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BDS1 > Muscle physiology > Flashcards

Muscle physiology Flashcards

1
Q

3 types of muscle cell

A

cardiac (cardiomyocyte), skeletal, smooth

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2
Q

How can muscle cells be classified?

A

Striated vs smooth or voluntary vs involuntary

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3
Q

Which muscle cells are striated?

A

Skeletal and cardiac

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4
Q

Why are skeletal muscle cells also known as fibres?

A

Due to varying length

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5
Q

Where is smooth muscle found?

A

Blood vessels, tracts, GIT, bladder, lungs

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6
Q

Which muscle cells are classed as involuntary?

A

Cardiac and smooth

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7
Q

Despite being involuntary, how can smooth muscle be indirectly controlled?

A

Exercising can bronchodilation and vasodilation of blood vessels supplying the active skeletal muscles and vasoconstriction of blood vessels supplying the viscera. Or eating a big meal

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8
Q

How can cardiac cells be controlled indirectly?

A

Exercising increases contraction

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9
Q

Function of muscle

A

contract and relax to create movement

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10
Q

Which part of the nervous system controls skeletal muscle?

A

Somatic NS

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11
Q

Which part of the nervous system controls cardiac and smooth muscle?

A

Autonomic NS

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12
Q

How is cardiac muscle contraction controlled?

A

By SAN in right atrium; however, can be altered by nervous input from ANS.

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13
Q

What does an electrochemical gradient refer to?

A

The difference in concentration and difference in charge (usually concentration difference (chemical gradient) has a greater influence than the electrical gradient).

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14
Q

What is the resting membrane potential (Em)?

A

The potential difference between the inside and outside of the cell (inside - outside)

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15
Q

What is the resting membrane potential (Em) in muscle?

A

-90mV

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16
Q

How is the resting membrane potential of muscle -90mV?

A

Na+/K+ ATPase pumps out 3 Na+ and 2 K+ in. Creates a net transfer of + charge out of the cell which makes the inside negative.

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17
Q

Why does Na+/K+ ATPase require ATP?

A

Because it moves Na+ and K+ against their concentration gradients

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18
Q

Name of channels that allow a continual small outflux of K+ and influx of Na+

A

passive leak channels

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19
Q

3 types of gated channels important for AP generation

A

Chemically regulated channels (e.g. ligand-gated at synapse), voltage-gated channels, mechanically regulated channels (e.g. stretch-mediated)

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20
Q

Stages of an AP

A
  1. Graded potential reaches threshold
  2. voltage-gated Na+ channels open causing depolarisation
  3. Once +40mV is reached, voltage-gated Na+ channels close and voltage-gated K+ channels open
  4. K+ ions move out of the cell causing repolarisation
  5. K+ overshoot causes hyperpolarisation
  6. resting membrane potential is restored.
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21
Q

Why is the AP described as being an all-or-nothing event?

A

Once threshold has been reached and voltage-gated Na+ channels open, there is no stopping the AP

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22
Q

How long does the refractory period last?

A

From the time the AP begins until resting potential is restored

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23
Q

What causes the static contraction of skeletal muscle?

A

Constant firing of APs

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24
Q

How do the duration of APs differ between muscle cells?

A

Cardiac muscle cells have a longer AP (200ms) than skeletal muscle cells (5ms) because there is a delay in the opening of voltage-gated K+ channels in cardiac muscle. This leads to longer, less frequent contractions.

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25
Q

Why can Na+/K+ ATPase only move 2 K+ compared to moving 3 Na+?

A

K+ has a steeper concentration gradient between ICF and ECF therefore it is more difficult to move K+ against its concentration gradient.

26
Q

What is an action potential?

A

a rapid change in membrane potential (Em) (caused by the movement of ions against the electrochemical gradient) that is propagated along the length of the cell, followed by a return to the resting Em.

27
Q

Stages of Excitation-Contraction coupling

A
  1. Depolarisation opens L type Ca2+ channel on sarcolemma causing a small Ca2+ influx
  2. Ca2+ entry activates release of more Ca2+ from SR via ryanodine receptors to amplify the amount of Ca2+.
  3. Intracellular Ca2+ concentration increases from 0.1 to 1 uM
  4. Ca2+ triggers myofilament contraction
28
Q

How is Ca2+ removed from the myofilament to allow relaxation?

A

Ca2+ is requestered into SR via SERCA ( SR Ca2+ pump) and is removed from the cell via Na+/Ca2+ exchanger (NCX) and Ca2+-ATPase pump at the sarcolemma.

29
Q

Name of Ca2+ channel on the sarcolemma

A

L type Ca2+ channel (LTCC)

30
Q

In smooth muscle, how can contraction occur without an AP?

A

Agonists can activate receptor-mediated Ca2+ channels on the sarcolemma causing an influx of Ca2+.

31
Q

In skeletal and cardiac muscle, how is Ca2+ released from the SR?

A

Via the ryanodine receptor (RyR2) - type of Ca2+ channel

32
Q

In smooth muscle cells, how is Ca2+ released from the SR?

A

Via ryanodine receptors (RyR2) and also inositol-triphosphate receptors (IP3R) therefore smooth muscle can also rely on agonists not just APs.

33
Q

What are sarcomeres?

A

Short contractile units of myofibrils

34
Q

What are the 3 subunits of troponin?

A

Troponin C (TnC) - Ca2+ binding site
Troponin T (TnT) - Troponin/tropomyosin complex
Troponin I (TnI) - inhibition site that also blocks myosin binding site

35
Q

How do sarcomeres contract? (only cardiac and skeletal muscles - striated)

A

Ca2+ binds to troponin at TnC, changing the shape of TnT which exposes the myosin-binding sites. Myosin heads can now bind to actin and pull to shorten the sarcomere and muscle (contraction).

36
Q

Myosin is a hexamer. What is meant by this?

A

It has 2 heavy chains and 4 light chains

37
Q

How much displacement is created by one sarcomere?

A

5-10nm

38
Q

Which myofilament is a molecular motor?

A

Myosin - generated movement

39
Q

Which muscle determines vascular lumen dimensions?

A

Smooth muscle (always active - more active or more relaxed)

40
Q

How is smooth muscle contraction different to striated muscle?

A

no troponin/ tropomyosin
1. Ca2+ entry via L type Ca2+ channel
2. Ca2+ influx triggers release of Ca2+ from SR via ryanodine AND inositol triphosphate receptors
3. Ca2+ binds to a protein called calmodulin
4. Ca2+-calmodulin complex activates myosin light chain kinase (MLCK)
5. MLCK phosphorylates myosin light chain
6. Phosphorylated myosin head groups bind to actin
7. Crossbridge cycle begins

41
Q

During the sliding filament mechanism, when is ATP required?

A

To relax the muscle. ATP binds to myosin head which breaks the crossbridge. ATP is then hydrolysed to pull back and energise the myosin head.

42
Q

Sequence of sliding filament theory

A
  1. ATP binds to myosin heads, breaking the crossbridge
  2. ATP is hydrolysed (to ADP and Pi) which pulls back and energises the myosin heads.
  3. Myosin heads bind to actin
  4. Pi is released
  5. Powerstroke (actin pulled to M-line)
  6. ADP released
  7. Rigor (muscle contracted, but myosin in low energy form).
43
Q

What happens to muscle if there is a depletion of ATP?

A

the muscle stays contracted (no ATP to break actin-myosin cross bridges)

44
Q

2 scenarios when muscle is depleted of ATP

A
  1. Cramps
  2. Rigor mortis
45
Q

What is the main cause of reduced muscle contractility?

A

Reduced intercellular / sarcoplasmic reticulum Ca2+ due to ryanodine receptor (RyR) abnormality.

46
Q

How can an abnormality in the ryanodine receptor result in reduced muscle contractility?

A

Ca2+ is released from single ryanodine receptors at irregular events (RyR leaks/sparks) which leads to the loss of SR Ca2+ as Ca2+ leaves the cell. Therefore, intracellular Ca2+ cycling is reduced and slowed down. When a muscle is stimulated, less Ca2+ is released from the SR.

47
Q

Effect of abnormal ryanodine receptor (RyR2) in cardiac muscle

A

Heart failure - reduced ability to pump blood

48
Q

Result of RyR2 dysfunction in skeletal muscle

A

muscular dystrophy

49
Q

What mutation can cause ryanodine abnormalities?

A

Mutations in dystrophin-glycoprotein complex

50
Q

2 modes of death in heart failure

A

Pump failure (50%) and sudden cardiac death (50%)

51
Q

What happens when a heart failure patient dies of pump failure?

A

not sudden or unexpected as there is progressive hemodynamic (blood flow) deterioration. This leads to profound bradycardia or asystole as the terminal event.

52
Q

What happens to a heart failure patient during a sudden cardiac death?

A

Abrupt onset of systems. Difficult to determine mode of death.

53
Q

What percentage of the population has heart failure?

A

1-2% (more prevalent in over 75)

54
Q

How can the extent of heart failure be classified?

A

Using NYHA class: class IV is most severe with highest mortality, while class I is least severe with the lowest mortality.

55
Q

Prognosis meaning

A

expected pathway of a disease / chance of improvement / mortality

56
Q

What is the most common type of muscular dystrophy?

A

Duchenne Muscular Dystrophy (usually affects boys in early childhood).

57
Q

Prognosis of Duchenne muscular dystrophy

A

muscle degeneration, loss of skeletal muscle function and therefore movement, paralysis including life support muscles. Leads to death (25 year life expectancy).

58
Q

Example of types of muscular dystrophy

A

Duchenne and Limb-Girdle MD

59
Q

How can muscular dystrophy affect oral health?

A

Reduced function of muscles of mastication leading to more chewing, malocclusion, poor skeletal muscle control can make it difficult to maintain oral hygiene.

60
Q

How can the effects of RyR abnormality be mitigated?

A

Exercising training to improve the uptake of Ca2+ into the SR by SERCA (therapeutically increased SERCA activity)

61
Q

Future possible treatment for RyR abnormality

A

gene therapy (dystrophin-glycoprotein complex mutation, SERCA)

BDS1 (50 decks)

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