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97 Cards in this Set

  • Front
  • Back
what is a muscle fiber?
a muscle cell
what does a typical muscle cell look like?
big and multinucleated
where does the alpha-motor neuron originate?
in the spinal cord
what are the compotents of the alpha-motor neuron
soma (cell body)
myelin and nodes of Ranvier
motor end plate and synapse
what is the job of the alpha-motor neuron?
it propagates the action potential
what are the components of the neuromuscular junction?
motor end plate
post-synaptic membrane
what makes up the motor end plate?
ACh vesicles
pre-synaptic membrane (which works by a secretory vesicle process)
what are the components of the post-synaptic membrane?
junctional folds
ACh receptors
Na+/K+ channels (ion channels)
what do the ion channels in the post-synaptic membrane do?
cause depolarization, which spreads from the initial point
what does an action potential do?
opens gates leading to depolarization, dep. spreads
what is the weird word Eng uses for the motor end plate?
how is the speed of conduction increased?
saltatory conduction via nodes of Ranvier
what is myelin?
a lipophilic structure laid down by schwann cells; it doesn't allow for leakage
what is a motor unit?
the alpha-motor neuron and all of the fibers that it innervates
what are the 3 types of motor units?
what are slow, small fibers?
dark due to lots of myoglobin which store O2 so the cell can use it to make E, have more mito, smaller peak
what are fast, big fibers?
light, larger in diameter, can produce a higher peak tensile strength, doesn't use mito or glycolysis, max tension quickly
why are there different types of fibers?
due to different ATPases
what are the characteristics of fibers?
a single fiber vs. a motor unit
functional unit of the motor unit
how do nerves and muscles communicate?
by the propagation of the action potential
what is the mechanism of electrochemical communication with the muscle fiber? 6 steps
mobilization of ACh vesicles
fusion with pre-syn membrane
ACh release into synapse
ACh binds to ACh-R
generation of the muscle fiber action potential
degradation of ACh
what is Curarae?
a paralytic
inhibits ACh release
no contraction occurs
what are OP's?
nerve agents, pesticides
block AChE and lead to constant depolarization
what is Myasthenia Gravis?
autoimmune disease where the body kills its own ACh receptors
signs: relaxed muscles, breathing tube paralysis, mega-esophagus, paralyzed
what is tetany?
continuous contraction
how is force regulated?
motor unit recruitment
rate coding
what is motor unit recruitment?
the number and size of motor units
more cells and more motor units lead to greater strength
when are small motor units recruited?
at low force outputs
what happens as force output increases?
progressively larger motor units are activated
when might all units be recruited?
at high force output
what is rate coding?
the frequency of stimulation
what is a twitch?
a single stimulus
what happens when there are multiple stimuli delivered at low frequency?
twitches sum and an unfused tetanus occurs
what happens when there are multiple stimuli at high frequencies?
a fused tetanus (maximal F) occurs
-the faster the axon fires, the higher the F
-fast=few mito, low O2
is there a close association between stimulation frequency and force output?
what are graded voluntary contractions?
don't know
what happens when force is low? (GVC)
small units are activated
individual activation frequencies begin to increase
what happens as force increases? (GVC)
activation frequencies continue to increase until a plateau is reached
larger units are recruited
activation frequencies increase
when does the process of graded voluntary contractions stop?
when all units are activated at their maximal frequencies
what are the parts of the muscle membrane structure?
what is the sarcolemma?
muscle membrane that functions as most cell membranes and contains myoplasm or sarcoplasm
what is the transverse tubular network? (T-tubule)
invagination of the sarcolemma, extention of the sarcolemma
what is the fuction of the T-tubules?
transports excitation into the interior of the fiber
transports extracellular fluid into the interior of the fiber
what is the SR?
highly specilized ER which stores and releases Ca++
what happens at the terminal cisternae of the SR?
Ca++ is released through channels
what happens at the longitudinal region of the SR?
Ca++ is sequestered, contains Ca++ ATPase (Ca++ pump, which pumps out of sarcoplasm and into ER)
how many muscle filaments are in each muscle cell?
100's or 1000's packed side by side and surrounded by SR
does every cell have a motor endplate in the middle of the cell?
what are the 2 types of filaments in myofibrils?
do the T-tubules and TC merge?
what are the components of the contractile apparatus?
thin myofilaments
thick filaments
cytoskeletal proteins
how do myofibrils appear?
what does the Z-line define?
the sarcomere
what is a thin myofilament
actin which is the backbone of the thin filament; myosin binding site
how many subunits does troponin have and what do they do?
3 subunits
C-binds calcium (causes a physical change of C which changes other subunit configuration; I no longer inhibits ATPases, T pulls on Tropomyosin and changes it's physical force which leaves myosin heads accessible)
I-inhibits ATPases
T-binds tropomysin
what is a thin myofilament made of?
troponin subunits
what is tropomyosin?
thin linear molecule that is bound to the T subunit of troponin
what happens when the myosin head is accessible?
ADP bound myosin heads bind to actin
head flexes
filaments move
ADP leaves
ATP comes in
breaks bond
ATPase cleaves ATP to ADP
what is needed for the head to release?
what is necessary for contraction?
where is the ATPase activity?
on the light chain
what constitutes a thick myofilament?
myosin heavy chain (MHC)
myosin light chain (MLC)
myosin ATPase
actin binding site
where does actin bind?
on the light chain
where are light chains found?
only on the head
what is the sliding filament theory?
heads bind to thin filaments
head releases, shifting thin & thick filaments
thin filament is released
what causes the mechanical event involved in the contractile apparatus?
an electrical event
what is necessary to pump Ca++ back into TC?
outline the overview of the contraction process
initiated at NM junction
sarcolemma AP spreads to T-tubules
Ca++ released into myoplasm
Ca++ binds to C subunit of troponin
where is the contraction process initiated?
at the NM junction
what does the sarcolemmal action potential do when it spreads to the T-tubules?
activates a voltage sensor located in T-tubular membrane which opens the release channels of the SR TC
what happens when Ca++ binds to the C subunit of troponin?
causes a conformational change in the thin filament
myosin x-bridges shift from weak binding to strong binding sites
ATP is hydrolyzed and F is produced
if there is adequate ATP and Ca++, myosin X-bridges cycle b/t weak and strong binding states and produce F
what happens in the relaxation step of muscle fiber contraction?
SR Ca++ release channels close
myoplasmic Ca++ is re-sequestered by the longitudinal SR via Ca++ ATPase
Ca++ dissociated from troponin
myosin X-bridges remain in the weak binding state
what is the only source of E for contraction?
what are the 2 major ATPases that account for the vast majority of E consumed during activity?
myosin ATPase
Ca++ ATPase
what does myosin ATPase need E for?
force production (2/3 of total)
active contraction
what does Ca++ ATPase need E for?
Ca++ transport (1/3 of total)
maintains pump
what is rigor mortis due to?
total lack of ATP
what is needed for contraction?
ATP and Ca++
is it true that the more Ca++ you have available the stronger the F can be?
how is force production regulated by Ca++?
-force production by contractile apparatus is dependent on myoplasmic [Ca++]
-sigmoidal relation between F and [Ca++]
-[Ca++] is regulated by SR
what is the concentration of Ca++ at rest?
what is the concentration of Ca++ during tetanic contraction?
how is [Ca++] regulated by the SR?
release rate
uptake rate
at rest, what state are the myosin crossbridges in?
weak binding state
what happens to myosin crossbridges at rest?
they attach and detach from actin very rapidly, with low affinity
ATP is hydrolyzed to ADP and Pi by the myosin ATPase
what remains bound to the head when ATP is hydrolyzed?
is force produced at rest (low Ca++)
what happens during contraction (high Ca++)
Ca++ binds to troponin
troponin I inhibition is removed
Pi is released from myosin head
X-bridges move to the strong binding site
what happens at the strong binding site?
-E is utilized and the myosin head contracts (produces F)
-ADP is released from the myosin head
-new ATP attaches to the myosin head and the rigor bond is broken
-X-bridges move back to the weak binding state
with adequate ATP and Ca++, what happens to crossbridges?
they cycle continually between the 2 states
what is the force of a contraction dependent on?
the number of cycling crossbridges
force per crossbridge
rates of crossbridge cycling
what are some changes which skeletal muscle makes to adapt under different circumstances?
strength and fatiguability
can weakness develop without noticible changes in muscle size?
force per unit muscle declines
what happens when weakeness develops without noticible changes in muscle size?
likely that one or more of the steps in the contraction process is impaired
what are the major steps of the contraction process?
1. initiation of the contraction in the motor cortex
2. activation of the motor neuron
3. propagation of the AP
4. NM communication
5. initiation of the sarcolemma AP
6. SR Ca++ release
7. Ca++ binding to troponin
8. X-bridge cycling and force generation
9. SR Ca++ uptake
what can happen in the case of a spinal cord injury?
inibility to activate the motor unit and paralysis
what happens when the communication b/t the motor cortex and the motor neuron is blocked?
severe weakness occurs