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My Body Logs > Lecture 11 And 12 - Muscle Structure And Function > Flashcards

Lecture 11 And 12 - Muscle Structure And Function Flashcards

1
Q

What is Muscle cell cytoplasm called?

A

Sarcoplasm

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2
Q

What is Muscle cell membrane called?

A

Sarcolemma

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3
Q

What is Muscle cell mitochondria called?

A

Sarcosomes

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4
Q

What is the role of Skeletal Muscle?

A

Movement of skeleton and other structure like the eye tongue
(Voluntary)

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5
Q

What is the role of Cardiac muscle?

A

Involuntary muscle in the heart

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6
Q

What is the role of Smooth muscle?

A

Involuntary visceral (organ) muscle that changes the volume of tubes and cavities

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7
Q

What is Endomysium?

A

The loose connective tissue that surrounds skeletal muscle fibres

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8
Q

What are Fascicles?

A

Bundles of muscle cell fibres

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9
Q

What is Perimysium?

A

Thicker loose connective tissue that surrounds the fascicles

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10
Q

What is Epimysium?

A

The thicker, denser connective tissue that surrounds bundles of fascicles

Dense irregular connective tissue

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11
Q

Basic structure of skeletal muscle

A

Muscle fibre surrounded by endomysium
Bundle of muscle fibres all surrounded by perimysium forms a fascicle
Bundles of fascicles surrounded by epimysium is a muscle

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12
Q

What is a Myofibril?

A

Groups of contractile proteins that contain many sarcomeres in Skeletal muscle

There are many Myofibrils in a striated muscle cell/fibre

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13
Q

What are the 2 points of attachment called that Skeletal muscle needs and describe how they move during contraction?

A

Origin (Doesn’t move during contraction)
Insertion (Normally moves in contraction)

Origin normally proximal
Insertion normally distal

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14
Q

What does Distal mean?

A

Further from the body

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15
Q

What does Proximal mean?

A

Closer to the body

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16
Q

What is a First class lever?

A

Like a see saw
Pivot point in middle, when force is applied, the opposite sid of where the weight is moves in the opposite direction
E.g Head extension at the neck

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17
Q

What is a Second class lever?

A

Like a wheelbarrow
Toes are fulcrum, weight is entire body and force is contraction of muscles in lower limb

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18
Q

What is a Third class lever?

A

Fulcrum at opposite end to the weight and force needs to be applied in the middle to raise the load
Like doing a bicep curl, force is bicep, fulcrum is elbow , weight is dumbbell

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19
Q

Differences of cardiac muscle to skeletal muscle

A

Muscle fibres not as wide
Nuclei are central and cigar shaped (Skeletal = peripheral nuclei)
Normally SINGLE nuclei per cell (skeletal = Multinucleated)
Muscle fibres branched (Skeletal = non branched)
Intercalated discs (Skeletal = no intercalated discs)

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20
Q

What are Intercalated discs of cardiac muscles??

A

Form junctions between cells
The specialised cell contacts like gap junctions allow fast electrical signal conduction between cardiomyocyte cells

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21
Q

What structure does Smooth muscle have if it has no striations?

A

Narrow, long spindle shaped cells
Has calveoli (Cave like structures)
The microtubules run between dense bodies

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22
Q

Skeletal muscle ultrastructure

A

Peripheral nuclei
Multi nucleated
Non branched fibres

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23
Q

What is the Sarcomere?

A

Smallest functional unit in striated muscle
Role is to draw the Z-line together
Distance between the 2 Z-lines marks a sarcomere

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24
Q

How can we tell that Myosin is thicker than actin?

A

Appears darker

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25
Q

Striated Muscle ultrastructure (Left to right)

A

I Band (Isotropic region)
Z-Line (Made of actin) in I Band
A-Band (Anisotropic)
I-Band (Isotropic region)
Z-Line in I-Band

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26
Q

What marks the start and end of a sarcomere?

A

The distance between the 2 Z-Lines

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27
Q

How does the I-Band appear and what is obtained within the I-Band?

A

Lighter region
Contains only thin actin filaments
Contains Z-line which is made out of actin

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28
Q

How does the A-Band appear and what does it contain?

A

The darker region in the sarcomere
Contains both thick myosin filaments and thin actin filaments
Contains the M-Line
Contains the H-Zone

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29
Q

What is the H-Zone and where is it?

A

Where the M-Line is found
Contains only myosin (No Actin)

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30
Q

What is the role of the M-Line?

A

Think myosin filaments are held in place by it.

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31
Q

What is a Myofibril?

A

Series of sarcomeres

Cylindrical organelle running length of the muscle fibre containing actin and myosin

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32
Q

What is in endomysium?

A

Reticular fibres
Nerves
Small capillaries

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33
Q

What is in Perimysium?

A

Blood vessels
Nerves
Lots of collagen (mainly 1)

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34
Q

What is epimysium?

A

Thick dense irregular connective tissue
It is contiguous with muscle tendon

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35
Q

What are Type 1/Slow striated muscle fibres and what colour do they appear?

A

Red muscle fibres

Slow oxidative fibres (Slow twitch)
Rich capillary/blood supply
MANY MITOCHONDRIA
Many cytochromes (for electron transport)
High myoglobin

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36
Q

What is the role of Slow twitch muscle fibres and what fuel source do they mainly use?

A

Fatty acid fuel source
Endurance type activities
E.g standing, maintaining posture

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37
Q

What are the 2 types of Fast Twitch fibres?

A

Type 2A(Fast oxidative glycolytic)
Type 2B(2X Fast glycolytic fibres)

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38
Q

What fuel sources do Type 2A fibres use and describe their structure? What colour are Type 2A skeletal muscle fibre?

A

Fatty acid and glycogen fuel source
Rich capillary supply
INTERMEDIATE mitochondrial numbers
Many cytochromes
High myoglobin
Lighter pinkish

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39
Q

What fuel source do Type 2B muscle fibres (The proper quick ones) use? Describe their structure? Are they aerobic or anaerobic? What colour are they?

A

Glycogen fuel source
Poor capillary supply
Few mitochondria
Few cytochromes
Low myoglobin
Rapid fatigue
WHITE/VERY PALE
ANEROBIC

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40
Q

Slow twitch Vs Fast twitch fibre comparison

A

Slow has BETTER blood supply
MORE Mitochondria
MORE myoglobin
SLow is RED, FAST is WHITE
SLOW = fatigue resistant fast is not

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41
Q

How does Mature Skeletal muscle get repaired?

A

Skeletal muscle cells can’t divide
Satellite cells undergo mitosis to regenerate muscle cells
HYPER PLASIA follows muscle injury

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42
Q

How can satellite cells also cause Skeletal Muscle Hypertrophy?

A

Satellite cells fuse with muscle cells to increase mass

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43
Q

Can Cardiac muscle be repaired?
What happens when cardiac muscle is damaged?

A

Cannot regenerate
FIbroblasts invade divide and produce scar tissue

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44
Q

Can Smooth muscle be repaired?

A

Retain mitotic activity so can form new smooth muscle cells

Very good at repairing self

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45
Q

What is Hyperplasia?

A

Multiplication of cells

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46
Q

What is Hypertrophy?

A

Cells enlargement

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47
Q

What is Heart atrophy?

A

Smaller than normal heart

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48
Q

What is Heart Hypertrophy?

A

Enlarged heart

49
Q

What is Deep Fascia?
What type of connective tissue is it?
What is its function?

A

Dense connective tissue
Surrounds a group of muscles
Binds them into functional groups
Contains large blood vessels, nerves and fat

50
Q

Where is Superficial fascia?

A

IS between SKIN and MUSCLES

51
Q

What is the Difference Between Deep Fascia and Superficial fascia?

A

Deep Fascia surrounds MUSCLES
Superficial Fascia is between SKIN AND MUSCLES

52
Q

What is the Agonist?

A

(MAIN MUSCLE) The prime mover

53
Q

What are Antagonists?

A

Oppose the prime mover/agonist

54
Q

What are Neutralisers?

A

Prevent agonist from doing unwanted movement

55
Q

What are Fixators?

A

Holds a body part in place while another body part is moving

56
Q

What are Synergists??

A

Assist prime movers

57
Q

What are Compartments of muscles?

A

Muscles with similar actions grouped together

58
Q

What is the Origin for Skeletal Muscle?

A

Origin is attachment site the normally doesn’t move
Tension created here

59
Q

What is the Insertion Point of Skeletal muscle?

A

Point at which moves when muscle contracts

60
Q

What is a tendon?

A

Fibrous cord the extends from the muscles connective tissue to the bone
Dense regular connective tissue

61
Q

What are Aponeruoses?

A

Broad and flat structure that attaches bone to other closet structures
Flat sheet like tendon (Bicipital aponeurosis)

62
Q

What is the Direction of skeletal muscle contraction determined by?

A

Direction of muscle fibres

63
Q

How does Smooth muscle contract?

A

Actin and myosin slide other each other but pull dense plaques together not Z-Lines
Not striated

64
Q

What is Muscle Remodelling?

A

Continually Replacement of contractile proteins
Exercise = more Myofibrils

Atrophy = Loss of contractile proteins
Destruction > replacement
Hypertrophy = Increase in cell size
Replacement > Destruction

65
Q

What is the mechanism for Muscle Hypertrophy?

A

Exercise
Overstretching (A and I Bands can’t touch)
New sarcomeres added in between existing sarcomeres

More Myofibrils made to adapt to be able to cope with dealing with more weight

66
Q

What are Purkinje Fibres? = Specialised muscle cells in heart
Describe the structure of Purkinje fibres:

A

LOTS OF GLYCOGEN STAIN VERY PALE
MANY GAP JUNCTIONS between them (Rapid action potential transmission = rapid conduction = strong synchronous contraction of heart)
FEW MYOFIBRILS (CONDUCTION DONT REALY NEED THEM)
CENTRAL NUCLEI

67
Q

What is the function of Purkinje fibres?

A

Transmit depolarisation/action potential from the bundle of his to the ventricles of the heart

68
Q

What is the Sino-Atrial Node?
Where is it located?

A

The pacemaker
In right atria wall
Initiates depolarisation of atria
Is BANANA Shaped

69
Q

How is the SAN Affected by neuronal activity?

A

Sympathetic nervous system increases rate it initiates depolarisation along sympathetic ganglia

Parasympathetic nervous system decreases rate

70
Q

What is Myoglobin?
Where is it found?
What colour is it?

A

Red protein
ONLY FOUND IN STRIATED MUSCLE
Like a single subunit of haemoglobin
Oxygen storing molecule
HAS MUCH HIGHER AFFINITY FOR OXYGEN THAN HAEMOGLOBIN

71
Q

What is Rhabdomyolysis?

A

Striated muscle damage
Rhabdo - Striated
MYo- Muscle
Lysis - Breaking apart

72
Q

What are the clinical signs (what can be seen in the blood) of Rhabdomyolysis?

A

Myoglobin released into blood (Myoglobinaemia)
Creatinine kinase in blood

73
Q

What can cause Rhabdomyolysis?

A

Falls/crush injuries
Compartment syndrome

74
Q

What are varicosities?

A

Autonomic nervous system fibres containing neurotransmitter which release these neurotransmitters into a wide synaptic cleft to stimulate smooth muscle contraction

75
Q

How is smooth muscle stimulated to contract?

A

Neurotransmitter from varicosities bind to receptor
Second messenger stimulates sarcoplasmic reticulum to release Ca2+
Voltage gated Ca2+ channel lets more Ca2+ in
Ca2+ binds to Calmodulin which binds to MLCK which Phosphorylates myosin
This allows actin to bind
Contraction continues until Ca2+ drops

76
Q

On a basic level, what regulates smooth muscle contraction?

A

Phosphorylation of myosin = contraction
Dephosphoryrlation of myosin = stops contraction

77
Q

What is a neuromuscular junction?

A

Region joining nerve to a skeletal muscle
The end of an axon before a skeletal muscle

78
Q

What happens at a neuromuscular junction?

A

Vesicles containing acetylcholine bind to the membrane of the synaptic knob releasing acetylcholine into cleft once a nerve impulse reaches the junction

This neurotransmitter in the cleft initiates an action potential along the muscle

79
Q

How does a nervous impulses reaching the end of a motor neuron stimulate muscle contraction?

A

The acetylcholine binds to receptors on the post synaptic membrane (Skeletla muscle)
Na+ ion channels open causing influx of Na+ causing muscle depolarisation
Depolarisation spreads through T tubules and over sarcolemma
Ca2+ voltage gated ion channels open causing influx of Ca2+

80
Q

What is the structure of a myosin molecule?

A

Rod like structure with 2 protruding heads
The thick myosin’s contain many myosin molecules and heads

81
Q

What is tropomyosin?

A

Protein which coils around the actin helix reinforcing it and blocking the binding sites for the myosin heads

82
Q

What complex is present on tropomyosin?

A

Troponin complex

83
Q

What is the most important protein in the Troponin complex on tropomyosin and why is it important?

A

TnC
Binding site for Calcium
When calcium binds causes conformational change to tropomyosin
Pulls tropomyosin away from actin exposing the binding sites to the myosin heads allowing for contraction to occur

84
Q

Describe the sequence of events in the sliding filament model of muscle contraction:

A

1.) ATP on the myosin head is hydrolysed to ADP + Pi energy is used to cock myosin head

2.) Actin myosin cross bridge forms

3.) Working stroke/power stroke occurs where the activated myosin head pulls the actin filament towards the M line and ADP + Pi is released

4.) ATP binds to myosin head and cross bridge detaches , cycle back to step 1

85
Q

When does the contraction of skeletal/striated muscle cease?

A

When the action potential ceases
Ca2+ taken back up into sarcoplasmic reticulum
Ca2+ unbinds from TnC in Troponin complex of tropomyosin
Tropomyosin goes back to block myosin binding sites on actin

86
Q

What is Ptosis?

A

Drooping eyelid

87
Q

What happens in terms of actin and myosin lengths and distance between Z-lines in muscle contraction?

A

Lengths of actin and myosin remain the same
Z lines come closer together/sarcomeres shorten

88
Q

What type of disease is Myasthenia Gravis?

A

Autoimmune disease

89
Q

What do the autoantibodies target in Myasthenia Gravis?

A

Block Acetylcholine receptors

90
Q

What does the blocking of acetylcholine receptors in Myasthenia Gravis cause?

A

Reduced synaptic transmission causing intermittent muscle weakness
E.g Ptosis

91
Q

What is compartment syndrome?

A

Trauma in a compartment of muscles causing internal bleeding
Increases internal pressure in compartment on blood vessel and nerves

92
Q

What are the signs/symptoms of Compartment syndrome?
The 6Ps

A

Compartment feeling tense and firm
Swollen shiny skin, sometimes obvious bruising
Prolonged capillary refill time
Deep constant localised pain

Pain
Pulselessness
Paraesthesia
Paralysis
Perishingly cold
Pallor

93
Q

How is compartment syndrome treated?

A

Fasciotomy

94
Q

What is a fasciotomy?

A

Where the fascia surrounding a compartment of muscles is cut open to relieve the building pressure in that compartment

Skin graft then given to cover

95
Q

What is Muscle tone?

A

The tension of muscle when its at rest

96
Q

How does exercise cause muscle hypertrophy?

A

New Myofibrils are created or existing Myofibrils increase in length

Due to A and I bands can’t re engage

97
Q

What causes muscle atrophy?
The 3 Ds

A

Disuse (sedentary lifestyle, bed rest)
Denervation of muscle (surgery)
Disease (Muscular dystrophies)

98
Q

What type of disease is Duchene Muscular dystrophy?

A

X-linked recessive inherited

99
Q

What is mutated in Duchene muscular dystrophy?

A

Dystrophin gene

100
Q

What occurs in Duchene muscular dystrophy due to the absence of Dystrophin?

A

Excess Ca2+ enters muscle cell
Ca2+ then water taken up into mitochondria
Mitochondria burst
Muscle cell bursts (Rhabdomyolysis)
Creatine Kinase and myoglobin in blood now high

101
Q

What is Creatine Kinase?

A

Enzyme important in metabolically active tissues like muscle
Adds phosphate to creatine (creatine phosphate) creating a molecule that’s a high energy store

102
Q

When is Creatine kinase released into the blood?

A

When skeletal muscle is damaged
Or when the brain is damaged

103
Q

Levels of what enzyme in the blood used to be used to diagnose heart attack?
What is now used to measure heart attacks?

A

Creatine Kinase levels
Now Troponin I and Troponin T assay used

104
Q

What can cause an increase in plasma creatine kinase levels?

A

Intramuscular injections (vaccines)
Vigours exercise
Falls
Rhabdomyolysis - (compartment syndrome, crush injuries)
Muscular dystrophy
Acute kidney injury (myoglobin not cleared)

105
Q

The smallest changes in what protein in the blood indicate cardiac muscle damage?

A

Troponin I or T levels

106
Q

What is the effect of the Botulism toxin produced by Clostridum botulinum?

A

Blocks neurotransmitter release at the end of the motor neurone
Causes paralysis of muscles (unable to contract remains relaxed)

107
Q

How does Botox utilise the Botulism toxin?

A

Treats wrinkles as it prevents the contraction of muscles

108
Q

What is the effect of Organophosphate poisoning on muscle contraction?

A

Affects activity of Acetylcholine esterase so Ach remains in cleft constantly stimulating muscle contraction

109
Q

What type of disease is Malignant hyperthermia?

A

Autosomal dominant inheritance

110
Q

What gene is affected in Malignant hyperthermia?

A

RyR1 gene

111
Q

What is caused by the mutation of the RyR1 gene in malignant hyperthermia?

A

Severe reaction to anaesthetics

Massive involuntary muscle contractions
Causes excessive heat and metabolic acidosis

Causes increased muscle breakdown and hyperkalaemia

112
Q

What is ANP?

A

Atrial natriuretic peptide

113
Q

What is ANP released by?

A

Atria

114
Q

What is BNP?

A

Brain natriuretic peptide

115
Q

What is BNP released by?

A

Ventricles

116
Q

When is ANP and BNP released?
What is the benefit of this?

A

During heart failure by heart
To increase Natriuresis (sodium excretion in urine)
This helps decrease BP and RAAS activity helping decrease pre-load on the heart

117
Q

What does Congestive heart failure lead to the release of?

A

ANP (Atrial Natiuretic peptide)

118
Q

What affect does ANP have on the kidneys?

A

Increases GFR
More Naturiesis (more Na+ lost in urine)

119
Q

When is BNP released?

A

During brain failure it’s released by the heart

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