Week 13 - muscle Flashcards
classification of muscles
skeletal muscle, smooth muscle, cardiac muscle
what is skeletal muscle activated by
somatic nervous system
motor unit
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
neuro-muscular junction NMJ
Synpase between a motor neuron and muscle fiber
contractile filaments in skeletal muscle
sarcomeres; striated
they have a well-developed sarcoplasmic reticulum
muscle
group of fascicles
muscle fibers extend the length of muscle from tendon to tendon
what is muscle fiber made up of
myofibrils, sarcolemma, t-tubule system, sarcoplasmic reticulum
T-tubule system
Invaginations of sarcolemma into muscle fiber
It allows the spread of action potential
sarcolemma
plasma membrane
sarcoplasmic reticulum
intracellular organelle, Ca2+ storage
3 broad categories of muscle fibers
- Slow twitch oxidative ; red muscle
- Fast twitch oxidative-glycolytic ; red muscle
- Fast twitch glycolytic ; white muscle
how muscle fibers of a motor unit contract
they all contract together
muscle contraction begins with small motor units being activated first
what do the smoothness and precision of movement depend on?
Number and timing of motor units that are activated
slow twitch oxidative fibers
slowly contracting
many mitochondria
oxidative metabolism
small diameter
important in posture
fast twitch oxidative - glycolytic
faster contracting
moderate amount of mitochondria
glycolytic metabolism but becomes oxidative with endurance training
Used for standing and walking
medium diameter
fast twitch - glycolytic
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
small diamater motor neurons
innervate slow oxidative fibers, more easily excited
large diameter motor neurons
innervate fast glycolytic fibers, less easily excited
Anatomy of neuromuscular junction
Terminal bouton = axon terminal (motor neuron)
Motor end plate = specialized muscle membrane at junction
properties of NMJ
all motor neurons release acetylcholine
all synapses are excitatory
what does activation of motor neurons depend on
summation of EPSPs and IPSPs
communication at NMJ - how does Ach bind to nicotinic receptors
- Action potential arrives at terminal bouton
- Voltage-gated calcium channels open
- Calcium enters the cell triggering the release of Ach
- Ach diffuses across cleft and binds to nicotinic receptors on motor end plate
communication at NMJ- what happens after Ach binds to nicotinic receptors
- Ach binding triggers opening of channels for small cations (Na and K)
- Net movement of positive charge, causes depolarization
- causes action potential in muscle cell
- action potential spreads through muscle causing contraction
how is the brain protected from toxins in the body
blood brain barrier
what is exposed to circulating toxins
peripheral tissues including muscles
toxins that block NMJ
nicotinic receptor blocker
exocytosis blocker
Ach-esterase inhibition
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.
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
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
cross bridge cycle
how muscles generate force
filaments in skeletal muscle fiber
thin filament - actin
thick filament - myosin
sarcomeres
actin and myosin are organized in overlapping arrangements with respect one another in units called saromeres
muscle contraction
sarcomere shortening
actin and myosin do not change length, instead they slide past one another
thick filament
made up of myosin molecuels
myosin head contains actin binding site and ATP binding site
thin filament
made up of 2 strands of actin molecules
actin molecule has a binding site for myosin
whats present on actin
troponin, tropomyosin, nebulin
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
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
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
power stroke
myosin head moves propelling the thin actin filaments towards the centre of the muscle
crossbridge cycle overview
power stroke
thick and thing filaments detach
myosin head returns to initial position, cycle starts again
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
what does myosin release at end of power stroke
ADP
what happens when there is no more ATP
tight binding in rigor state, muscles contracted and cross bridge cant detach
what happens when ATP binds to myosin
Myosin releases actin
what happens when myosin hydrolyzes ATP
myosin head rotated to cocked position, myosin weakly binds to actin
when does power strok begin
when tropomyosin moved off the binding site
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
what happens when acetylcholine is released from motor neurons
bidning oc acetylcholine
na+ entry, leading to muscle ap
what happens when calcium binds to roponin
actin-myosin binding, power stroke occurs
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
how is contraction terinated
calcium must leave binding sites
how is calcium moved from the cytosol
Ca2+ ATPase in sarcoplasmic reticulum
transport calcium from cytosol into sarcoplasmic reticulum
3 phases of muscle twitch
latent period, period of contraction, period of relaxation
muscle twitch
its a single contraction-relaxation cycle
to generate force u need to have many twitches working together
period of relaxation
intracellular Ca2+ levels fall, eventually tension gradually falls to 0
period of contraction
intracellular Ca2+ levels are high, cross-bridge cycling occurring
latent period
excitation-contraction coupling occurring
summation
stimuli close together do not let muscle to relax fully
what happens in muscle with increased AP frequency
succesive twitched fuse with each other, contractile force rises
summation leading to unfused tetanus
stimuli are far enough aparat to allow muscle to relax slightly between stimuli
summation leading to complete tetanus
muscles reached steady tension, In muscle fatigues, tension decreases rapidly
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
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
classification of smooth muscle
by location
by communication with neighbouring cells (single unit or multi-unit smooth muscle)
single unit smooth muscles - wehre are they found
ntestinal trcact, blood vessels, etc
activity of single unit smooth muscles
spotaneous acitvity (but also activated by ANS)
able to actively exert tension in absence of external stimulation w
where are multi unit smooth muscles found
large airways and arteries
activity of multi unit smooth muscles
each fiber acts individually, heavily innervated, generally contracts only when nervous supply is stimulated
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
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
relaxation of smooth muscle
Phosphatase removes phosphate from myosin
* Calcium removed from cytoplasm
– Ca-ATPase
– Ca-Na counter transport
cells in cardiac muscle
contractile and conductile cells
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)
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+
how long does cardian contractil cell AP last
almost as long as contraction and relaxation
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)
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
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
