B1W3: Skeletal Muscle Flashcards
Organization of Muscles
- Whole muscle
- Muscle fiber (muscle cell)
- Myofibrils (within cell, sarcomeres)
- Contractile filaments/proteins/structural proteins
Titin
Attaches to Z line and keeps thick filaments in line during contraction
CapZ
attaches actin filaments to Z line
prevents actin depolarization
Nebulin
On thin filament
Maintains constant length of each filament
Z line
Boundary of sarcomere
Where thin filaments attch
I band
Thin filaments (and z disks)
“I is a thin letter”
Disappears during contraction
A band
length of thick filaments
Thhin and thick filaments may overlap here
H zone
Thick filaments only
“H is a thick letter”
disappears during contraction
M line
Center of the thick filament
Structural protein
Label
Myosin components
Thick filaments
Two heavy chains for the tail, 4 light chains that form two globular heads
–actin binding site
–ATPase activity
Two of the light chains necessary, other two regulatory for smooth muscle
Thin filaments
Two F-actin strands and two strands tropomyosin
Actin contains myosin binding sites
Troponin: 3 subunits, one binds Ca2+ and the other two bind tropomyosin and actin
Tropomyosin: regulatory protein that binds to actin and troponin (blocks active myosin binding sites)
Hinges of myosin
One allows head to reach up and grab onto the myosin filament, another is at the myosin head and grabs onto actin
Muscle Contraction Steps
- Mysoin head is attached to actin in rigor state
- ATP binds to myosin and myosin head releases actin
- Myosin hydrolyzes ATP to “cock” myosin head
- Myosin binds actin to form new cross bridge
- Phosphate is released and myosin head has power stroke
- ADP released
How would no ATP impact skeletal muscle contraction?
- Myosin head would not release actin
- Ca2+ not pumped out of cell via (Ca/H+) pump
- Ca2+ not pumped into SR
How are skeletal muscles activated? How many nerve action potentials are needed for a muscle action potential?
Motor nerve impulses
Every nerve action potential will cause a muscle action potential
What is the neurotransmitter released and ion that helps release it at neuromuscular junction?
AcH
Ca2+
What kind of receptors does AcH in muscle cells bind to?
Ach binds to nicotinic receptor, increasing Na+ and K+ conductance
Depolarization because Na+ conductance has greater effect
How does curare block muscle contraction?
Blocks Ach binding to nicotinic receptor completely
Are you supposed to see end plate potentials?
NO! Every EPP=AP
if you see one, the neuromuscular transmission is fucked up (maybe Curare?)
How does botulinum toxin block muscle contraction?
Cleaves V and T Snares on vesicles of presynaptic neuron
AcH is not released, muscle will not contract
How would giving a patient with myasthenia gravis neostigmine (Acetylcholine esterase inhibitor) help treat their condition?
Neostigmine inhibits acetylcholinesterase
By blocking that enzyme, AcH builds up and not deraded, increases likelihood of muscle contraction
T Tubules
Network of muscle cell membrane that carries depolarizations from action potentials
Contains DHP receptors that attach to ryanodine receptors on SR
Sarcoplasmic reticulum
Stores calcium, releases it and re-uptakes it
Ryanodine receptors are opened by voltage-gated DHP receptors, cause release of Ca2+ into cell
Calsequestrin binds to calcium in SR to maintain low free conc.
SERCA helps pump Ca2+ in
Triad
T tubule
SR–terminal cisternae
Excitation-Contraction Coupling
Action potential due to Na+ current leads to Ca2+ release into the cell from the sarcoplasmic reticulum
AP causes depolarization of DHP receptor, which releah opens ryanodine channel and Ca2+ into cell from SR
When done, SERCA pumps Ca back into cell
Maliganant hyperthermia
SR Ca2+ channels genetically altered, and this appears under anesthesia
SR Ca2+ channels do not close properly, Ca2+ leaks into cytoplasm causing sustained contractions, generating heat (NOT GOOD!)
Isometric
Same length, contraction without shortening of muscle
i.e. lifting bar
Isotonic
Same force, muscle contraction with shortening of muscle
Lifting dumbell over and over again
Quantal summation
As more motor units are recruited, the strength of the muscle contraction increases
Temporal summation
Stimulating contractions at a higher frequency, causing increased strength
Treppe
after a long period of rest, initial muscle contraction may not be as strong as later stimuli of same strength (i.e. why warm up before working out)
Tetanization
Contrations so frequent muscle cannot relax bc Ca2+ not pumped into SR fast enough
Twitch contractions
Summate to one steady contraction
Passive tension
Tension developed by stretching muscle to diff. lengths
Active tension
Total tension-passive tension
=degree overap between filaments capable of generating cross bridges
What happens to muscle as length increases above normal?
Tension before contraction increases and contractile force decreases at longer lengths
At a long enough length, tension before contraction=total force, no contractile force generated
Resting length and filaments
Optimal overlap thin and thick filaments
Force-Velocity relationships
Velocity decreases as load increases
Vmax constant for specific given skeletal muscle
Load is so much, V=o at isometric contraction
V=max when load is 0
When is active force maximum?
Normal length, resting length, or optimal length (all the same)
Fast fibers (white)
Larger fibers
Fast twitch myosin isoform
Less extensive blood supply
No myoglobin; abundant glycolytic enzymes, fewer mitochondria
Slow fibers (red)
smaller fibers
slow twitch myosin isoform
more mitochondria, contain myoglobin
extensive blood supply
adapted for slow, continuous activity
