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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
what is exposed to circulating toxins
peripheral tissues including muscles
25
toxins that block NMJ
nicotinic receptor blocker exocytosis blocker Ach-esterase inhibition
26
nicotinic receptor blocker
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.
27
exocytosis blocker
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
28
Ach esterase inhibition
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
29
cross bridge cycle
how muscles generate force
30
filaments in skeletal muscle fiber
thin filament - actin thick filament - myosin
31
sarcomeres
actin and myosin are organized in overlapping arrangements with respect one another in units called saromeres
32
muscle contraction
sarcomere shortening actin and myosin do not change length, instead they slide past one another
33
thick filament
made up of myosin molecuels myosin head contains actin binding site and ATP binding site
34
thin filament
made up of 2 strands of actin molecules actin molecule has a binding site for myosin
35
whats present on actin
troponin, tropomyosin, nebulin
36
troponin and tropomyosin action when there is no calcium
troponin holds tropomyosin over myosin binding sites on actin no cross-bridges form between actin and myosin - muscle relaxed
37
troponin and tropomyosin action when there is calcium present
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
what does myosin switch back and forth between
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
power stroke
myosin head moves propelling the thin actin filaments towards the centre of the muscle
40
crossbridge cycle overview
power stroke thick and thing filaments detach myosin head returns to initial position, cycle starts again
41
increase of calcium - cross bridge cycle
myosin head and actin filaments bind strongly powerstroke occurs, myosin head moves propelling the thin filament toward centre of muscle
42
what does myosin release at end of power stroke
ADP
43
what happens when there is no more ATP
tight binding in rigor state, muscles contracted and cross bridge cant detach
44
what happens when ATP binds to myosin
Myosin releases actin
45
what happens when myosin hydrolyzes ATP
myosin head rotated to cocked position, myosin weakly binds to actin
46
when does power strok begin
when tropomyosin moved off the binding site
47
excitation-contraction coupling
sequence of events wherebt an action potential in the sarcolemma causes contraction dependent on neural input from motor neuron requires calcium release
48
what happens when acetylcholine is released from motor neurons
bidning oc acetylcholine na+ entry, leading to muscle ap
49
what happens when calcium binds to roponin
actin-myosin binding, power stroke occurs
49
what does the action potential in t-tubule cause
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
how is contraction terinated
calcium must leave binding sites
51
how is calcium moved from the cytosol
Ca2+ ATPase in sarcoplasmic reticulum transport calcium from cytosol into sarcoplasmic reticulum
52
3 phases of muscle twitch
latent period, period of contraction, period of relaxation
53
muscle twitch
its a single contraction-relaxation cycle to generate force u need to have many twitches working together
54
period of relaxation
intracellular Ca2+ levels fall, eventually tension gradually falls to 0
54
period of contraction
intracellular Ca2+ levels are high, cross-bridge cycling occurring
55
latent period
excitation-contraction coupling occurring
56
summation
stimuli close together do not let muscle to relax fully
57
what happens in muscle with increased AP frequency
succesive twitched fuse with each other, contractile force rises
58
summation leading to unfused tetanus
stimuli are far enough aparat to allow muscle to relax slightly between stimuli
59
summation leading to complete tetanus
muscles reached steady tension, In muscle fatigues, tension decreases rapidly
60
smooth muscles
found in internal organs, blood vessels eg. vasculature, GI tracts, urinary, reporductive tracts, etc not arranges in sarcomeres, its undervoluntary control by ANS
61
how do smoothe muscles operate
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
classification of smooth muscle
by location by communication with neighbouring cells (single unit or multi-unit smooth muscle)
63
single unit smooth muscles - wehre are they found
ntestinal trcact, blood vessels, etc
64
activity of single unit smooth muscles
spotaneous acitvity (but also activated by ANS) able to actively exert tension in absence of external stimulation w
65
where are multi unit smooth muscles found
large airways and arteries
66
activity of multi unit smooth muscles
each fiber acts individually, heavily innervated, generally contracts only when nervous supply is stimulated
67
excitation contraction coupling - smooth muscles
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
mechanism of excitation contraction coupling - smooth muscles
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
relaxation of smooth muscle
Phosphatase removes phosphate from myosin * Calcium removed from cytoplasm – Ca-ATPase – Ca-Na counter transport
70
cells in cardiac muscle
contractile and conductile cells
71
cardiac muscle
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
cardia muscle action potential
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
how long does cardian contractil cell AP last
almost as long as contraction and relaxation
74
cardiac muscle contraction
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
excitaiton contraction coupling - cardiac muscle
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
digitalis
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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