muscle contraction Flashcards
motor unit
motor neuron + it’s muscle fibers
large fibers - large movement
small - fine movement (eye)
NMJ
presyn = axon terminal
postsyn = muscle endplate
steps at the NMJ
- Ap conducted into pre-syn terminal
- depolarize pre-syn terminal
- Opening of VG-Ca2+ channels and entry
- fusion of vesicles w membrane - Ach into cleft
- Ach binds receptor on post-syn membrane
- opening of channels on post-syn membrane - Na and K travel down gradient
- generation of EPP
- Ach broken down into coline and acetate - choline back to pre-syn
10.
EEP characteristics
latency - delay from AP –> muscle
graded - size dep on how many vesicles of Ach released
quantal - goes up step by step (each vesicle) - adds up to full potential
decremental conduction - gets smaller further away from end plate
high safety factory (skel muscle) - as long as EPP what it’s supposed to be you will get AP!
decremental conduction
if EEP but NOT AP
at nmj you can still see the EEP but it goes away (still see same strong AP far away)
muscle structure
muscle - fascile - muscle cell (fiber) - myofibrils (in muscle cell covered by SR) - myofibrils - sarcomere (with actin and myosin)
T tubules
formed from invaginations of plasma membrane
triad
sarcoplasmic reticulum cisterna on either side of transverse tubule
skeletal muscle excitation
- AP into T tubules
- VG L-type Ca channel conformational change
- Ca release channel open (mechanically cated, Ca gated)
- mytoplasmic [Ca] increases
Ca DOES NOT MOVE through L-type channels in the T tubules
how do skeletal and cardiac muscle excitation differ
- Ca enters through L type channels
- no mechanical link between L type and SR ca release (80% from SR, 20% from membrane)
- can be modulated
tropomyosin
binds to actin and troponin
TnT
troponin T
binds to tropomyosin
TnC
tropinon
binds to Calcium
TnI
interferes
troponin
how does troponin work
increased Ca –> binds to TnC –> actomyosin complex formed –> tension increases
E-C coupling in skeletal muscle
muscle action potential
increase in Ca - myoplasm
Ca-troponin
increase muscle tension
decrease muscle tension
SERCA
Ca-ATPase - pumps Ca back into SR
primary active transport
calsequestrian
bound to ca in SR
relaxation in skeletal musche
- l type Ca channels close
- Ca-gated channel inactivated
- SERCA pump back in
- Ca binding proteins in cytoplasm
differences betwen cardiac and skeletal uscle relaxation
sarcolemma:
Ca-Na pump
Ca pump
SR:
PLN –> increases SERCA
all can be regulated
Ca release channels in skeletal muscles
mechanically and ionically
crossbridge system
isometric tension
length - no change
tension - increasing
head rotates developing isometric contraction
acheives 45% by stretching neck of myosin (not enough tension to shorten sarcomere)
recruits more and more muscle fibers until enough muscle tension
isotonic tension
length - shortening
tension - no change
muscles can’t change length and tension at same time
muscle resting length-tensison
more stretched - increased resting tension
Titan
mechanism of passive and restoring force generation
when tighten muscle - titan stretches
molecular basis for resting tension
fused tetanus
summation of tetanic stimulus until it fuses
how to increase active tension
increase stimulus frequency
recruit motor units
active tension
total tension when contract (measured) - resting tension
hihest at resting length
sliding filament model
- F due to interaction of thick and thin filaments
- muscle filament length is constant
- filaments can slide past each other
- isometric F is proportional to thick and tin filament overlap
isometric force and length
due to interaction of thick and thin filaments
0 tension when 0 overlap or full over lap
most tension when meet - no overlap
middle when slight overlap
same in cardiac and skeletal muc
length-tension plot
shows changesin isometric tension with sarcomere (muscle) length
isometric
for more tension - add crossbridges and muscle fibers
same length - recruit more
don’t shorten until have enough tension
isotonic
when muscle begins to shorten - no more crossbridges or muscle fibers are added
what if lifting more than you can hold up isometrically?
first need titan to lift for a second but then will drop it
preload
determines initial muscle length
determined by amt of blood in the heart
(resting tension)
afterload
determines force required to shorten and end muscle length
pressure in orta (what pushing against but doesn’t know it’s there)
shortening velocity
depends on myosin isoform (ATPase)
and force against which muscle contracts (afterload)
at heaviest load - muscle can’t contract - V = 0
AND preload (at heavy - few xb available for fast cycling, at light - many xb available for fast cycling)
high BP- can’t contract as fast bc so much afterload
- afterload 2. preload 3. myosin isoform(ATPase)
velocity and afterload
bigger F pumping against - lower Velocity
shortening velocity and myosin ATPase
Myosin ATPase (EC 3.6.4.1) is an enzyme with system name ATP phosphohydrolase (actin-translocating). [1] This enzyme catalyses the following chemical reaction ATP + H2O ADP + phosphate. ATP hydrolysis provides energy for actomyosin contraction.
shortening velocity and preload
resting length - number of crossbridges ready to be formed for fast cycling
power
afterload x velocity of showertening
max power = 1/3 max load
rate of doing work
dep on:
- myosin ATPase
- load (afterload)
- resting load (preload)
