Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Excitable Cells > Muscle 2 > Flashcards

Muscle 2 Flashcards

1
Q

What is the typical duration of a muscle action potential?

A

Around 2ms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How long does a muscle twitch last?

A

20-100ms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why does a muscle twitch have the start delayed and what does this allow?

A

start delayed due to neuronal and muscle action potential – allows force to be maintained without having to fire action potentials continuously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is and isn’t muscle contraction dependent on?

A
  • Muscle contraction isn’t directly dependent on electrical activity of muscle membrane
  • Muscle contraction is dependent on calcium – this takes longer than an action potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

If a second stimulus arrives before the muscle is relaxed what do we see?

A

If a second stimulus arrives before the muscle is relaxed we see summation and unfused tetanus with increased rate. The calcium concentrations will reach much higher levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the force produced by muscle proportional to?

A

Calcium concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do higher rates of AP lead to?

A

fused tetanus (not the disease – here it is the state at which a muscle is maximally contracted)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the smallest contractile unit and what is this?

A

• Smallest contractile unit of muscle is a motor unit

  • Set of muscle fibres that are controlled by a single motor neurone
  • The bigger the motor neurone cell body size the more fibres it will innovate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Henneman’s size principle?

A
  • As a muscle is stimulated to contract by a neurone in the CNS motor units will become recruited in order of size
  • Smaller neurones fired first – more likely to fire an action potentials at low stimuli than larger neurones
  • As stimulus size is increased we recruit the larger motor neurones increasing contraction force
  • By recruiting different motor neurones with different size motor units we can regulate the size of contraction and produce very small and very large contractions of a muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the different skeletal muscle types?

A
  • Slow-twitch oxidative
  • Fast-twitch glycolytic
  • Fast-twitch oxidative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give features of slow fibres (type I)

A
  • Used for posture maintenance etc.
  • Have myoglobin (red) as oxygen store
  • Many mitochondria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give features of Fast Fibres (Type IIa, IIb)

A
  • Both have fast myosin isoform
  • Fast Ca transient (high SERCA pump)
  • Allows rapid shortening but at high energy cost as ATP is hydrolysed quickly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give features of type IIa oxidative fibres

A
  • Lots of mitochondria
  • Pretty good blood supply
  • Good glycogen stores
  • Resist fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give features of type IIb glycolytic fibres

A

Lactate accumulation and acidosis can limit contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Give features of muscle fibre differentiation

A
  • Depends heavily on neuronal input
  • Plastic somewhat – can use training to influence distribution of type II fibres
  • Differences in ATPase activity are because the different fibre types have different levels of myosin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Look at the table in notes to find the properties of different fibre types

A

Look at the table in notes to find the properties of different fibre types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Duchenne Muscular Dystrophy

A
  • Duchenne muscular dystrophy is an X-linked disorder caused by a mutation in the dystrophin gene and it affects about 1:3500 male births
  • The mutations cause skeletal muscle fibres to not be linked properly to the extracellular matrix
  • Excess calcium enters the cells and the muscle fibres die and are replaced by fat or connective tissue.
  • Patients with Duchenne experience progressive muscle weakness and have an average life expectancy of 25 to 30 years
  • There is no treatment for Duchenne muscular dystrophy but it may be a candidate in the future for gene therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does a myostatin deficiency do?

A

Myostatin normally regulates muscle growth and animals that have mutations in this proteins often have extra muscle mass and very little body fat

19
Q

How is cardiac muscle similar and different to skeletal muscle?

A
  • both striated
  • basics of sliding filament mechanisms are identical
  • contractile protein subtypes differ
  • control mechanisms are different
  • action potentials are different
  • excitation contracting coupling is different
20
Q

What is a syncytium?

A

Series of fused cells

21
Q

Give features of cardiac muscles

A
  • Branched syncytium
  • Cells incompletely fused
  • Joined by intercalated discs
     Cells drawn together by desmosomes
     We have gap junctions which electrically couple the cell together
  • only found in the heart
22
Q

Give features of cardiac muscle action potentials

A
  • Cardiac muscle can fire action potentials
  • Initial rising phase bought about by the opening of sodium channels
  • Broad Plateau phase due to opening of voltage sensitive calcium channels – these inactivate much more slowly than sodium channels
  • Duration of action potential much longer – 200ms
23
Q

What is the trigger for actin myosin crosslink formation in cardiac excitation contraction coupling?

A

The trigger for actin myosin crosslink formation is an increase in intracellular calcium which largely comes out of the sarcoplasmic reticulum

24
Q

What channels are present in the cardiac muscle membrane?

A

L type calcium channels - they are not physically linked to the ryanodine receptor

25
Q

What is calcium induced calcium release?

A

Calcium that has come through the L type calcium channel triggers the release of calcium from sarcoplasmic reticulum, calcium activates the ryanodine receptor and causes it’s channel to open

26
Q

What are the sources of Ca in Cardiac excitation contraction coupling?

A

 80-90% from SR via CICR

 10-20% Ca current from outside

27
Q

What is the initiation of cardiac contraction?

A
  • Myogenic (originates from the muscle itself)
  • Pacemaker cells in SA node generate pacemaker potential
  • When membrane potential brought to threshold potential the SA node will fire an action potential. After this SA node will return to pacemaker potential
  • Once an action potential has been initiated in the SA node it will spread through the atria to the AV node and then to the ventricles
28
Q

How is cardiac contraction controlled by pacemaker potential?

A
  • Pacemaker potential has a characteristic slope
     The steeper the slope the quicker the cell will get to threshold potential and fire an action potential
  • Sympathetic activation will result in steepening of slope of pacemaker potential increasing heart rate
  • Parasympathetic activation decreases the slope of the pacemaker potential decreasing heart rate
29
Q

How is cardiac contraction controlled by force of contraction?

A
  • Force of contraction determined by
     Degree of stretch of cardiac muscle (Frank-Starling Law of the Heart). The more blood returned to the heart the more the cardiac muscles are stretched when blood returns to the heart. This increases the force of contraction
     Concentration of cytoplasmic Ca2+ - this can be modulated by the autonomic nervous system: sympathetic – increase; parasympathetic – decrease. This helps control force of contraction
30
Q

What is the cardiac muscle energy metabolism?

A
  • Heart needs to beat continuously so can’t use glycolytic ATP production
  • Uses oxidative metabolism
  • Cardiac muscle needs a good blood supply
  • Deprivation of blood (Ox) supply -> angina, heart attack
31
Q

How is smooth muscle histologically distinct from skeletal and cardiac muscle?

A
  • No striations
  • No t-tubules
  • Small, spindle shaped cells
32
Q

How are smooth muscle cells often coupled?

A

Cells often electrically coupled by gap junctions

33
Q

What is it called when smooth muscle cells are coupled and when they are not?

A

Cells often electrically coupled by gap junctions (‘unitary’ – acts as syncytium) but can be independent (‘multiunit’)

34
Q

Where is smooth muscle often found around?

A

• Smooth muscle often found around hollow organs

  • Blood vessels
  • Gut
  • Bladder
  • Uterus
  • Bronchi
35
Q

What is the function of smooth muscle?

A
  • Propel contents (gut, bladder, uterus)

- Regulate flow (blood vessels, bronchi)

36
Q

What is smooth muscle controlled by?

A

autonomic nervous system

37
Q

what is the contraction mechanism of smooth muscle and how is it different to skeletal and cardiac muscle?

A
  • Actin-myosin cross bridges (same as skeletal/cardiac)
  • But:
  • Contracts slowly
  • More energy efficient than skeletal and cardiac
  • Different mechanism of Excitation contraction coupling
  • Contracts well over greater range (important in terms of function e.g. bladder) – actin and myosin is much less ordered
  • troponin is not involved
  • not all smooth muscle requires an action potential to contract
  • the way calcium enters the cytoplasm is different
38
Q

What are the different sources of Calcium in smooth muscle for excitation-contraction coupling?

A
  • L type calcium channels
  • IP3
  • Store operated calcium channels
39
Q

How do smooth muscles source calcium from L type calcium channels?

A
  • Smooth muscle has L-type calcium channels in plasma membrane – depolarisation activates calcium channels and allows entry of calcium
  • Calcium can then trigger calcium-induced-calcium release via ryanodine receptor
40
Q

How do smooth muscles source calcium regarding IP3?

A
  • On the sarcoplasmic reticulum in smooth muscle we have IP3 receptors – ligand gated calcium channel. When IP3 binds to it, it opens and allows calcium to leave the SR
  • IP3 produced by actions of phospholipase C on membrane lipids, it cleaves off phospholipid headgroups
  • Phospholipase C needs to be activated by G protein coupled receptors
  • When an agonist binds to a G protein coupled receptor it will activate phospholipase C, release IP3 and we will get the IP3 receptor activated and calcium will leave the SR
  • M1, M3 and M5 types of muscarinic acetylcholine receptors are G protein coupled receptors that will do this – means that we can get contraction without membrane depolarisation or an action potential
41
Q

How is calcium sourced from store operated calcium channels?

A

When the SR becomes depleted of calcium it sends a signal to store operated calcium channels in the plasma membranes. The consequence is that the store operated calcium channels open and more calcium enters the cytoplasm

42
Q

What is the role of calcium in smooth muscle?

A

In smooth muscle the heavy chain heads have much lower ATPase activity. The role of calcium is to increase the ATPase activity in smooth muscle heavy chain heads

43
Q

How does calcium increase ATPase activity in smooth muscle heavy chain heads and then how is the signalling stopped?

A
  • Calcium binds to Calmodulin protein
  • Calmodulin converts myosin light-chain kinase enzyme from an inactive form to an active form
  • Myosin light-chain kinase then phosphorylates the regulatory light chains on the myosin and this switches on the ATPase activity of the myosin heavy chain heads
  • Then we can get cross bridge formation and we get our muscle contracting
  • To switch this signal off we need to remove calcium and the regulatory light chains need to have their phosphate groups removed
  • Myosin light-chain phosphatase removes phosphate group from regulatory light chain
44
Q

What are the different ways smooth muscle can be excited?

A
  • Can be myogenic – some smooth muscles e.g. gut have pacemaker-like activity
  • Can be initiated by action potentials triggered by neuronal stimulation
  • Can get action potentials superimposed on myogenic activity
  • Can be a graded response to depolarisation (no AP)
  • Can be modulated by neurotransmitters/ hormones

Excitable Cells (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions