Skeletal Muscle Flashcards

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1
Q

Three main types of muscle and main function

A

1) Skeletal: attached to bones, responsible for movement
2) Cardiac: heart mass, contracts causing blood to pumped
3) Smooth: lines hollow organs, blood vessels, regulates their dimensions

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2
Q

Skeletal muscle

A

Voluntary

Striated

Long cylindrical cells

Multiple nuclei pushed to side

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3
Q

Cardiac Muscle

A

Involuntary

Striated

Connected via intercalated discs

Branched cells w/ 1-3 central nuclei

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4
Q

Smooth Muscle

A

Involuntary

NOT striated

Spindle shaped, one nucleus per cell

Lines internal organs

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5
Q

Motor unit

A

Motor neuron and all the muscle fibers it innervates

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6
Q

Skeletal muscle structure

A

Are attached to bone via tendons

Long (up to 35cm), Wide (0.1mm)

Cells are composed of fibrils (actin and myosin), containing contractile filaments

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7
Q

A-band

A

Both Actin and Myosin

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8
Q

I-band

A

Actin only

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9
Q

H zone

A

Myosin only

Filaments don’t overlap

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10
Q

Z-discs

A

Anchor thin filaments (actin)

Connect myofibrils to one another

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11
Q

T-tubules

A

Circle each sarcomere

At the end of each of the A bands and I bands meet

Allows AP to be carried deep within muscle cell

Extracellular fluid can go through T-tubule

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12
Q

Sarcoplasm reticulum (SR)

A

Calcium storage site

Terminal cisternae of SR lie close to T-tubule

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13
Q

Sarcolemma

A

Plasma membrane of muscle

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14
Q

Triad

A

T-tubule surrounded by terminal cisternae on either side

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15
Q

Titin

A

Anchors thick filament to Z-line

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16
Q

Thick filament

A

Myosin (globular head + tail)

Head is an ATPase (hydrolyses ATP)
that binds to actin

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17
Q

How is the myosin head arranged

A

Pointing away from M-line when stretched

Pointing in when relaxed

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18
Q

What Thin filaments structure, composed of

A

Double stranded helical actin chain

Troponin and tropomyosin are regulatory proteins
in skeletal and cardiac muscles

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19
Q

Tropomyosin

A

Thing strand

Can block myosin head from binding to actin

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20
Q

Troponin

A

Regularly arranged on tropomyosin

Calcium binding site
- changes shape when Ca2+ binds

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21
Q

Sliding filament theory

A

Thin filament pulled over thick filaments

Z-line pulled towards M-line

I band and H zone become narrower

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22
Q

4 major steps of Cross bridge cycle

A

1) Cross bridge formation
2) Power stroke
3) Detachment
4) Energisation of myosin head

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23
Q

Cross bridge formation

A

Myosin binds to actin binding site

Calcium binds to troponin, change shape, myosin-actin binding site exposed

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24
Q

Power Stroke

A

ADP released

Myosin head rotates

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25
Q

Importance of Calcium

A

Binds to troponin, the tropmyosin moves to expose the myosin binding sites on actin

Cross bridge cycle continues as long as calcium levels remain above threshold

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26
Q

Calcium regulation

A

Active Transport pumps move Ca2+ back into SR

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27
Q

Isotonic contraction of muscles

A

Shortening
SAME tension
Velocity variable

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28
Q

Isometric contraction of muscles

A

No shortening
Constant length
Different tension

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29
Q

Length-tension relationship

  • what type of contraction does this occur?
  • definition/theory
A

Isometric contraction- when muscle doesn’t shorten but tension increases

Maximum active force (tension developed) of sarcomere is dependent on degree of actin/myosin overlap determining the number of cross-bridges

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30
Q

@ optimal length what is actin and myosin like

A

Maximum number of cross-bridges formed

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31
Q

@ reduced size of zone overlap what is actin and myosin like

A

Fewer cross-bridges formed and reduced tension

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32
Q

@ zero zone of overlap what is actin and myosin like

A

Zero tension due to no interactions between myosin and actin

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33
Q

Active tension when less tension than normal

A

sarcomere lengths less than 2.0um filaments collide and interfere

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34
Q

What um is maximal force developed of muscle (normal working range of muscle)

A

2.0-2.2 um

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35
Q

Active tension when more tension than normal

A

Sarcomere length greater than2.2 active forces decline , less overlap, less cross bridges

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36
Q

Total tension equation

A

Sum of active tension and the passive tension

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37
Q

Passive tension

A

Resistance from CT around muscle cells resist stretch

More you stretch more the collagen and muscle prevents your from stretching

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38
Q

Total tension when stretching

A

The more you stretch, active force decreases, passive force decreases

Total can be more than 100%

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39
Q

Excitation-Contraction Coupling

A

AP enters T-tubules causing Ca2+ channels in SR to open

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40
Q

What happens when AP travels down motor neuron?

A

Axon terminal voltage gated channels open Ca2+ enters axon terminal

Vesicles containing Ach fuse with terminal membrane, releasing Ach into neuromuscular junction (synaptic cleft)

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41
Q

How are Ach receptors on activated on post-synaptic neuron?

A

Ach binds to ligand (Ach) gated channels causing them to open ;predominantly Na+, enters, K+ leaves muscle cell making it less negative (end plate potential) aka depolarisation of Post-SN

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42
Q

How is muscle AP triggered

A

Sufficient ligand channels are open and causes threshold to be reached

Voltage gated Na+ channels open and AP triggered

AP travels along sarcolemma into T-tubule

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43
Q

Excitation contraction coupling

- Ca2+ released

A

AP conducted down T-tubule causing coming into close contact with SR

Voltage-gated Ca2+ channels open in SR

Ca2+ released into cytosol/sarcoplasm

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44
Q

Ca2+ binds to

A

2 Ca2+ binds troponin, causing conformational change

When Ca2+ concentrations reach critical threshold myosin binding sites on actin exposed

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45
Q

When does muscle contraction end

A

Ends when Ca2+ levels fall

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46
Q

How is calcium levels reduced

A

Pumped back into SR by Ca2+ ATP-ase pumps

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47
Q

What is the result of actin on Ca2+ leaving

A

Troponin moves back covering myosin binding site

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48
Q

Creatine Phosphate

A

Can act as an ATP “store”

Creatine phosphate + ADP = creatine + ATP

Anaerobic

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49
Q

Anaerobic glycolysis properties

A

Good for short intense exercise: Fast but inefficient

Build up of lactate and H+ max. 120s

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50
Q

What does acidification of cell inhibit

A

phosphofructokinase (PFK)

51
Q

Aerobic metabolism

A

Efficient, slower

Requires Oxygen, therefore good blood supply

Max 300W

52
Q

What substances break down to form products of cellular respiration

A

Fatty acids, amino acids, pyruvic acid, oxygen from haemoglobin, myoglobin in muscle fibers

53
Q

Myoglobin

A

High affinity for O2, and stores it

54
Q

Two ways to increase muscle tension

A

Increase frequency of stimultion (e.g. AP’s)

Recruiting additional motor units

55
Q

Temporal Summation

A

Additional AP’s initiated before Ca2- levels return to resting

Causes calcium levels to remain high and continuing force development

56
Q

Tetanus

A

Muscle contraction sustained, by high frequency of AP’s

57
Q

Type 1

A
Slow oxidative
Moderate SR pumping capacity
Small Diameter
High mitochondria/myoglobin/blood supply
Moderate glycolytic capacity
Aerobic 

Darker due to more mitochondria

58
Q

Type 1 muscle fiber properties

A

Slow twitch
Units with neurons innervating slow aerobic cells

Maintain posture, walking, low intensity exercise

POSTRUAL

59
Q

Type 2B

A

Fast twitch
Fast ATPase Rate- High SR pumping
Larger diameter, not relying on blood supply as much
Low mitochondria/myoglobin/blood supply

High glycolytic capacity

Anaerobic glycolysi

60
Q

Glycolytic capacity

A

Measure of maximum capacity of glycolysis to generate ATP

61
Q

which type of muscle fiber is recruited first

A

Type 1

62
Q

Regulation of force dependent on

A

Number of AP’s coming down motor unit

The number of motor units recruited

63
Q

Hypertrophy

A

Increase/growth in muscle size

64
Q

Atrophy

A

Reduction in activity- loss of innervation

65
Q

Relationship between motor unit and tension

A

As more units recruited, tension increases, as fast twitch fibres starting to be recruited

66
Q

Atrial cells structure

A

100um long 10um wide

No t-tubules
Contract relatively weak

Allows co-ordinated contraction of all myocytes

67
Q

How are atrial cells joined and what is the purpose of this?

A

Joined by gap junctions, allows electric activity to spread from one cell to next

68
Q

Ventricular cells structure

A

100um long 30um wide

Branched

Have well developed T-tubular system which carries excitation into interior of cell

69
Q

How are ventricular cells joined and what is the purpose of this?

A

By numerous gap junctions forming ‘sheets’ that wrap around ventricles

70
Q

What is the purpose of desmosomes in relation to contraction

A

Prevent cells from separating during contraction

71
Q

Intercalated disc function in relation to contraction

A

co-ordinated contraction of all myocytes

unlike skeletal muscle where fibres are recruited via motor neurons

72
Q

Myogenic muscle

A

Initiates contractions without nervous input

73
Q

How is AP generated in cardiac muscle

A

Sino-atrial node located in right atria

74
Q

Where does this AP spread

A

Spreads throughout atria then Purkinje Fibres to the ventricles

75
Q

How long is cardiac AP

- length relative to skeletal and nerve

A

> 100ms long

AP much longer than nerve and skeletal due to presence of ionic currents that hold the cell depolarised for a period comparable to that of a twitch

76
Q

Why is there a plateau in tension development

A

Due to large Ca2+ current, slow to open slow to close, L-type channel, K+ moves out barely in little amounts

77
Q

Can cardiac muscle tetani

A

No highly unlikely, due to absolute refractory period (long AP)

78
Q

Three major stages in cardiac muscle AP

A

0- rapid depolarisation fast voltage gates Na+ channel

2- plateau due to slow voltage gated Ca2+ channel (L-type Ca2+ channel)

3- Repolarisation due to closing of Ca2+ and opening of K+ channels

79
Q

Excitation coupling cardiac muscle

A

Depolarisation wave opens L-type Ca2+ channels in T-tubule

Ca2+ influx balanced by Na+/Ca2+ exchanger

80
Q

What happens after Ca2+ enters Cytoplasm

A

Calcium induced calcium release
or RyRa

Ca2+ binds to RyRa opening channel allows Ca2+ to leave SR

81
Q

What happens after Ca2+ released from RyRa

A

Ca2+ intracellular conc. allows Ca2+ to bind to troponin

82
Q

What is special about troponin for cardiac muscle excitation?

A

Only ONE calcium specific site (skeletal muscle has TWO)

83
Q

How is Ca2+ transported out of cell

A

Ca2+ ATPase into SR

sarcolemmal Na+/Ca2+ exchange
(3Na in, 1 Ca out)

mitochondria

sarcolemma Ca- ATPase

84
Q

How is AP graded in skeletal muscle?

A

Recruiting more muscles

85
Q

How is AP graded in cardiac muscle

A

Changing Ca2+ conc.

86
Q

How is Heart rate (HR) set, and how is it modified

A

set by pacemaker in SAN

Rate modified by autonomic nerves releasing neurotransmitters

87
Q

How is Stroke volume increased

A

Increased HR
Increased stretch of ventricles (length)
Certain neurotransmitters

88
Q

Pacemaker potential

A

Slow depolarisation due to If channel ‘funny’ (mostly Na+ driven), SPONTANEOUSLY

89
Q

Vagus nerve

Parasympathetic

A

Decreases heart rate

RELEASES ACh

90
Q

What is special about ACh in innervation in cardiac muscle?

A

It is INHIBITORY, slows down HR

91
Q

Sympathetic cardiac nerves

A

Can innervate both pacemakers, and ventricular myocytes

Affect heart rate AND stroke volume

Releases noradrenaline

92
Q

How does ACh slow down heart rate

A

by hyperpolarising RMP, so takes longer to reach threshold

Decreases rate of spontaneous depolarisation

93
Q

How does Noradrenaline increase heart rate

A

Increases rate of spontaneous depolarisation = increasing heart rate

94
Q

“Automaticity”

Increasing HR increases… because…

A

Contractile force (Stroke volume)

Less time available for Ca2+ to be pumped out of cell = more Ca2+ in cell, increase CICR by SR = stronger contraction

95
Q

Passive tension in heart

A

Lot of collagen, more stretch more total tension = more stroke volume

96
Q

How Noradrenaline acts

A

INCREASES Ca2+ release

Increases frequency of discharge of SAN thus frequency of AP

binds to B receptors and via second messengers acts on
L-type channel (more Ca2+ entering cell)

Ca2+ ATPase in SR
so more Ca2+ ready to be released when next AP comes

97
Q

Sympathetic Nervous System

A

Fight of flight response

98
Q

Parasympathetic Nervous System

A

Rest and digest

99
Q

Increase in Inotropy

A

Strengthening of muscle contraction

100
Q

Basic structure of smooth muscle

A

Spindle shape
100-400um long 5um wide
Central nucleus

No sarcomeres
Poor developed SR
No troponin
No t-tubules 
Few mitochondria
No striation
101
Q

Dense bodies

A

Act as z-lines to anchor actin to sarcolemma

Intermediate filaments attached

102
Q

Single unit (visceral) smooth muscle

WAVE like contractions

A

Sheets of electrically coupled cells act in unison

e.g. hollow organs
Spontaneously active

103
Q

Where is single-unit SM located

A

Blood vessels, hollow organs (digestive, respiratory, urinary, reproductive) RRUD

104
Q

Multiunit SM

A

Independent cells contract to its own innervation

E.g. iris, vas deferens, piloerectors (hairs)

105
Q

Why can smooth muscle contract further than skeletal and cardiac

A

Less organised, actin filaments don’t overlap as much and interfere

but slower

106
Q

Initiation of contraction in smooth muscle

A

Due to voltage-gated Ca channels for cross bridge cycle

Increase in intracellular Ca, enter mostly through cell membrane channels

107
Q

Contraction of smooth muscle can occur 3 three ways

A

Neural (iris)
Hormonal (uterus)
Spontaneous (gut) (myogenic)

108
Q

What is the source of Ca in SM

A

Extracellular and SR via IP3

109
Q

Ways which SM is regulated

A

Voltage, hormones, neurotransmitters, specific ions

110
Q

How is Ca released from SR in SM

A

By ligand-gated second messenger pathways (IP3) and by RyR

111
Q

What is activated when Ca2+ increase in SM

- what does it activate in turn

A

Calmodulin (binds 4 Ca2+ ions)

Activates myosin light chain kinase (MLCK)
which upregulates contraction

112
Q

How is MLCK activated

A

regulation in SM is MYOSIN (not actin) based

Regulatory protein turned on by phosphate, then allowing myosin to hydrolyse ATP

113
Q

When does contraction end in SM

A

when myosin light chain phosphatase (MLCP) removes phosphate group on myosin light chain

114
Q

Why is SM contraction slower

A

Enzyme regulated (NOT calcium regulated)

Slow but efficient

115
Q

What favours relaxation in SM

A

Increased MLCP

Decrease intracellular Ca2+

116
Q

What favours contraction in SM

A

Increased MLCK activity (Ca2+ regulated)

117
Q

How can SM contraction be graded

A

Difference in modulation of MLCK and MLCP

118
Q

What can modulate SM contraction

A
Stretch
Neurotransmitters
Hormones
Environment
Histamine
Adenosine
Prostacyclin
Nitric oxide (NO)
119
Q

Nitric Oxide (NO) function in modulating

A

Inhibits cGMP-dependent mechanism which contract proteins

120
Q

What innervates SM what do they do

A

Autonomic nerve fibres branch, “diffuse junction”

121
Q

What are the subunits of Autonomic nerve fibres and what do they contain

A

Varcosities (in terminal axon) release neurotransmitters into synaptic cleft

122
Q

What happens when you stretch smooth muscle

A

Initially contract, effectively resisting the stretch

(e. g. blood vessels trying to maintain blood flow constant)
- Stretch activated calcium channels

Over time slowly relaxes, adapting to change in length (e.g. gut)
- via Ca dependent K+ channels, hyperpolarising membrane potential

123
Q

Stress relaxation

A

Your constant deformation (e.g. stomach) can be steady but your stress relaxation can decrease therefore you can eat more