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BDS1 BAMS: Locomotor System > Muscle Physiology 1 + 2 > Flashcards

Muscle Physiology 1 + 2 Flashcards

1
Q

Which types of muscle are striated?

A

Cardiac and skeletal

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2
Q

What are cilia and flagella made of?

A

Microtubules

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3
Q

Which type(s) of muscle is/are voluntary?

A

Skeletal

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4
Q

Which type(s) of muscle is/are non-voluntary?

A

Smooth and cardiac

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5
Q

What is the function of a muscle cell?

A

To contract and relax in order to create movement

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6
Q

Which types of muscle contain sarcomeres?

A

Skeletal and cardiac

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7
Q

How long are sarcomeres?

A

1-2 micrometres

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8
Q

Which muscles contract longitudinally ONLY?

A

Skeletal and heart muscle

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9
Q

Which muscles contract longitudinally and transversely?

A

Smooth muscle

2 axis contraction

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10
Q

What is the electrochemical gradient?

A

Chemical and electrical gradients across the plasma membrane. Created by distribution of ions outside/inside the plasma membrane.

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11
Q

Which is more negative: inside the cell or outside the cell?

A

Inside the cell

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12
Q

What is the concentration of Na+ inside/outside the cell?

A

145mM Na+ outside the cell, 12mM Na+ inside the cell

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13
Q

What is the concentration of K+ inside/outside the cell?

A

160mM K+ inside the cell

3.5mM K+ outside the cell

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14
Q

What is the Na+K+ATPase?

A

Sodium potassium pump - actively pumps Na+ and K against their concentration gradients (3 Na+ out for 2 K+ in, causes net transfer of +ve out of the cell => inside of cell is negative

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15
Q

What is the resting membrane potential in a muscle cell?

A

-90mV

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16
Q

What is the resting membrane potential in a nerve cell?

A

-70mV

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17
Q

What is the action potential?

A

A rapid change in the membrane potential caused by rapid activation of ion channels, and fluxes of ion currents followed by a return to the resting Em

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18
Q

Which process is the basis for neuronal communication and elicits muscle contraction?

A

The action potential

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19
Q

What is membrane potential expressed as?

A

Voltage inside the cytoplasm minus the voltage in the ECF

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20
Q

Which active channel balances the ‘leak’?

A

Na+K+ATPase by moving ions against their electrochemical gradient

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21
Q

What are the 3 types of gated channels?

A
  1. Chemically regulated channels
  2. Voltage-regulated channels
  3. Mechanically-regulated channels
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22
Q

What does the ‘all or none’ principle refer to in generating an action potential?

A

Once the threshold is reached, the neuron will fire an action potential. The response will be the same, independent of the size of stimulus, so long as the threshold is reached.

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23
Q

What is the refractory period of an action potential?

A
  • Refractory period lasts from the time the action potential begins until normal resting potential returns
  • During this period, the neuron cannot elicit another action potential
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24
Q

Which channels are activated by depolarization (When voltage-gated Na+ channels are opened)?

A

Ca+ channels

Calcium flows into the cell

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25
Q

Which cells generate action potentials in the heart?

A

Cells in the SA node

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26
Q

Once an action potential is generated in the SA node, where does it spread to?

A

Through the AV node, bundles of His and Purkinje fibres

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27
Q

Which ion is the main activator of contraction?

A

Calcium (Ca2+)

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28
Q

Describe excitation-coupling in smooth muscle

A
  1. Depolarisation (action potential) and/or agonists in smooth muscle
  2. Activates inward Ca2+ channel current
  3. This activates Ca2+ release from sarcoplasmic reticiulum.
  4. Release is mediated by RyRs and IP3Rs
  5. Intracellular [Ca2+] increases from 0.1 to 1.0 uM
  6. Ca2+ triggers myofilament contraction
  7. Ca2+ sequestered into the SR via the SR Ca+pump (SERCA - an ATPase), and removed from the cell by the plasma membrane Na/Ca exchanger (NCX) and Ca-ATPase
  8. This removes Ca2+ from myofilaments whereby their relax
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29
Q

Which receptors mediate the release of intracellular Ca2+ from the sarcoplasmic reticiulum in smooth muscle excitation-contraction coupling?

A
  • Ryanodine receptors (RyR)

- Inositol triphosphate receptors (IP3R)

30
Q

Which pump mediates the re-uptake of calcium into the sarcoplasmic reticulum?

A

SERCA - an ATPase (Sarco/endoplasmic reticiulum Ca2+ ATPase)

31
Q

Which pumps remove Ca2+ from the cell?

A

Na2+/Ca2+ exchanger (NCX) and Ca2+-ATPase

32
Q

Which type of calcium channel is long lasting (remains open for a long time)?

A

L-type

33
Q

Which type of calcium channel is short lasting (transient)?

A

T-type

34
Q

Which receptors are stimulated causing Ca2+ amplification within the cell?

A

RyRs and IP3Rs

ryanodine receptors and inositol triphosphate receptors

35
Q

What does Ca2+ released from the sarcoplasmic reticulum do?

A

Acts on myofilaments causing them to contract

36
Q

What causes relaxation of myofilaments?

A

Removal of Ca2+ from the myofilaments

37
Q

Which receptor is stimulated in skeletal and heart muscle causing Ca2+ release from the sarcoplasmic reticulum?

A

Ryanodine receptors (RyR)

38
Q

Which receptor is stimulated in smooth muscle but NOT skeletal and heart muscle causing Ca2+ release from the SR?

A

Inositol Triphosphate receptor (IP3R)

39
Q

Describe excitation-contraction coupling in striated muscle (cardiac and skeletal)

A

Action potential occurs, SR Ca2+ channels stimulated. Following Ca2+ release from the sarcoplasmic reticulum via RyRs:

  1. Cytoplasmic Ca2+ binds to troponin C
  2. This induces a conformational change in the troponin/tropomyosin complex that exposes the myosin-binding sites on actin filaments
  3. Myosin heads can then attach to the binding sites on actin, creating contraction -> this shortens the sarcomere and results in muscle shortening
40
Q

Which part of myosin retains the motor function?

A

Myosin head

41
Q

What is the displacement in the myosin power stroke?

A

5-10 nm

42
Q

Describe excitation-contraction coupling in smooth muscle

A
  1. Ca2+ binds to calmodulin
  2. Changes configuration
  3. Ca2+-calmodulin complex activates myosin light chain kinase (MLCK)
  4. MLCK phosphorylates myosin light chain to catalyse cross-bridge activation
  5. Myosin heads bind to actin
  6. Rest of crossbridge cycle is similar to skeletal and cardiac muscle
43
Q

What does MLCK stand for?

A

Myosin light chain kinase

44
Q

Which complex activates myosin light chain kinase (in smooth muscle excitation-contraction coupling)?

A

Ca2+-calmodulin complex

45
Q

Describe excitation-contraction coupling in skeletal and cardiac muscle

A
  1. Calcium concentration in cytoplasm increases (mediated by RyRs in the SR)
  2. Calcium binds to troponin C
  3. Conformational change in troponin/tropomyosin complex
  4. Tropomyosin moves away from myosin binding sites on actin, exposing them
  5. Myosin head bind to binding sites on actin
  6. Crossbridge cycle begins
46
Q

Describe excitation-contraction coupling in smooth muscle

A
  1. Calcium concentration in the cytoplasm increases (mediated by RyR and IP3R in the SR)
  2. Calcium binds to calmodulin
  3. Calcium-calmodulin complex activates MLCK (myosin light chain kinase)
  4. MLCK phosphorylates myosin light chain
  5. Myosin heads bind to actin
  6. Crossbridge cycle begins
47
Q

What is the sarcomere composed of?

A

Actin and myosin filaments

48
Q

Which type of muscle contains sarcomeres?

A

Skeletal and cardiac

49
Q

What is a sarcomere?

A

Contractile unit in striated muslce composed of actin and myosin filaments

50
Q

What effect does hydrolyzing ATP have on muscle?

A

Causing muscle relaxation (myosin head is cocked)

51
Q

How many chains does myosin have?

A

6 (myosin is a hexamer)

4 light chains and 2 heavy chains

52
Q

Why does muscle cramp occur?

A

When the muscle is depleted of ATP: ATP required for muscle relaxation

53
Q

What do RyR abnormalities lead to?

A
  • RyR abnormalities lead to Ca2+ sparks: aberrant Ca2+ release events from single RyR clusters, lead to loss of SR Ca2+
  • Intracellular Ca2+ cycling is reduced and impaired
54
Q

What effect does RyR abnormalities have in the heart?

A

Heart failure

55
Q

What is the MAIN reason for reduced contractility in heart failure?

A

Reduced intracellular Ca2+ amplitude

56
Q

What are the 2 modes of death in heart failure?

A
  1. Pump failure: progressive haemodynamic deterioration lead to profound bradycardia or asystole as the terminal event. These deaths are neither sudden nor unexpected.
  2. Sudden cardiac death: Mode of death difficult to determine. Abrupt onset of symptoms and death within 1 hour.
57
Q

Which study was the biggest epidemiological survey?

A

Framingham survey

58
Q

What is a major risk factor for heart failure?

A

Age: older people are more susceptible to heart failure

59
Q

What are the main causes of heart disease?

A
  • Smoking, high BMI, lack of physical activity, poor diet, high cholesterol, high blood pressure, diabetes
  • Heart disease is mainly a life-style associated disease
60
Q

Describe the effects of RyR abnormalities on skeletal muscle

A
  • Typically due to a genetic mutation rather than lifestyle factors
  • Examples include Duchenne Muscular Dystrophy and Limb-Girdle Muscular Dystrohy
61
Q

What is Duchenne Muscular Dystrophy?

A
  • Recessive X-linked mutation - Prevalence = 1/3,500 boys
  • Prognosis: muscle degeneration, loss of skeletal muscle function, loss of movement, paralysis
  • Life expectancy = ~25 years
  • No cure
62
Q

What is Limb-Girdle Muscular Dystrophy?

A
  • Less severe than Duchenne Muscular dystrophy but typically reduces lifespan as life support muscles eventually affected
  • Limb girdle muscles affected i.e. muscles that attach the limbs to the body
63
Q

Mutations in which protein complex leads to muscular dystrophy?

A

Dystrophin-glycoprotein complex

64
Q

What is a potential therapy currently in development for treating RyR abnormalities?

A
  • Increasing SERCA activity: pumping Ca2+ back into the sarcoplasmic reticulum
  • RyR abnormality is still present but effect is mitigated by therapeutic intervention of SERCA
65
Q

What causes the generation of an action potential?

A

If the depolarising ion (Na+) current of the plasma membrane is large enough (reaches threshold), an action potential will be propagated across the cell

66
Q

Which process activates L-type Ca2+ channels?

A

Action potential

67
Q

What effect does hydrolyzing ATP to ADP + Pi have on myosin heads?

A

Myosin heads are charged by hydrolyzing ATP to ADP and Pi

68
Q

What effect does release of Pi have on myosin heads?

A

Causes power stroke: myosin heads release from myosin binding site on actin to relax

69
Q

Which pumps remove calcium from tropomyosin C/calmodulin?

A
  • SERCA (Ca2+ reuptake into the sarcoplasmic reticulum)
  • NCX
  • PMCA
70
Q

What do muscular dystrophies cause?

A

Progressive muscle weakening and degeneration

BDS1 BAMS: Locomotor System (7 decks)

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