Unit 8 muscles Flashcards
Cardiac muscle
In heart- involuntary
Muscle fibres are
branched and striated
One nucleus per fibre
Skeletal muscle
It is what attaches to bone (by tendons)
movement (controlled by somatic nervous system)
Striated, fibres are long cylinders multi nucleotide
Smooth muscle
Involuntary
No striations, one nucleus per fibre, fibre is spindle shaped
In arteries, veins, digestive system, etc
Attachment points of a muscle: origin and insertion
Origin: attached to fixed part of bone
Insertion: attached to bone that will move
Flexer vs extensor
Decrease angle between 2 bones
Increase angle between 2 bones
Agonist vs antagonists in muscle movement
Agonist= main mover/muscle doing the work
Antagonist= does opposite action (help keep position)
Ex bicep and tricep are antagonist muscle group since they have opposite actions (extension and flexor)
Skeletal muscle made up of
Many muscle fibre, inside muscle fibre are multiple myofibrils (long cylinders), and each myofibril has sections that repeat called sarcomeres (this is what makes it have striated look)
Sarcolemma, sarcoplasm, sarcoplasmic reticulum
- Muscle cell membrane
- Cytoplasm of muscle cell
- Extensive network of smooth Er of muscle cell
Transverse tubules (t-tubules)
Help transmit atp deep into muscle cells ensuring all sarcomeres receive the contraction signal
Triad
T-tubule along with 2 terminal cisternae on either side
What do muscle cells contain to support high atp demand
Numerous mitochondria and glycogen granules
Actin vs myosin
Actin=thin filaments
Myosin= thick filaments (golf club shape)
Myosin function and its important binding sites
Myosin head to form crossbridges between thick and thin filaments
Has actin binding site and myosin atpase binding site (to hydrolysis)
G-actin
Thin- globular shape but assembled into long chains
Functions in contraction and is the primary structural protein of thin filaments
Trypomyosin and troponin
Threadlike- regulates contractions of sarcomere. Blocks binding site of myosin (so no contraction- unless ca++ binds)
Set of more regulatory proteins
3 polypeptide units
One binds with actin, ca++, and tropomyosin
Z-lines
Where sarcomere ends and where thin filaments attach
What shortens during muscle contraction
Sarcomere
-not myosin or actin (they overlap)
Z-lines move closer together
A band same
Hzone and i band shorten
M-line
Thick filaments held together by accessory proteins called m-line
Center of A band
Does not change length during contraction
Powerstroke
Myosin head bound to atp, hydrolyses it and turns it to pi and adp- myosin head can now bind to actin (crossbridge), powerstroke occurs which releases ado and pi and new atp binds to stop. Process repeats
Titin (function and why important)
Large elastic protein
Joins m-line and z-line at opposite ends of sarcomere
- stabalize position of thick and thin filaments
- improves muscle elasticity (return to resting length after contraction)
Nebulin
An aligning protein
Aligns actin chain
Sarcomere divided into bands/zones: A-band
Contains both actin and myosin
Areas where actin and myosin overlap
Dark band= myosin
Sarcomere divided into bands/zones: H zone
Contain only myosin
Light band at centre of A-band
As myosin and actin progressively get overlapped, h-zone disappears
Sarcomere divided into bands/zones: i-band
Contain only actin
-Light band that spans 2 adjacent sarcomeres
-shortens during contraction
-z disk in centre of the i band
Skeletal muscle: physiology
Controlled by nervous system
Upper motor neuron vs lower motor neuron synapse w/
- Synapse on lower motor neuron
- Synapse on skeletal muscle cells
Resting/relaxed muscle
Tropomyosin covers myosin binding site. No ca++ because…
Ap stop arriving at neuromuscular junction, ach on end plate broken down therefore ryanodine receptor channels close
End plate potential
Impulse on nerve terminal causes release of ach which opens na+ channels causing depolarization (threashold reached- AP generated) leads to contraction of muscle
How is ca++ released in order to form crossbridge
AP spreads from motor end and plate to all directions (same as ripples on pond)
Reach t-tubles and reaches down stimulates change in dhp receptor
Dhp touches ryanodine receptor (mechanical gated c++ channels) on the sr and opens it
Ca flows from sr into cytosol (down conc) and bind to troponin
Rigor mortis
Stiffness of death
Ca still leaks out of SR . Since dead- no atp to stop crossbridge no detaching
