Muscle test Flashcards
Skeletal muscle tissue
Attached to bones and skin
Striated
Voluntary (i.e., conscious control)
Powerful
Cardiac muscle tissue
Only in the heart
Striated
Involuntary
Smooth muscle tissue
In the walls of hollow organs
Not striated
Involuntary
functions of muscle
Movement of bones or fluids
Maintaining posture and body position
Stabilizing joints
Heat generation
skeletal muscle characteristics
Excitability
Contractility
Extensibility
Elasticity
excitability
responsiveness or irritability: ability to receive and respond to stimuli
Contractility
ability to shorten when stimulated
Extensibility
ability to be stretched
Elasticity
ability to recoil to resting length
Epimysium
dense regular connective tissue surrounding entire muscle
Perimysium
fibrous connective tissue surrounding fascicles (groups of muscle fibers)
Endomysium
fine areolar connective tissue surrounding each muscle fiber
muscle flow chart
muscle is covered by epimysium
muscle is made up of fasicles covered by perimysium
fasicles are made of muscle fibers (muscle cells) covered by endomysium
muscle fibers made of myofibrils which are made up of filaments (actin and myosin)
muscles attach directly
epimysium of muscle is fused to the periosteum of bone or perichondrium of cartilage
muscles attach indirectly
connective tissue wrappings extend beyond the muscle as a ropelike tendon or sheetlike aponeurosis
skeletal muscle cells
Cylindrical cell up to 30 cm long
Multiple peripheral nuclei
Many mitochondria
myofibrils, sarcoplasmic reticulum, and T tubules
densely packed rodlike elements (80 percent of cell volume)
striations
glycosomes for
glycogen storage
myoglobin for
oxygen storage
striations in muscle cells
perfectly aligned repeating series of dark A bands and light I bands
Sarcomere
Smallest contractile unit (functional unit) of a muscle fiber
The region of a myofibril between two successive Z discs
Composed of thick and thin myofilaments (actin myosin)
thick filaments (myosin)
run the entire length of an A band
thin filaments (actin)
run the length of the I band and partway into the A band
Z disc/line
coin-shaped sheet of proteins that anchors the actin and connects myofibrils to one another
H zone
lighter midregion where filaments do not overlap
m line
line of protein myomesin that holds adjacent thick filaments together
protein myosin tails contain
2 interwoven, heavy polypeptide chains
protein myosin heads contain
2 smaller, light polypeptide chains that act as cross bridges during contraction
Have binding sites for actin of thin filaments
Also have binding sites for ATP
Has ATPase enzymes
Actin contains
Twisted double strand of fibrous protein F actin
Tropomyosin and troponin
F actin consists of
of G (globular) actin subunits
G actin consists of
active sites for myosin head attachment during contraction
tropomyosin
block binding site for myosin
troponin
changes shape when calcium binds to it which moves tropomyosin out of the way
thick filament
myosin molecules whose heads protrude at opposite ends
thin filament
two strands of actin subunits twisted into a helix plus troponin and tropomyosin
Sarcoplasmic Reticulum
network of smooth endoplasmic reticulum surrounding each myofibril
Pairs of terminal cisternae form perpendicular cross channels
Functions in the regulation of intracellular Ca2+ levels
T-tubules
Continuous with the sarcolemma
Penetrate the cell’s interior at each A band–I band junction
part of triads
conduct impulses deep into muscle fiber
triad
terminal of cisternae of SR, t tubule, terminal of cisternae of SR
t tubule proteins
voltage sensors
SR foot proteins
gated channels that regulate calcium release from the SR cisternae
why does generation of force does not necessarily cause shortening of the fiber
when the load is greater than the muscle can move, the muscle doesnt shorten
ex trying to pick up a car
Shortening occurs when
tension generated by cross bridges on the thin filaments exceeds forces opposing shortening
muscle contraction steps with actin and myosin: relaxed state
In the relaxed state, thin and thick filaments overlap only slightly
muscle contraction steps with actin and myosin: during contraction
myosin heads bind to actin, detach, and bind again, to propel the thin filaments toward the M line
As H zones shorten and disappear
sarcomeres shorten, muscle cells shorten, and the whole muscle shortens
steps to contraction
activation and excitation
activation
neural stimulation at a neuromuscular
Excitation-contraction coupling
Generation and propagation of an action potential along the sarcolemma
Final trigger: a brief rise in intracellular Ca2+ levels
skeletal muscle stimulation travel path
Skeletal muscles are stimulated by somatic motor neurons
Axons of motor neurons travel from the central nervous system via nerves to skeletal muscles
Each axon forms several branches as it enters a muscle
Each axon ending forms a neuromuscular junction with a single muscle fiber
neural muscular junction
Situated midway along the length of a muscle fiber
contain synaptic cleft
Synaptic vesicles of axon terminal contain the neurotransmitter acetylcholine (ACh)
Junctional folds of the sarcolemma contain ACh receptors
how neural muscular junction works
Nerve impulse arrives at axon terminal
ACh is released and binds with receptors on the sarcolemma
Electrical events lead to the generation of an action potential
which travels down t tubule to cause SR to dump calcium which causes troponin to shift and unblock tropomyosin
ach affects are terminated by
achesterase
What does achesterase do
which prevents continued muscle fiber contraction in the absence of stimulation
steps after ach binds to receptor on sarcolemma when crossing synaptic cleft
local depolarization (end plate potential)
generation and propagation of action potential
repolarization
local depolarization (end plate potential)
ACh binding opens chemically (ligand) gated ion channels
Simultaneous diffusion of Na+ (inward) and K+ (outward)
More Na+ diffuses, so the interior of the sarcolemma becomes less negative
and loses polarity
Generation of an action potential
End plate potential spreads to adjacent membrane areas
Voltage-gated Na+ channels open
Na+ influx decreases the membrane voltage toward a critical threshold
If threshold is reached, an action potential is generated
propagation of an action potential
Local depolarization wave continues to spread, changing the permeability of the sarcolemma
Voltage-regulated Na+ channels open in the adjacent patch, causing it to depolarize to threshold
repolarization of an action potential
Na+ channels close and voltage-gated K+ channels open
K+ efflux rapidly restores the resting polarity
Fiber cannot be stimulated and is in a refractory period until repolarization is complete
Ionic conditions of the resting state are restored by the Na+-K+ pump
What maintains polarity
3 clacium going out and 2 potassium going in leads to repolarization
latent period
Time when E-C coupling events occur
Time between AP initiation and the beginning of contraction
stopping contraction At low intracellular Ca2+ concentration
Tropomyosin blocks the active sites on actin
Myosin heads cannot attach to actin
Muscle fiber relaxes
stopping contraction At higher intracellular Ca2+ concentrations
Ca2+ binds to troponin
Troponin changes shape and moves tropomyosin away from active sites
Events of the cross bridge cycle occur
When nervous stimulation ceases, Ca2+ is pumped back into the SR and contraction ends
Continues as long as the Ca2+ signal and adequate ATP are present
cross bridge cycle
Cross bridge formation—high-energy myosin head attaches to thin filament
Working (power) stroke—myosin head pivots and pulls thin filament toward M line
Cross bridge detachment—ATP attaches to myosin head and the cross bridge detaches
“Cocking” of the myosin head—energy from hydrolysis of ATP cocks the myosin head into the high-energy state (pull back to gain another actin)
what makes myosin heads let go and cock
atp makes it let go, hydrolysis makes it cock
why rigamortes people are stiff
stiff dead person, no ATP made so cross bridges are stuck. When pumps stop, calcium leaks and causes myosin heads to grab, get stiff, but ATP is gone so cant move
