

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30
Q

filaments in skeletal muscle fiber

A

thin filament - actin
thick filament - myosin

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31
Q

sarcomeres

A

actin and myosin are organized in overlapping arrangements with respect one another in units called saromeres

32
Q

muscle contraction

A

sarcomere shortening
actin and myosin do not change length, instead they slide past one another

33
Q

thick filament

A

made up of myosin molecuels
myosin head contains actin binding site and ATP binding site

34
Q

thin filament

A

made up of 2 strands of actin molecules
actin molecule has a binding site for myosin

35
Q

whats present on actin

A

troponin, tropomyosin, nebulin

36
Q

troponin and tropomyosin action when there is no calcium

A

troponin holds tropomyosin over myosin binding sites on actin
no cross-bridges form between actin and myosin - muscle relaxed

37
Q

troponin and tropomyosin action when there is calcium present

A

it binds to troponin, causing movement of troponin, which causes the movement of tropomyosin, exposing binding sites for myosin on actin
Crossbridges form between actin and myosin - muscle contracts

38
Q

what does myosin switch back and forth between

A

it undrgoes conformation chnages swiveling back and forth between the high energy form (high affinity for actin) and the low energy form (low affinity for actin)
it relies on ATP hydrolysis

39
Q

power stroke

A

myosin head moves propelling the thin actin filaments towards the centre of the muscle

40
Q

crossbridge cycle overview

A

power stroke
thick and thing filaments detach
myosin head returns to initial position, cycle starts again

41
Q

increase of calcium - cross bridge cycle

A

myosin head and actin filaments bind strongly
powerstroke occurs, myosin head moves propelling the thin filament toward centre of muscle

42
Q

what does myosin release at end of power stroke

A

ADP

43
Q

what happens when there is no more ATP

A

tight binding in rigor state, muscles contracted and cross bridge cant detach

44
Q

what happens when ATP binds to myosin

A

Myosin releases actin

45
Q

what happens when myosin hydrolyzes ATP

A

myosin head rotated to cocked position, myosin weakly binds to actin

46
Q

when does power strok begin

A

when tropomyosin moved off the binding site

47
Q

excitation-contraction coupling

A

sequence of events wherebt an action potential in the sarcolemma causes contraction
dependent on neural input from motor neuron
requires calcium release

48
Q

what happens when acetylcholine is released from motor neurons

A

bidning oc acetylcholine
na+ entry, leading to muscle ap

49
Q

what happens when calcium binds to roponin

A

actin-myosin binding, power stroke occurs

49
Q

what does the action potential in t-tubule cause

A

alteration of DHP (dihydropyridine L-type calcium channel)
DHP receptor open RyR (ryanodine receptor channel) and there’s calcium release in sarcoplasmic reticulum
Ca2+ enters cytoplasm

50
Q

how is contraction terinated

A

calcium must leave binding sites

51
Q

how is calcium moved from the cytosol

A

Ca2+ ATPase in sarcoplasmic reticulum
transport calcium from cytosol into sarcoplasmic reticulum

52
Q

3 phases of muscle twitch

A

latent period, period of contraction, period of relaxation

53
Q

muscle twitch

A

its a single contraction-relaxation cycle
to generate force u need to have many twitches working together

54
Q

period of relaxation

A

intracellular Ca2+ levels fall, eventually tension gradually falls to 0

54
Q

period of contraction

A

intracellular Ca2+ levels are high, cross-bridge cycling occurring

55
Q

latent period

A

excitation-contraction coupling occurring

56
Q

summation

A

stimuli close together do not let muscle to relax fully

57
Q

what happens in muscle with increased AP frequency

A

succesive twitched fuse with each other, contractile force rises

58
Q

summation leading to unfused tetanus

A

stimuli are far enough aparat to allow muscle to relax slightly between stimuli

59
Q

summation leading to complete tetanus

A

muscles reached steady tension, In muscle fatigues, tension decreases rapidly

60
Q

smooth muscles

A

found in internal organs, blood vessels
eg. vasculature, GI tracts, urinary, reporductive tracts, etc
not arranges in sarcomeres, its undervoluntary control by ANS

61
Q

how do smoothe muscles operate

A

must operate over a range of lengths
layers may run in several directions
it contracts and relaxes much more slowly
uses less energy “and sustains contractions for extended periods

62
Q

classification of smooth muscle

A

by location
by communication with neighbouring cells (single unit or multi-unit smooth muscle)

63
Q

single unit smooth muscles - wehre are they found

A

ntestinal trcact, blood vessels, etc

64
Q

activity of single unit smooth muscles

A

spotaneous acitvity (but also activated by ANS)
able to actively exert tension in absence of external stimulation w

65
Q

where are multi unit smooth muscles found

A

large airways and arteries

66
Q

activity of multi unit smooth muscles

A

each fiber acts individually, heavily innervated, generally contracts only when nervous supply is stimulated

67
Q

excitation contraction coupling - smooth muscles

A

Lacks specialized receptor regions
* Ca2+ is from the extracellular fluid and sarcoplasmic reticulum
* Ca2+ initiates a cascade ending with phophorylation of myosin light chain and activation of myosin ATPase

68
Q

mechanism of excitation contraction coupling - smooth muscles

A

Opening of calcium channels in
plasma membrane
* Calcium triggers release of calcium
from sarcoplasmic reticulum
* Calcium binds to calmodulin
* Ca-Calmodulin activates MLCK
* MLCK phosphorylates myosin
* Crossbridge cycling

69
Q

relaxation of smooth muscle

A

Phosphatase removes phosphate from myosin
* Calcium removed from cytoplasm
– Ca-ATPase
– Ca-Na counter transport

70
Q

cells in cardiac muscle

A

contractile and conductile cells

71
Q

cardiac muscle

A

Contractile filaments in sarcomeres; striated
* Intermediate development of SR
* Gap-junctions for synchronous beat
* Activity modulated by ANS (unlike skeletal muscle = somatic nervous system)

72
Q

cardia muscle action potential

A

AP duration 300ms in ventricles
* AP plateau due to slow Ca2+ channels allows time for forceful contraction from single AP
* Plateau allows muscle contraction to last 300ms (20-50x longer than in skeletal muscle)
* AP shape and duration reflects changing permeability to Na+, Ca2+

73
Q

how long does cardian contractil cell AP last

A

almost as long as contraction and relaxation

74
Q

cardiac muscle contraction

A

frank startling law
One way to increase force of
contraction:
* Unable to increase force of contraction by motor unit
recruitment or by enhanced
excitation/contraction coupling
* Unable to increase force of
contraction by increasing stimulation
frequency to tetanus
* Increase force of contraction by
increasing muscle length (Starling
law)

75
Q

excitaiton contraction coupling - cardiac muscle

A

Significant Ca2+ source from ECF, rest
from SR
* Contractile proteins in presence of
increased cytosolic [Ca2+] power
contraction (systole)
* Ca2+ pump in the SR removes Ca2+
from cytosol allowing for relaxation
(diastole)
* Na+/Ca2+ membrane exchange
removes Ca2+ from cytosol allowing
for diastole

76
Q

digitalis

A

cardiac glycoside used to treat conditions such as congestive heart failure and it works directly on the heart muscle to strengthen heart. beatc by increasing ca levels and inhibiting na-k atpase. high intracellular Na levels, low Na influx, low ca efflux, high ca

PSL300 (19 decks)

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