6 Muscle Physio Flashcards
What are muscle cells?
Highly specialized cells for the conversion of chemical energy (ATP) to mechanical energy
Describe the skeletal muscle cell in terms of: A. Control (Voluntary or involuntary) B. Striation C. Number of nucleus/cell D. Characterize E. Organization
A. Voluntary
B. Striated
C. Multinucleated
D. Fibers in fibers in fibers arranged in parallel
E. Organization
Muscle (epimysium) -> muscle fasciculus (perimysium) -> muscle fiber (endomysium) -> myofibril composed of many, repetitive sarcomeres
What do you call an individual muscle cell?
Muscle fiber
Part of a muscle fiber
- Cell membrane
- Cytoplasm
- ER
- Cell
- Sarcolemma
- Sarcoplasm
- Sarcoplasmic Reticulum
- Muscle fiber
What is the fundamental/functional unit of a skeletal muscle? Describe components
Sarcomere
- From Z-Z disk
- I band - thin band (mainly actin) only
- H band - thick (myosin) band only
- A band - entire length of thick filaments, including overlap with thin
- M line - line in the middle which helps organize or align thick filaments; where thick filaments connect
- Z line - where sarcomere will be connected to the sarcolemma and endomysium through costameres
What is the largest protein in the body? Function?
Titin. It tethers myosin to the Z disk
Arrangement of skeletal muscle fibers?
Hexagonal lattice where every thick filament is surrounded by thin filaments allowing optimal interaction between thin and thick filaments
When the sarcomere contracts, which part/s of the sarcomere shortens? Lengthens? Stays the same?
Shortens: H and I band, Z-Z distance
Same: A band and M & Z line
What composes the thin filaments?
Actin double helix/filamentous actin
Nebulin -regulates length of thin filament
Tropomyosin - blocks actin binding sites
Troponin complex
>Troponin T - binds to tropomyosin
>Troponin I - inhibits actin-myosin binding; strengthens actin-tropomyosin interaction
>Troponin C - binds to Ca2+
Thick filament composition? Briefly describe
Thick filament = myosin filament
Consists of 200+ myosin molecules
Each myosin molecule has 2 heavy chains and 4 light chains: 2 light chains (essential light chains) which enable myosin to utilize ATP; 2 light chains (regulatory light chains) influence actin-myosin binding strength/kinetics
What is the “cross-bridge”?
Protruding arm and head of the myosin
What is a costamere? Function?
Consists of the dystrophin-glycoprotein complex + integrins + other related proteins
>Connects Z line to the sarcolemma and endomysium (connective tissue surrounding muscle fiber) maintaining muscle integrity
What is the sarcotubular system? Function?
Sarcotubular system = SR + T-tubules
Function: Envelops the myofibrils
What is a triad?
>Location?
>Function of each composition of the triad
> Composition: 2 terminal cisternae of SR + 1 t-tubule of the sarcolemma
Located in the A-I junction
Terminal Cisternae - where you’ll find the most conc of Ca2+ in the AR
T-tubule - ensures AP will get transferred to each and every myofibril
How does a muscle contract?
Excitation-contraction coupling >STEPS Step 1: NMJ Nerve-to-muscle connection AP reaches end of motor neuron/nerve -> inc. Ca2+ Influx (VG channels will be open bc of AP) -> cause fusion of vesicles cont NT with the membrane = release of Ach -> ACh bind to ACh receptor (Ligand-gated Na+ channel) Ach binding = open Na+ will go in = build up local potential once LP reaches threshold, VG Na+ channels will open = AP Ach degraded by acetylcholinesterase *so ACh rec will be ready to receive another signal Step 2: Sarcolemma and SR
AP travels along membrane and goes down through T-tubules (and reaches each & every myofibril inside the muscle cell) ->
AP arrival in T-tub = Activates DHPR aka L-type Ca2+ channels -> DPHR activation = Activates RYR in terminal cisternae -> (RYR are your calcium release channels thus when activated, Release of Ca2+ (from terminal cisternae) into myofibril
How do DHPR and RYR interact?
In heart/cardiac muscle, DHPR opens, causes Ca2+ influx, then Ca2+ influx causes RYR to open (CICR: Calcium induced Calcium release)
flow of Ca2+ in DHPR would cause RYR to open
In skeletal muscle, DHPR is mechanically attached to RYR. So if DHPR changes shape, RYR mechanically opens, allowing Ca2+ to flow to the myofibrils (MECHANICAL OPENING MAJOR not CICR)
Step 3: Actin-myosin interxn
At rest, tropomyosin blocks binding site; myosin has ADP Is already attached to myosin head = has processed that ATP = “cocked” position (nakakasara siya)
When we have influx of Ca2+:
A) Ca2+ binds to Troponin C, which causes troponin to change shape. Once troponin changes shape, it’ll move tropomyosin away from binding site, which exposes the binding site in actin
B) Myosin head attaches to binding site (aka cross-bridging). ADP is released causes: Myosin head rotates to pull actin inward (*myosin Flexes). Sarcomere shortens
“Power stroke”
C) Myosin head now has a free binding site. ATP attaches, weakening the myosin-actin bond. Myosin detaches.
D) Myosin head hydrolyzes ATP, producing ADP + P. This provides energy to “re-cock” the myosin head.
*Light chains
*As long as ATP is present and binding sites are exposed,power stroke will continue/cycle will continue = “Cross-bridge cycle” = mech of sliding filament theory
Step 4: Muscle relaxation
Once signals from AP stops -> no stimulation of DHPR, RYR (bc Ca2+ not longer released by RYR)
SERCA: Pumps 2 Ca2+ back into (SR) terminal cisternae per ATP hydrolyzed; pump that’s always active but can’t complete its job when Ca2+ floods your myofibril
(*Once very low Ca2+, troponin will return to original shape and will cause tropomyosin to cover the binding sites again so no longer have the actin-myosin interxn)
Decreased Ca2+ -> Tropomyosin blocks actin binding site again -> decreased actin-myosin interaction
