Muscle Part 1 Flashcards
Muscle tissue transforms chemical energy ______ to directed mechanical energy
ATP
Muscle tissue characteristics
-Highly vascular
-Highly innervated
-Huge nutrient and oxygen need
-Generates large amount of waste
-Excitability: Receive and respond to stimuli
-Contractility: Shorten forcibly when stimulated
-Extensibility: Ability to be stretched
-Elasticity: Ability to recoil to resting length
– Insertion
– Origin
– movable bone
– immovable (less movable) bone
Muscle is made up of ________ which are composed of _______ which are composed of ________ which are composed of _________ which are made of ________
Fascicles
Muscle cells
Myofibrils
Sarcomeres: Functional, structural contractile unit
Filaments: Actin and Myosin and Titan
Skeletal Muscle Fiber (Cell)
Long, cylindrical cell (up to 20 cm)
Multiple peripheral nuclei:
- From fusion of myoblasts during development
- Regulation of gene expression and protein synthesis
Satellite cells (stem cells):
Can form myoblasts after damage. Repair or form new muscle fibers.
Sarcolemma= Plasma membrane
Sarcoplasm= Cytoplasm
Myofibrils
Densely packed, rodlike elements
About 80% of cell volume
Contain sarcomeres - contractile units
Sarcomeres contain myofilaments
Sarcomere
Region between two successive Z lines
M line runs down the middle
Composed of thick (myosin) and thin (actin) myofilaments made of contractile proteins
A band (Dark)
I band (White)
H zone
-where there is myosin
-the area around the Z disc where there is no myosin
-the area around the M line where there is no actin
– Actin myofilaments
– Myosin myofilaments
= thin filaments, anchored to Z discs
= thick filaments, connected at M line
Elastic filament
– Composed of protein titin
– Holds thick filaments in place
– Helps recoil after stretch
– Resists excessive stretching
Sarcoplasmic Reticulum & T-tubules
Can you label them?
Sarcoplasmic Reticulum (SR)
Network of smooth ER surrounding each myofibril
Most run longitudinally
Functions in regulation of
intracellular Ca2+ levels
Stores and releases Ca2+
Transverse Tubules (T-tubules)
- Continuations of sarcolemma
- Lumen continuous with extracellular space
- Increase muscle fiber’s surface area
Penetrate cell’s interior
Triads = 1 T tubule + 2 terminal cisternae of SR
T-Tubules interact with the terminal cisternae of SR= release of stored Ca+2 in the cytosol
Physiology of a Muscle Contraction
For skeletal muscle to contract:
1- Membrane Excitation (at neuromuscular junction)
* Must be nervous system stimulation
* Must generate action potential in sarcolemma
2- Excitation-contraction coupling
a) Action potential propagated along sarcolemma= Intracellular Ca2+ increased
b) Cross bridge Cycling
Neuromuscular junction
– Neuron–muscle connection
– Axon of neuron contacts
sarcolemma of muscle cell (fiber)
– Also called a motor end plate
Motor Unit
1 neuron + all of the muscle fibers it contacts
Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber.
1) Motor neuron action potential.
2) Ca2+ enters voltage gated channels
3) Acetylcholine release
4) Acetylcholine binding opens ion channels
5) Na+ entries
6) Local current between depolarized end plate and adjacent muscle plasma membrane.
7) Muscle fiber action potential initiation
8) Propagated action potential in muscle plasma membrane
9) Acetylcholine degradation
End-plate potential (EPP)
- graded potential at motor end plate
- All EPPs are excitatory
EPP = EPSP - All EPPs lead to APs
AP in motor neuron= AP in muscle
fiber - Acetylcholinesterase in cleft degrades
ACh to stop signal= return to resting
membrane potential
Mechanism of Cytosolic Increase in Ca2+
T-tubules conduct impulses deep into
muscle fiber
– Every sarcomere
- T-tubules contact with SR cisternae by junctional feet (2 proteins)
T tubule proteins
– Dihydropyridine receptor (DHP)
– Voltage sensors
– Change shape in response to voltage changes
SR proteins
– Ryanodine receptor (RYR)
– Channels that release Ca2+ from SR
cisterns when voltage sensors
change shape
Tropomyosin
blocks binding of myosin head
Troponin
holds tropomyosin over myosin binding site on actin
Cross-bridge Cycle
1) Cross-bridge binds to actin
2) Cross-bridge moves
3) ATP binds to myosin, causing cross-bridge to detach
4) Hydrolysis of ATP energizes cross-bridge
Sliding Filament Model of Contraction
Contraction
– Generation of force
Shortening
– Tension generated by cross bridges on thin filaments > opposing forces
Relaxation
– Cross bridges detach
– Tension declines
in fully contracted sarcomere
– I band narrows,
– H zone disappears,
– A band remains unchanged
Overview of muscle contraction
1) Action potential propagated along muscle cell membrane and into T-tubules
2) Ca2+ released from terminal cisternae
3) Ca2+ binding to troponin removes blocking action of tropomyosin
4) Cross bridges bind, rotate, and generate force.
5) Ca2+ transported back into sarcoplasmic reticulum
6) Ca2+ removal from troponin restores tropomyosin blocking action
Rigor mortis
Because ATP is required for cross-bridge detachment
Dying cells take in calcium= cross bridge formation
No ATP generated to break cross bridges after death
How does curare work?
– Blocks N-ACh receptors
– No EPP
* no AP= no contraction
– Muscle paralysis and Asphyxiation
How does botox (botulinum toxin) work?
Botulinum toxin works by breaking down a protein complex called the SNARE complex, which is crucial for the release of acetylcholine (ACh), effectively blocking the neurotransmitter’s release at the neuromuscular junction, leading to muscle paralysis; essentially, it prevents the synaptic vesicles containing ACh from fusing with the cell membrane and releasing their contents.
