bmsc 207 muscle Flashcards

(65 cards)

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
oxidative (aerobic) metabolism
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
24
muscle fatigue
a decrease in muscle tension as a result of previous contractile activity that is reversible with rest (hours)
24
central fatigue peripheral fatigue
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
determinants of muscle force/tension development
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
how does muscle length influence tension development
the overlap between actin and myosin
27
single twitch vs summation what causes a twitch? how long does it last
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
tetanus
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
motor unit motor neuron pool
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
why doesnt the large diameteer neuron reach threshold?
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
size principle
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
asynchronous recruitment
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
isotonic contrations (con/ecc)
concentric: muscle shortens while generating force eccentric: muscle lengthens while generating force acts to decelerate the joint at the end of a movement
33
how do the sacrcromeres shorten during isometric contraction without the muscle changing lenght?
elastic elements in tendons, elastic and connective tissue in and around muscle fibres
34
skeletal muscle adpatations
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
muscle hypertrophy
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
skeletla muscle atrophy
protein degradtion > protein synthesis can occur due to disuse: immobilization, bed rest, and unloading (0 gravity)
37
cachexia
weakness and or wasting due to chronic disease cancer is often associated with a loss of weight and weakness of muscles
38
skeletal muscle reflexes
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
monosynaptic reflex polysnaptic reflexes
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
proprioceptors
provide info into the CNS about the position of our limbs in space, movements, and the effort exerted by skeletal muscles
41
muscle spindles
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
golgi tendon organ
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
joint receptors
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
alpha gamma neuron
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
a flexion reflex pulls limbs from painful stimuli? what is it driven by what is crossed extensor
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
cardiac muslce what is it made of what connects them electrically and mechanically
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
does cardiac muscle have larger t tubules compared to skeletal muscle? less or more of SR mitochondria?
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
contraction is not initiated by neurons for cardiac
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
AP's in autorhythmic myocardial cells
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
AP's in contractile myocardial cells
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
how the autorhytmic and contractile myocardial connected
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
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
53
Excitation-contraction coupling in cardiac muscle
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
enhancing contractile force in cardiac muscle
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
in cardiac muscle, the SERCA pump
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
the heart has neuronal input that modifies conduction/contraction para/sympathetic
the sympathetic increases heart rate/conduction and contractibility (autorhymic and contractile) the parasympathetic decreases heart rate/ conduction (autorhythmic)
57
phosphorylation effect on Ca, ryanodine receptors, and SERCA
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
cardiac length tension relationship
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
heart rate is under tonic control
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
modulating pacemaker activity (parasympathetic)
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
modulating pacemaker activity (sympathetic)
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