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Physiology with Pharmacology > Muscle > Flashcards

Muscle Flashcards

1
Q

What is skeletal muscle responsible for?

A
  • Voluntary movement of bones - locomotion
  • Control of inspiration - diaphragm contraction
  • Skeletal muscle pump - venous return to heart
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2
Q

What is the structure of skeletal muscle?

A
  • Muscle cells come together to form the fascicle
  • Fascicle surrounded by the perimysium (sheath)
  • Muscle units made up of many fascicles, surrounded by epimyosin sheath
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3
Q

What is the basic unit of contraction?

A

Sarcomere

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4
Q

What are myofibrils?

A

Units of contraction that are made up of multiple sarcomeres running end to end

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5
Q

What are the thick and thin filaments made of?

A

Thick - myosin
Thin - mainly actin

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6
Q

What are the I bands?

A

Predominantly actin
Lighter appearance

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7
Q

What are the A bands?

A

Overlap of actin and myosin filaments

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8
Q

What is the Z line?

A

At the end of each sarcomere

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9
Q

Which proteins are involved with sarcomeres?

A

Nebulin is linked around the actin filaments
Titin helps anchor the myosin to the Z-disk
Both have roles in sensing the length and state of the sarcomeres

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10
Q

What happens to the bands as the sarcomere contracts?

A

Actin pulled inwards
I band becomes smaller
A band stays same length

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11
Q

How is contraction initiated?

A
  • Release of ACh at neuromuscular junction initiates action potential in plasma membrane of muscle fibre
  • Wave of depolarisation passes along sarcolemma, through T-tubules to interior of cell
  • T-tubule runs near two areas of the SR forming a Triad
  • Depolarisation triggers increase in IC Ca2+
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12
Q

What is fine and course control of muscle action?

A

Fine control - each motor neuron innervates a few muscle fibres e.g. eye
Course control - in larger muscles each may be innervating hundreds e.g. leg

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13
Q

What would cause rigour mortis?

A

Absence of ATP

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14
Q

What is the mechanism for contraction of the sarcomere?

A

1) ATP binds to myosin head - causes dissociation of myosin head from actin
2) ATP hydrolysed forming ADP and Pi (remain attached) - gives conformational change in myosin head to open position
3) Myosin head reaches down actin filament binding to new actin molecule - forms cross-bridge
4) Phosphate released - gives strong association between actin and myosin
5) Second conformational change - myosin head goes back, pulls actin in towards middle of sarcomere
6) ADP released from myosin head

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15
Q

How can twitch be measured?

A

Measured physiologically in isolated muscles - stimulate muscle electrically to mimic ACh release

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16
Q

What is the latent period?

A

Where action potential passes down sarcolemma causing calcium release

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17
Q

What is summation in muscle fibres?

A

Where contraction phase much slower than actional potential and repolarisation - so is possible to depolarise membrane again before first contraction finished

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18
Q

What is unfused tetanus?

A

25 Hz - plateau in force generation is reached, calcium is released, before this is taken up we get the next twitch

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19
Q

What is fused tetanus?

A

50 Hz - no chance for calcium to be taken back up so present in sarcoplasm all the time - constant force generation

20
Q

What are the properties of slow oxidative muscle fibres?

A
  • Oxidative phosphorylation to generate ATP for contraction
  • High myoglobin for O2 storage
  • Resistant to fatigue
  • Red colour
  • Low glycogen content
  • Low frequency needed to be able to go into unfused tetanus state
    e.g. soleus muscle
21
Q

What are the properties of fast oxidative muscle fibres?

A
  • Oxidative phosphorylation for ATP
  • Not as resistant as type 1
  • High glycogen (energy in O2 absence)
  • Red colour
  • High myoglobin
  • Type 2A
    e.g. gastrocnemius
22
Q

What are the properties of fast glycolytic muscle fibres?

A
  • Glycolytic glycolysis to generate ATP
  • Lower myoglobin levels
  • High force but tire quickly
  • High glycogen
  • White colour
    e.g. biceps brachii
23
Q

What is the speed of contraction of slow and fast muscle fibres?

A

Slow - take longer to contract after nerve stimulation
Fast fibres - take less time to contract - are double the diameter of slow fibres

24
Q

What is isometric contraction?

A

Muscle at fixed length, tension is generated e.g. plank

25
What is isotonic contraction?
Muscle stimulation causes a change in length e.g. bicep curls
26
How is an action potential transmitted at a NMJ?
1) Action potential arrives 2) Neuronal Na+ channels open and sodium enters neurone 3) Causes wave of depolarisation which activates Ca2+ channels, Ca2+ enters 4) Causes fusion of vesicles containing ACh with membrane 5) ACh released into synaptic cleft and stimulates nicotinic receptors 6) Causes activation of VG Na+ channels, wave of depolarisation passes down muscle
27
How is overstimulation prevented?
Acetylcholinesterase released which breaks down acetylcholine so it is not bound to the receptors continually - Allows relaxation
28
What causes repolarisation?
Opening of VG K+ channels Potassium moves out
29
What are the inhibitors of ACh release?
Tetanus toxin Botulinum toxin
30
What are the inhibitors of acetylcholinesterase?
Physostigmine DFP
31
What is an inhibitor of K+ channels?
Dendrotoxin
32
What are the symptoms caused by botulinum toxin?
1st - dry mouth, double vision 2nd - diarrhoea, vomiting 3rd - paralysis of limbs or respiratory muscles
33
What is botulinum toxin?
Produced by Clostridium botulinum bacteria Is an endoproteinase that cleaves proteins required for exocytosis of ACh in ANS - prevents vesicular fusion
34
What are the clinical uses of botulinum toxin
Strabismus treatment - cross-eyed Blepharospasm Cosmetic treatments
35
What are the properties of cardiac muscle?
- Specific to the heart - Striated cardiomyocytes - Myocytes are shorter and branched - join together at intercalated disks - Electrical coupling between adjacent myocytes at ID by gap junction
36
Where are action potentials initiated in cardiac muscle?
In the pacemaker cells of the sino-atrial node and propagates between cells via gap junctions
37
What processes is smooth muscle involved in?
Mechanical control of organ systems - digestive, urinary, reproductive Control of blood vessel and airway diameter
38
What are the classes of smooth muscle?
Multiunit Unitary - cells coupled to each other so waves of depolarisation can be transmitted to neighbouring cells
39
What are the properties of smooth muscle?
Non striated - multiple actin fibres join at dense bodies, thick filaments intersperse around the thin filaments Large variations in action potential depending on muscle type
40
How is IC Ca2+ increased in skeletal muscle?
- Depolarisation activates L-type Ca2+ channels in the T-tubule membrane - Leads to opening of the channel and influx of calcium into cell - Causes mechanical tethering between the L-type Ca2+ channels in the T-tubule and Ca2+ release channels (ryanodine receptors) in the SR membrane - The Ca2+ release channels open and Ca2+ moves into cytoplasm
41
How is IC Ca2+ increased in cardiac muscle?
Cardiac muscle has T-tubules - in dyad structure that lie at the Z line - No mechanical interaction between VG Ca2+ channels in T-tubule and Ca2+ release channels (ryanodine receptors) in SR - Influx of Ca2+ through T-tubule channels activates the ryanodine receptors - calcium induced calcium release
42
How is muscle contraction terminated?
Ca2+ is removed from the cytoplasm: - Across cell membrane by plasma membrane calcium ATPase (PMCA) or electrogenic sodium/calcium exchanger (NCX) - Back into SR via sarco/endoplasmic reticulum calcium ATPase
43
How is IC Ca2+ increased in smooth muscle?
- SM has shallow invaginations instead of T-tubules - Change in Vm or action potential activates L-type Ca2+ channels - Leads to CICR via activation of ryanodine receptors in SR membrane - Activation of Gq-coupled membrane receptors leads to IP3 production and stimulation of IP3 receptors in SR membrane
44
What is troponin?
- Site of Ca2+ binding - Changes shape to reveal myosin binding site - Sits on top of myosin binding site in resting state
45
What is the mechanism of contraction in smooth muscle?
(No troponin) Calponin and Caldesmon tonically inhibit interaction between actin and myosin - Stimulation of contraction involves stimulation of calmodulin by Ca2+ Downstream effects:] - Activation of myosin light chain kinase - phosphorylates MLC - Removes inhibitory effects of calponin and caldesmon - facilitates crossbridge formation and contraction
46
How is contraction stopped in smooth muscle?
Need to dephosphorylate MLC by using myosin light chain phosphatase (MLCP)

Physiology with Pharmacology (11 decks)

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