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Kin 121 > bmsc 207 muscle > Flashcards

bmsc 207 muscle Flashcards

1
Q

function of muscle

A

primary function is generate force and movement in response to stimulus
- body movement
maintenance of posture
respiration
production of body heat
communication
constriction of organs and vessels
heartbeat

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2
Q

types of muscles

A

skeletal: voluntary by somatic motor neurons, striated and multinucleated

cardiac: involuntary, spontaneous electrical activity can be altered by autonomic NS hormones
striated and uninucleated

smooth:involuntary, autonomic control, spontaneous, hormones, pararcrines and autocrines
non striated and uninucleated
control of: digestive tract, urinary tract, reproductive tract, blood vessels, airways

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3
Q

skeletal muscle
how is it attached?
antagonstic muscle
extensor/flexor
origin/insertion

A

usually attached to bones by tendons
40% of total body weight

origin: closest to the trunk or to more stationary bone
insertion: more distal or more mobile attachment
antagonistic muscle groups: flexor-extensor pairs
flexor: brings bone together
extensor: moves bones away

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4
Q

myofilaments
thin filaments

A

F-actin: back bone of thin filaments, double stranded alpha helical polymer of G-actin molecules. contains binding site for thick filaments (myosin)

tropomyosin: two identical alpha helicies that coil around each other and sit in the two grooves formed by actin strands, regulates the binding of myosin and actin

troponin complex: heterotrimer consisting of
1) troponin T: binds to a single molecule of tropomyosin
2) troponin C: Ca binding site
3) troponin I: under resting conditions is bound to actin inhibiting contraction

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5
Q

thick filaments

A

consist of a bundle of myosin molecules
myosin head contains a region for binding actin as well as a site binding and hydrolyzing ATP (ATPase)
regulatory light chain regulates ATPase activity of myosin
essential light chain stabilizes myosin head

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6
Q

titin
nebulin

A

titin: very large protein extending from M line to Z line, appears to be involved in stabilzation of thick filaments and the elastic recoil behaviour of muscle

nebulin: a large protein that interacts with the thin filaments, believed to regulate the length of thin filaments and contribute to the structural and contribute to the structural integrity of myofibrils

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7
Q

sarcomere (bands and line/discs)

A

z disk: zigzag protein structure that is the attachment site for the thin filaments

I bands- lightest band of sacromere, region occupied only by actin

a band: darkest band, encompasses entire lenght of the thick filament, including very dark are where thin and thick filaments overlap

H zone: central region of A band, consists only of thick filaments.

M line- proteins form the attachment site for the thick filaments, equilvalent to z disk for thin filaments

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8
Q

neuromuscular junction

A

point of synaptic contact between somatic motor neuron and individual muscle fibre
the synapse of a lower motor neuron to a muscle fiber

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9
Q

brain regions involved in voluntary movement

A

primary motor cortex
-basal ganglia
- premotor cortex
- thalamus
- cerebellum
- midbrain

corticospinal tract: descending tract (ventral and interior lateral white matter)

upper motor neuron: brain to brainstem or spinal cord

alpha (lower) motor neuron: spinal cord or brain stem to muscle

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10
Q

amyotrophic lateral sclerosis (ALS)

A

neurodegenerative motor neuron disease

upper and lower motor neurons degenrate leading to muscle atrophy and weakness from disease

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10
Q

alpha motor neuron and motor units
the amount need varies b/c.

A

large, myelinated axon, 15-120 m/sec
each axon branches and inneravtes serveral muscle fibers
all muscle fibers respond simultaneously (all or nothing)
number muscle fibers/motor units varies
- <10 for delicate precise work
>100’s for powerful, less precise contractions
hennans

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11
Q

nicotinic acetylcholine receptor
where are they found?

A

sacrolemma of muscle fiber contains nicotonic acetlycholine receptors

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12
Q

ceasing neural transmittion

A

once AP’s stop firing in the alpha motor neuron acetylcholine in the synaptic cleft must be removed and will diffuse away or be broken down to acetate and choline by the enzyme acetylcholinesterase

choline is transported back into the motor neuron and combined with acetyl CoA produced from mitochondria by the enzyme choline acetyltransferase to make acetylcholine

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13
Q

myasthenia gravis
autoimmune

A

means severe weakness of muscle
disorder of neuromuscular transmission
can be restricted to extracular muscles or generalized

autoimmune: body produces antibodies that bind to ACH receptors

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14
Q

excitation-contraction coupling

A

the ultimate intracellular signal that triggers contraction in all muscle types is a rise in intracellular calcium
depending on the muscle type, Ca can enter the sacroplasm from the extracellular space via voltage gated Ca channels or can be release into sacroplasm from the intracellular SR

the process by which electrical excitation of the surface membrane triggers an increase of Ca in muscle is known as excitation-contraction coupling

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15
Q

T- tubules

A

t tubule penetrate the muscle fiber and surround the myofibrils at two points in each sacromere, at the A and I band junctions

along its length the tubules are associated with two cisternae (specialized end regions of the SR) to form a traid

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16
Q

DHP receptor
RyR ryanodine receptor

A

DHP receptor: L-type Ca channel, voltage sensitive

RyR ryanodine receptor: Ca release channel on SR

DHP receptor opens RyR Ca release channels in SR, and Ca enters the cytoplasm

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17
Q

An increase in Ca triggers contraction by removing

A

the inhibition of cross bridge cycling
Ca binds low affininty sites on troponin C which induces a conformational change in the troponin complex:
causes the troponin complex as well as tropomyosin to move revealing the myosin binding site on the actin.

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18
Q

sliding filament theory

A

1) ATP binding: ATP binds to the head of myosin heavy chain reducing affinity of myosin for actin
2) ATP hydrolysis: ATP is broken down to ADP and inorganic phosphate resulting in the myosin head pivoting around hinge into cocked state. the cocked head is now aligned with and binds to a new actin molecule on thin filament.
3) the powerstroke: disassociation of Pi from myosin head strenghtens bond between actin and myosin and triggers power stroke, a conformational change in which the myosin head returns to its un-cocked state and while doing so pulls the actin generating force
4) ADP releases: dissociation of ADP from myosin casues myosin to remain bound to actin until ATP initiates the cycle again

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19
Q

termination of contraction requires removal of Ca

A

one the AP has subsided Ca must be removed so myosin binding site on actin can be covered by tropomyosin

Ca can be remove to the extracellular space by the Na-Ca exchanger or by the Ca pump which uses ATP

-would eventually deplete the cell of any CA, leaving the SR empty and becasue of this plays a minor role

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20
Q

rigid mortis

A

development of rigid muscle several hours after death
Ca leaks into the sarcoplasm and binds to troponin

ATP production stops:
Ca cannot be removed
ATP needed to release myosin head from actin
remains in latched cross bridge formation until muscle begin to deteriorate

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21
Q

timing of E-C coupling

A

slight delay between motor neuron AP and muscle fiber AP (synaptic release)
delay between muscle fiber AP and contraction time when Ca is being release and binding to troponin

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22
Q

ATP is needed for
and sources of ATP

A

myosin ATPase (contraction)
Ca Atpase: SERCA (relaxation)
Na/K ATPase (after AP in muscle fiber)

sources: free intracellular ATP (few seconds)
ATP formed from phosphcreatine (10 seconds)
ATP produced through anaerobic metabolism
ATP produced through aerobic metabolsim

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23
Q

anaerobic metabolism

A

process has no oxygen
one glucose molecule can then be broken down to pyruvate by glycolysis resulting in the production of two ATP molecules
takes place in the sacroplasm of the muscle

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24
Q

oxidative (aerobic) metabolism

A

if O2 and mitochondria are present
after glycolysis pyruvate then enters the citric acid cycle producing two more molecules of ATP as well as high energy electrons and H
the high energy electrons and H combine with O2 in the electron trasnport chain to produce an additional 26-28 molecules of ATP
occurs in mitochondria and oxygen is neccesary

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24
Q

muscle fatigue

A

a decrease in muscle tension as a result of previous contractile activity that is reversible with rest (hours)

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24
Q

central fatigue
peripheral fatigue

A

central fatigue: feeling of tiredness and a desire to cease activity. Precedes physiological cell fatigue meaning your muscles are not fatigue yet

peripheral fatigue: at the NMJ : proposed ACH synthesis cant keep up with neuron firing, decreased neurotransmitter release> decrease ACHR activation on muscle>muscle fails to reach threshold for firing AP
most experimental evidence
very unlikely theory tho

points to problems with EC coupling or the process following

action potential propgation: at the t tubule: potassium build up in the t tubule the amount of K leaving will be higher than the speed of the sodium-potassium ATPase putting it back causing hypoclemia

25
Q

determinants of muscle force/tension development

A

force/muscle cell
fiber diameter
- fatiguability
- initial resting length
- frequency of activation

force/entire muscle
number of muscle cell activated
number of muscle cells/motor unit
number of motor units activated

26
Q

how does muscle length influence tension development

A

the overlap between actin and myosin

27
Q

single twitch vs summation
what causes a twitch? how long does it last

A

a single AP in a single muscle fiber results in a individual muscle twitch
muscle can relax between stiumuli
AP last 1-3ms twitch lasts up to 100ms

summation: AP occurs before the muscle fobre is allowed to relax a more forceful contraction occurs.
a single AP does not cause a release of the entire Ca store from the SR

the Ca released from one AP may not lead to all troponin complexes being activated for a sufficient amount of time, some regions of actin may be recovered by tropomyosin before crossbridge cycling can actually begin

a second AP causes a sceond wave of Ca that may keep additional troponin complexes activated allowed for more cross bridges to be formed
Ca remains elevated for a longer period of time allowing increased cross bridge cycling and further shortening of the sacromeres

28
Q

tetanus

A

a maintained contractile response to a repeated stimuli

unfused tetanus: reaches steady state of contraction but stimuli are far enough apart that the muscle fiber slightly relaxes between stimuli

fused tetanus: the stimulation rate is fast enough that the fibre does not relax, instead it reaches max tension and remians there

to increase tension developed by muscle fiber increase the rate AP occur in the fibre

29
Q

motor unit
motor neuron pool

A

motor unit: a single motor neuron and all the muscle fibres it innervates; one motor neuron innervates one fibre type

motor neuron pool: the group of all motor neurons innervating a single muscle

29
Q

why doesnt the large diameteer neuron reach threshold?

A

yes, cytoplasmic resistance would be lower in larger diamter neuron but current would encounter resistance over a much greater distance
more leakage in large diameter due to the large length

in small neurons, its smaller distance

30
Q

size principle

A

small motor neurons innervate smaller muscle fibres and smaller motor units (type 1 slow oxidative)
intermediate size motor neurons innervate intermediate number of muscle fibers establishing intemediate sized motor units (type iia fast oxidative glycolytic
large motor neurons tend to innervate a large number of muscle fibres making up large motor units

slow oxidative–> fast oxidative glycolytic—> fast glycolytic

31
Q

asynchronous recruitment

A

during submaximal contraction the CNS modulates firing rates of upper motor neurons to allow different motor units to maintain contraction in order to prevent to fatigue

32
Q

isotonic contrations (con/ecc)

A

concentric: muscle shortens while generating force

eccentric: muscle lengthens while generating force
acts to decelerate the joint at the end of a movement

33
Q

how do the sacrcromeres shorten during isometric contraction without the muscle changing lenght?

A

elastic elements in tendons, elastic and connective tissue in and around muscle fibres

34
Q

skeletal muscle adpatations

A

hypertriphy/atrophy
increase in ATP synthesizing capacity
increase in mitochondria size and number
increased capillary density increase in glycolytic enzymes

neural adaptations: increased ability to recruit more units
reduced inhibitory input from GTO

35
Q

muscle hypertrophy

A

when skeletal muscle is subjected to an overload stimulus, it causes perturbations in muscle fibers and the related extracellular matrix. this sets off a chain of myogenic events that ultimately leads to:
increase size in sarcomeres and number of contractile proteins
increased number of sarcomeres within a muscle length increased myofibrils
increased sacroplamic storage (glycogen)
more in type ii fibres

36
Q

skeletla muscle atrophy

A

protein degradtion > protein synthesis
can occur due to disuse: immobilization, bed rest, and unloading (0 gravity)

37
Q

cachexia

A

weakness and or wasting due to chronic disease
cancer is often associated with a loss of weight and weakness of muscles

38
Q

skeletal muscle reflexes

A

involved in almost all movements
receptors sense changes in joint movements, muscle tension and muscle lenght and feed info into the CNS which responds in one of two ways:
if muscle contraction is needed the CNS activates motor neurons to the muscle fibres
if relaxation is needed sensory input activates inhibitory interneurons in CNS which inhibit activity in motor neuron leading to relaxation

four components: sensory receptor, integrating center, efferent neurons, effectors

39
Q

monosynaptic reflex
polysnaptic reflexes

A

monosynaptic reflex: has a single synapse between the afferent and efferent neurons

polysynaptic reflexes: has two or more synapses. this somatic motor reflex has both synapses in CNS

40
Q

proprioceptors

A

provide info into the CNS about the position of our limbs in space, movements, and the effort exerted by skeletal muscles

41
Q

muscle spindles

A

small elongated stretch receptors scattered among and arranged parallel to skeletal muscle fibres.
send info to the CNS about muscle length and changes in muscle length
made up of sensory neuron wrapped around intrausal muscle fibres
extrafusal muscle fibres are regular muscle fibres innervated by alpha motor neurons
tonically active (muscle tone) meaning always firing AP to the CNS
causes a contraction in the agonist

42
Q

golgi tendon organ

A

sensory neuron interwoven among collagen fibres inside a connective tissue capsule

respond to muscle tension (not tonically active)

originally proposed to primarily control inhibitory reflexes to prevent muscle damage
control force within muscles and stability around joints

GTO causes relaxation in the agonist muscle

43
Q

joint receptors

A

these are found in the capsules and ligaments around joints and are stimulated by mechanical distortion that accompany changes in position of bones

dont iniate skeletal muscle reflex

44
Q

alpha gamma neuron

A

it fires when the alpha neuron fires
get contraction on the ends, make sure there is some tension in the middle
when muscle contracted make sures the ends contract
maintains spindle function when muscle contracts

45
Q

a flexion reflex pulls limbs from painful stimuli? what is it driven by
what is crossed extensor

A

painful stimulus activates nociceptor
prim sensory neurons enters the spinal cord and diverge

one collateral activates ascending pathways for pain and postural adjustment
withdrawl reflex pulls foot away from painful stimulus
crossed extensor reflex supports body as weight shifts away from painful stimulus

46
Q

cardiac muslce
what is it made of
what connects them electrically and mechanically

A

made up of cardiac myocytes, which are shorter, branched cells and usually contain a single nucleus

interconnected by intercalated disks: desmosomes link mechanically
gap junctions link them electrically

its striated and has sacromeres like skeletal

47
Q

does cardiac muscle have larger t tubules compared to skeletal muscle?
less or more of SR
mitochondria?

A

less abundant but larger T tubules
smaller amounts of SR, requires the entry of extracellular Ca

a abundance of mitochondria (1/3 of cell volume)

48
Q

contraction is not initiated by neurons for cardiac

A

approx 1% of myocardial cells are specialized non-contracting authorhytmic cells (pacemakers) that generate AP spontaneously. the depolarization begins in the sinoatrial node (main pacemaker of the heart)

smaller and contain few contractile fibres
dont produce force

49
Q

AP’s in autorhythmic myocardial cells

A

unstable resting membrane potential at -60mV, never truly rest

HCN channels (funny current) open from -60 to nearly -40mV and allow a net influx of Na, causing the cell become depolarized

just before reaching threshold (-40mV) HCN channels close and T-type Ca channels open, allowing Ca to flow in, further depolarizing the cell to reach threshold

one reaching threshold L-type Ca open allowing an influx of Ca, causing the depolarizing spike of the AP

L-type Ca close and K channels open causing K to flow out of the cell, casuing the cell to repolarize and return to -60 now HCN channels open adn start the cycle again

50
Q

AP’s in contractile myocardial cells

A

2 potassium channels (slow and fast)
1 Ca voltage gated channel
1 Na voltage gated channel

ions that entered from an AP transfered to adjacent cells through gap junctions leading to depolarization of adjacent cell
RMP is -90mV
once reach threshold voltaged gated Na channels open causing the Na spike of AP.
the positive voltage charge of the AP slowly opens L-type Ca channels.
there is a brief repolarization from fast K channels before the Ca influx
L-type Ca channels occur and the fast K channels close leading to sustained depolarization (the plateau)
once the Ca channels open, slow K channels repolarize the cell

51
Q

how the autorhytmic and contractile myocardial connected

A

there would be spontaneous AP firing in the autorhymic, causing an inc in Ca

the Ca that comes in will go into the next cell (the contractile)

gap junctions will be linking the autoryhtmic cell 1 to contractile cell 2
Ca will be travelling through the gap junctions
high Ca will bring the membrane to threshold, opening the voltage gated channels in the next contractile cell

52
Q

very long refractory period is caused by the contractile myocardial cell. which prevents summation in the heart, need a brief pause in between contractions so there can be blood in the heart

A
53
Q

Excitation-contraction coupling in cardiac muscle

A

in cardiac muscle L-type Ca channels (DHP receptors) are not mechanically coupled to ryanodine receptors therefore Ca entry is necessary for contraction

Ca induced Ca release
Ca coming in during the AP from the extracellular fluid binds to ryondine receptors, iniating Ca release

but same that Ca binds to troponing ripping off tropomyosin allowing contraction

54
Q

enhancing contractile force in cardiac muscle

A

in cardiac an increase in intracellular Ca in the cardiac myocytes enhances contractile force

cardiac muscle is capable of graded single twitch contractions (force can be different)
if cytosolic Ca is low some actin remains covered by tropomyosin
increased Ca—> additiional troponin complexes activated and increased cross bridge formation leading to inc force of contraction

length tension relationship: cardiac muscle generates a greater force when slightly stretched

55
Q

in cardiac muscle, the SERCA pump

A

it is regulated by phospholamban
it will influence the SERCA pump activity
when it is dephosphorylated PLN inhibits SERCA
when phosphorylated: it increase Ca removal, enhancing relaxation and contractability
rate and uptake of Ca is inc
causing quicker relaxation and a larger store of Ca

56
Q

the heart has neuronal input that modifies conduction/contraction
para/sympathetic

A

the sympathetic increases heart rate/conduction and contractibility (autorhymic and contractile)

the parasympathetic decreases heart rate/ conduction (autorhythmic)

57
Q

phosphorylation effect on Ca, ryanodine receptors, and SERCA

A

phosphorylation of Ca channels increases Ca during action potentials

phosphorylation of ryanodine receptors enhance sensitivity to Ca, inc release of Ca from SR

increases rate of myosin ATPase

phosporylation of SERCA (PLN) inc the speed up of Ca re-uptake which in Ca storage

58
Q

cardiac length tension relationship

A

a slightly stretched sarcomere inc the Ca sensitivity of the myofilaments
a stretched sarcomere has a decreased diameter which may reduce the distance that Ca needs to diffuse, increasing probability of cross-bridging cycling

a slightly stretched sarcomere puts additional tension on stress-activated Ca channels, increasing Ca entry from extracellular space and increasing ca induced Ca release

59
Q

heart rate is under tonic control

A

autorhythmic cells can be modulated by sympathetic and parasypathetic neurons and therefore heart is under tonic control

Sa node would fire 90 Ap per min
if you want to lower, below 90 there has to be inc in parasympathetic input in the Sa node
at resting heart rate of 70-72 BPM parasympathetic is dominant
sympathetic would be 90<

60
Q

modulating pacemaker activity (parasympathetic)

A

parasympathetic neurons containing ACH mainly innervate the SA and AV node
influnecing autorhymic myocardial cells, decreasing the frequency of AP (dec heart rate)

ACH acts on muscarinic cholinergic receptors opening K channels and closing T-type Ca channels and HCN channels.
since the pacemaker activity does not usually reside within the AV node, theses mechanisms act at the AV node to dec conduction velocity

61
Q

modulating pacemaker activity (sympathetic)

A

beta1 adrenergic receptors can be activated by NE released from sympathetic neurons or epinephrine from the adrenal medulla

increased Na conductance through HCN channels and Ca through T-type channels causes:
cells reach threshold rapidly
a decreased level of repolarization

Kin 121 (8 decks)

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