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Musculoskeleton > Physiology Of Muscle > Flashcards

Physiology Of Muscle Flashcards

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1
Q

Total body mass made up of skeletal muscle

A

40%

10% is cardiac and smooth

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2
Q

Actin

A

2 parallel strands of G-actin molecules that form a double helix structure.

Has three classes based on where it is found

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3
Q

Classes of actin and the tissues where it is found

A

(A)-actin: skeletal, cardiac and smooth muscles

(B) and (y) actin: every other non-muscle cell

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4
Q

Myosin

A

Proteins found on thick filaments that use ATP to generate force/contraction when bound to actin filaments

  • Contain 4 myosin light chains
  • Contain 2 essential light chains
  • Contain 2 regulatory light chains
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5
Q

How are myosin fibers classified?

A

By the length of their neck region and the speed of contraction.

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6
Q

Actin-binding proteins (ABPs)

A

Regulate actin filament formation and actin-myosin interactions.

Very common in non muscle cells however tropomyosin is in muscle cells.

(A)-actinin binds thin filaments to the Z-lines in skeletal muscle.

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7
Q

Force of muscle contraction is transmitted how?

A

Longitudinally to the tendon

Laterally to ECM tissues at costameres

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8
Q

Costameres

A

Facilitates the lateral transmission of force of contraction.

Helps stabilize the sarcolemma in muscle cells.

Contains 2 major protein complexes

Dystrophin and integrins

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9
Q

Dystrophin-glycoproteins complex (DGC)

A

Contains dystrophin proteins that anchor the cytoskeleton muscle cells to the ECM.

Disruption causes poor transmission of tension in contracting muscles causing muscle weakness and damage to muscle cells.

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10
Q

What signals damaged dystrophin molecules?

A

High creative kinase levels and section of abnormal dystrophin protein via muscle biopsy.

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11
Q

Pseudohypertrophy of muscles

A

Inflammatory response due to damaged muscle causes the appearance of hypertrophy.

Replaces damaged muscle with scar tissue that causes pseudohypertrophy

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12
Q

Proteins that can be mutated to cause various types of muscular dystrophy

A

Myosin

Actin

Tropomyosin and troponin

Nebulin

Desmin

Dystrophin

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13
Q

Integrin-vinculin-talin complex

A

Talin protein binds multiple integrins via Vinculin allowing for great stability to to the cytoskeleton.

Also allows for cell-matrix communication.

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14
Q

Major myopathys caused by myosin

A

Late onset distal myopathy

Myosin storage myopathy (MSM)

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15
Q

Characteristics of sarcomeres during muscle contraction

A

Muscle as awhile shortens about 1/3 length

  • shortening is caused by the distance between the thin and thick filaments shrink as they slide past each other
  • the H and I band shrink in size
  • The thin and thick filaments do not shrink in size
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16
Q

Specific changes in bands and lines during contraction

A

H zone and I band narrow/shrink

A band, M line, Z disc and thick and thin filaments remain unchanged

Distance between Z discs shrink, but not actual disc

“HI-AZ”

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17
Q

Myotendinous junctions

A

Force of contraction moves from the end of the muscle fibers to the tendon via connections with numerous collagen fibers.

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18
Q

Triad junction contents

A

T-tubule and the neighboring terminal cisternae (SR)

Terminal cisterna release calcium and the T-tubule moves the calcium into the muscle fibers for uptake.

Around all skeletal and cardiac fibers.

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19
Q

Muscle spindles

A

Sensory receptors located in the muscle

Function is to detect changes in muscle length and speed of contraction.

Centrally clumped nuclei in central fibers (nuclear bags)

Afferent fibers =. Excessive stretching sensation (inhibits muscle stimulation)

Efferent fibers: regulate sensitivity of Afferent endings

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20
Q

Neuromuscular junction

A

Chemical synapse formed between motor neurons and muscle fibers

Allows motor neurons to send chemical to muscles fibers to initate an action potential and ultimately contraction

Contain cholinergic receptors

(ACh is primary neurotransmitter)

  • also known as END PLATE*
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21
Q

1 motor neuron innervates how many skeletal muscles?

A

1 muscle (but multiple fascicles)

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22
Q

Action potential

A

Rapid depolarization of cell membranes via neurotransmitter signals from motor neurons.

Followed by rapid repolarization of the membrane once muscle contraction has ceased.

Depolarization = rapid influx of sodium

Repolarization = rapid influx of potassium

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23
Q

Ryanodine receptors

A

Receptors found in the gap between T-tubule and SR or terminal cisterna.

A result of depolarization causes calcium release into the mycoplasma of the muscle fibers

Binds the drug ryanodine: antagonist

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24
Q

Dihydropyridine receptor

A

Interacts with the ryanodine receptor. Induces the ryanodine receptors and plays just as essential of a role in release of calcium

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25
Troponin T subunit
Binds to tropomyosin and releases from actin
26
Troponin I
Binds to myosin heads Inhibits the binding of myosin to actin
27
Troponin C
Binds calcium molecules Allows for movement of tropomyosin *only found in striated muscle*
28
Does increasing calcium increase the force?
Yes but only to the maximal achieved force of that muscle.
29
1st step of cross bridge movement
Binding of myosin to actin *phosphate is released*
30
2nd step of cross bridge movement
Power stroke (muscle contraction)
31
3rd step in cross bridge movement
Rigor from the power stoke * ADP is released* * low energy form*
32
4th step of cross bridge movement
Unwinding of myosin and actin via ATP binding to the myosin head.
33
5th step of the cross bridge movement
Cocking of the myosin head preparing for porter stroke *high energy form*
34
Two broad components of muscle relaxation
Motor neuron action potentials stop signaling for release of ACh at End plate. Calcium ions are actively pumped back into terminal cisternae.
35
4 specific components of muscle relaxation
Acetylcholinesterase degrades remaining ACh. Sodium channels close and end plate potential ends causing repolarization Sarcolemma and T-tubules returns to resting membrane potential Calcium ions are actively pumped back into terminal cisternae. Troponin and tropomyosin block myosin heads and myofilaments slide back into original positions
36
Most important component of muscle relaxation
Removal of calcium ions.
37
Slow red muscle motor units
Type 1 MHC expression Contain very low ATPase activity Muscle Function is weight baring and sustained movement Fatigue resistant Aerobic metabolism Numerous mitochondria
38
Fast oxidative red muscle motor units
MHC expression 2a and 2x High levels of ATPase activities Muscle function is sustained locomotion Fatigue resistant Moderate mitochondria
39
Fast glycolytic white muscle motor units
MHC expression 2b and 2x High ATPase activity Muscle function is for quick burst power Easily fatigued Anaerobic metabolism Few mitochondria
40
Molecular Difference between motor units
Different amino acid components however both have 2 heavy and 2 light chains. Very difficult to interconvert slow and fast twitch muscles
41
Types of staining for muscle fibers
``` ATPase staining = Fast white (Dark brown) fast red (Light brown) Slow red (white) ``` ``` SDH staining = Fast white (white) Fast red (light brown) slow red (Dark brown) ```
42
Patent period
Time for action potential to propagate across sarcolemma *1st phase*
43
Contraction period
Repetition of cross bridge cycles Generates tension/force *2nd phase*
44
Relaxation period
Calcium ions are reduced in cytosol via uptake in terminal cisternae Lowers tension *3rd step*
45
Tension produced during twitch is affected by what factors?
Timing and frequency of stimulation Length of sarcomere at rest Type of muscle fibers
46
Refractory period
Muscle fiber is unable to fire and generate tension due to influx of potassium ions Occurs after relaxation briefly *4th phase*
47
Force summation occurs in what two ways?
Caused by either increased frequency of contractions or increase motor units contracting simultaneously Force/tension generated increases in summative fashion due to not allowing muscles to fully relax.
48
Infused tetanus
Force summation that has small muscle relaxation between stimuli Hits maximum tension level still.
49
Complete tetanus
Muscle reaches complete tension with no relaxation in between Causes muscle to completely fatigue over time.
50
Parallel (side-by-side) Orientation of sarcomeres
Enables double the force production but no increase in velocity or shortening capacity of the muscle
51
Series (in a line) orientation of sarcomeres
No change in force but doubles the velocity and shortening capacity of the muscle
52
Does increasing the sarcomere length from its original length increase tension/force?
No, there is an optimal length for tension/force generation.
53
Shortening of sarcomere causes what?
No tension formation since the sarcomere cant shorten
54
Lengthening of the sarcomere causes what?
No tension because thin and thick filaments cant interact (no overlapping)
55
Recruitment
Increase in number of active motor units by the nervous system
56
Size principle
Smaller motor units are called upon to stimulate small focused forces Larger motor units are called upon to stimulate large non-focused forces Larger motor units require larger stimulation to fire Increased action potential causes increased contraction
57
Type 1 motor units Characteristics
Small cell diameter with high excitability (sensitivity) Conduction velocity is fast Few fibers, low force, low fatiguability Oxidative metabolism SLOW TWITCH
58
Type 2 motor units characteristics
Large cell diameter with low excitability (sensitivity) Conduction velocity is very fast Many fibers, high force, easily fatiguable Glycolysis metabolism FAST TWITCH
59
Isotonic concentric muscle contraction
Muscle contracts, shortens and creates enough force to move the required load “Normal” muscle flexion contraction
60
Isotonic eccentric contraction
Muscle contracts, lengthens and creates enough force to move the required load “Normal” muscle extension contraction
61
Isometric contraction
Muscle contractions but does not shrink or lengthen causing no load movement (muscle force does not exceed load requirement)
62
Isometric contractions are caused by what?
Flexible elements equaling contraction components in force.
63
Pathways to regenerate ATP in muscle activity
Direct phosphorylation via creative kinase Anaerobic pathway metabolism (2 ATP) Aerobic pathway metabolism (32 ATP)
64
Changes in muscle caused by endurance training
Increased oxidative enzymes Increased # of mitochondria and blood vessels
65
Changes in muscle caused by resistance training
Increased # of myofibrils Increased diameter of muscle fiber and myofibrils
66
Changes in muscle caused by disuse of muscle for prolonged times
Decreased oxidative enzymes Decreased # of myofibrils and decreased diameter of muscle fibers
67
PGC-1
Transcriptional coactivator that is the key player in remodeling protein based on adaption needs. Almost all pathways go through PGC-1 at some point
68
Mitochondrial Transcription factor A (TFAM)
Key activator in generating additional mitochondria in muscle when needed. Also activates glucose, FA oxidation when cellular energy is low.
69
Two main causes of muscle fatigue
Limitations of a nerve ability to generate a sustained signal (neural fatigue) Reduced ability of the muscle fiber to contract (metabolic fatigue)
70
High-frequency fatigue
Impaired membrane excitability due to high frequency of stimulation. Causes down regulation of voltage gated channels.
71
Limb-girdle muscular dystrophy
Muscle Wasting in the pelvic region Caused by deficient titin protein
72
Calreticulin and calsequestrin
Proteins in sarcolemma that bind calcium for 2 reasons 1) prevent it from leaving sarcolemma until needed 2) stabilize calcium gradient
73
Force-velocity relationship
Heavier the load = longer it takes to contract fully.

Musculoskeleton (36 decks)

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