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BM213: Introduction to Pharmacology > Block B Lecture 3: Exercise - Physiology and Pharmacology > Flashcards

Block B Lecture 3: Exercise - Physiology and Pharmacology Flashcards

1
Q

How do you calculate flow?

A

Change in pressure / Resistance
(Lecture 3, Slide 4)

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2
Q

What is Po2?

A

The concentration of oxygen
(Lecture 3, Slide 4)

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3
Q

Where does gas exchange occur and what 2 gases are exchanged and what direction?

A

It occurs between the alveoli and the blood (and eventually the tissues), and O2 is put into the blood whereas CO2 is taken out
(Lecture 3, Slide 5)

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4
Q

What are the 5 steps of gas exchange?

A

Ventilation
Diffusion
Bulk flow
Diffusion
End-point
(Lecture 3, Slide 5)

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5
Q

What occurs in the ventilation stage of gas exchange?

A

Bulk flow exchange of air
(4L/min at alveoli)
(Lecture 3, Slide 5)

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6
Q

What occurs in the first diffusion stage of gas exchange?

A

Diffusion of O2 and CO2 occurs at lung capillaries
(Lecture 3, Slide 5)

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7
Q

What drives diffusion in gas exchange?

A

Concentration gradients
(Lecture 3, Slide 5)

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8
Q

What occurs in the bulk flow phase of gas exchange?

A

Transport of O2 and CO2 through circulation
(Lecture 3, Slide 5)

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9
Q

What occurs in the second diffusion stage of gas exchange?

A

Diffusion of O2 and Co2 at tissues
(Lecture 3, Slide 5)

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10
Q

What occurs in the end-point stage of gas exchange?

A

Cells use O2 and produce CO2
(Lecture 3, Slide 5)

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11
Q

How much oxygen does 5L of arterial blood contain?

A

1L
(Lecture 3, Slide 6)

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12
Q

5Ls of arterial blood contains 1L of O2, how much of this is physically dissolved and how much is bound to haemoglobin?

A

15 mil physically dissolved, 985 ml bound to haemoglobin
(Lecture 3, Slide 6)

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13
Q

What curve does haemoglobin make on a oxyhaemoglobin dissociation curve (Conc of oxygen vs haemoglobin O2 saturation)?

A

Sigmoidal
(Lecture 3, Slide 7)

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14
Q

What is the sigmoidal curve that haemoglobin makes on an oxyhaemoglobin dissociation curve (conc of oxygen vs haemoglobin O2 saturation) useful for?

A

Rapid transfer of oxygen into tissue that is using up oxygen
(Lecture 3, Slide 7)

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15
Q

What is the difference in the oxyhaemoglobin dissociation curve of foetal haemoglobin compared to normal?

A

It moves the curve to the left and makes it steeper
(Lecture 3, Slide 8)

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16
Q

What 2 things does lower pH (from increased Co2) and higher temperature do the oxygen haemoglobin curve?

A

it shifts it to the right and makes it less steep
(Lecture 3, Slide 8)

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17
Q

What 3 physiological conditions are present in more metabolically active tissue and what do these result in?

A

Lower PO2
Higher PCo2
Higher temperature
All leading to greater O2 unloading
(Lecture 3, Slide 8)

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18
Q

What happens when breathing in and out?

A

In: Diaphragm and external intercostal muscles contract
Out: abdominal organs press upwards and lung elasticity recoils
(Lecture 3, Slide 9)

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19
Q

What is the role of carotid chemoreceptors?

A

To pick up chemical inputs that stimulate ventilation and to act as excitatory input to medulla inspiratory neurons
(Lecture 3, Slide 10)

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20
Q

What 3 chemical inputs stimulate ventilation?

A

Decreased arterial Po2
Increased production of non-Co2 acids
Increased Arterial PCo2
(Lecture 3, Slide 10)

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21
Q

What effect do α adrenoreceptor agonists have on smooth muscle?

A

They cause vascular smooth muscle contraction
(Lecture 3, Slide 11)

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22
Q

What effect do ß adrenoreceptor agonists have on smooth muscle?

A

Pulmonary smooth muscle relaxation
(Lecture 3, Slide 11)

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23
Q

What is the difference in pulmonary and vascular smooth muscle?

A

Pulmonary smooth muscle is found in walls walls of bronchi and bronchioles in the respiratory system
Vascular smooth muscle is found in the walls of blood vessels throughout the body, including all types of veins and arteries
(Lecture 3, Slide 11)

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24
Q

What does supplementary O2 increase?

A

The driving force for O2 uptake
(Lecture 3, Slide 11)

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25
Q

How do deaths from opioid abuse occur?

A

As they decrease activity of neurons in the medulla that drive breathing
(Lecture 3, Slide 11)

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26
Q

What does carbon monoxide poisoning result in?

A

Haemoglobin binds CO more readily than O2 and also loses co-operativity when it does - resulting in no oxygen reaching tissues
(Lecture 3, Slide 11)

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27
Q

What nerves control the skeletal muscle?

A

Somatic motor nerves
(Lecture 3, Slide 12)

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28
Q

What does an action potential in muscle increase the concetration of and what does this lead to?

A

An increase in calcium (Ca2+) ions , resulting in contraction
(Lecture 3, Slide 12)

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29
Q

What is a skeletal muscle fibre also known as?

A

A muscle cell
(Lecture 3, Slide 12)

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30
Q

How many nuclei and myofibrils exist per skeletal muscle fibre?

A

Multiple nuclei and hundreds of myofibrils
(Lecture 3, Slide 12)

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31
Q

What are myofibrils?

A

Very fine contractile fibres
(Lecture 3, Slide 12)

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32
Q

What are myofibrils made of?

A

Thick (myosin) and thin (actin + troponin) myofilaments
(Lecture 3, Slide 12)

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33
Q

What are 2 organelles contained in skeletal muscle fibres that are specific to these cells?

A

Transverse-tubules
Sarcoplasmic reticulum
(Lecture 3, Slide 14)

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34
Q

What is the role of transverse-tubles?

A

Extend plasmalemma (cell/plasma membrane) deep into the cell
(Lecture 3, Slide 14)

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35
Q

What is the role of the sarcoplasmic reticulum?

A

Ca2+ store
(Lecture 3, Slide 14)

36
Q

What does cholinergic innervation mean?

A

Cholinergic refers to acetylcholine whereas innervation refers to the process of suppling nerves to an organ or part of the body
(Lecture 3, Slide 15)

37
Q

What are neuromuscular junctions?

A

Cholinergic innervation from the brainstem/spinal cord
(Lecture 3, Slide 15)

38
Q

Are neuromuscular junctions excitatory?

A

Yes
(Lecture 3, Slide 15)

39
Q

How do neuromuscular junctions result in an action potential?

A

Acetylcholine released binds to nicotinic acetylcholine receptors causing an Na+ ion influx which creates an end-plate potential which leads to an action potential
(Lecture 3, Slide 15)

40
Q

What is an end-plate potential?

A

A change in the membrane potential of a muscle fibres cell membrane at a neuromuscular junction
(Lecture 3, Slide 15)

41
Q

What does Ca2+ release from the sarcoplasmic reticulum as a result of an action potential propagating into the transverse tubules lead to?

A

Ca2+ binds to troponin resulting in tropomyosin moving, resulting in myosin being able to bind troponin
(Lecture 3, Slide 16)

42
Q

What drives myosin like a “ratchet”?

A

Cycle of ATP binding, hydrolysis and ADP/Pi release
(Lecture 3, Slide 16)

43
Q

What 3 things does ATP hydrolysis drive in skeletal muscle?

A

Cross bridge cycling (through myosin ATPase)
Restoration of plasma-membrane ion gradients (through the sodium potassium pump)
Removal of Ca2+ from the cytosol back into the sarcoplasmic reticulum (through Ca2+-ATPase)
(Lecture 3, Slide 17)

44
Q

Skeletal muscle contraction consumes a lot of ATP, how much can ATP consumption increase during muscle contraction?

A

Upwards of 100x
(Lecture 3, Slide 17)

45
Q

What 3 processes supply the skeletal muscle with ATP?

A

Phosphocreatine (through transfer of a phosphate group to an ADP to form ATP)
Mitochondrial oxidative phosphorylation
Glycolysis
(Lecture 3, Slide 18)

46
Q

What are the 4 types of skeletal muscle fibre?

A

Red oxidative fibres
White glycolytic fibres
Slow-twitch fibres
Fast-twitch fibres
(Lecture 3, Slide 19)

47
Q

What 3 things do red oxidative skeletal muscle fibres contain?

A

Lots of:
Mitochondria
Myoglobin
Small blood vessels
(Lecture 3, Slide 19)

48
Q

What 3 things do white, glycolytic fibres contain?

A

Few mitochondria
Lots of glycolytic enzymes
Large glycogen stores
(Lecture 3, Slide 19)

49
Q

What kind of myosin ATPase do slow-twitch skeletal muscle fibres contain?

A

Slower-acting myosin ATPase
(Lecture 3, Slide 19)

50
Q

What do fast-twitch skeletal muscle fibres contain?

A

Fast-twitch fibres
(Lecture 3, Slide 19)

51
Q

What are the 3 classes of skeletal muscle fibres?

A

Type I
Type IIa
Type IIb
(Lecture 3, Slide 21)

52
Q

What 2 skeletal muscle fibres does the Type I class contain?

A

The red, oxidative fibres and the slow-twitch fibres
(Lecture 3, Slide 21)

53
Q

What skeletal muscle fibre does the Type IIa class contain?

A

The white, glycolytic fibres
(Lecture 3, Slide 21)

54
Q

What skeletal muscle fibre does the Type IIb class contain?

A

The fast-twitch fibres
(Lecture 3, Slide 21)

55
Q

Which skeletal muscle fibre classes are oxidative and glycolytic?

A

Type I is oxidative
Type IIa is both (but main energy source is oxidative)
Type IIb is glycolytic
(Lecture 3, Slide 21)

56
Q

Compare the mitochondria, myoglobin and capillary count of the 3 skeletal muscle fibre classes.

A

Types I and IIa have many of all of these whereas
Type IIb has few of all of these
(Lecture 3, Slide 21)

57
Q

Compare the glycogen level and ability glycolytic enzyme count (ability to undertake glycolysis) of all 3 classes of skeletal muscle fibres.

A

Type I has low glycogen and glycolytic enzymes and therefore a low ability to undertake glycolysis
Type IIa has an intermediate amount of glycogen and glycolytic enzymes and therefore a medium level to undertake glycolysis
Type IIb has high glycogen and glycolytic enzymes and therefore a high ability to undertake glycolysis
(Lecture 3, Slide 21)

58
Q

Compare the speed of myosin ATPase (and therefore rate of ATP use) of all 3 skeletal muscle classes.

A

Type I has slower Myosin ATPase and therefore a slow rate of ATP use
Type IIa has faster Myosin ATPase and therefore a faster (medium) rate of ATP use
Type IIb has even faster Myosin ATPase and therefore a very fast rate of ATP use
(Lecture 3, Slide 21)

59
Q

What are multiple muscle fibres of the same type innervated by?

A

A motor neuron / motor unit
(Lecture 3, Slide 24)

60
Q

Are whole skeletal muscles made up of motor units?

A

Yes, they are made up of many, and they are different types
(Lecture 3, Slide 24)

61
Q

What 3 things do motor neurons do?

A

They generate muscle action potential, calcium rises and they allow myosin-actin cross-bridge cycling to contract muscle
(Lecture 3, Slide 25)

62
Q

What do neuromuscular blocking drugs (NMJs) do and when are they used?

A

They cause paralysis and some are used alongside anaesthetics during surgery
(Lecture 3, Slide 26)

63
Q

What are depolarising NMJ blockers (neuromuscular blocking drugs)?

A

Acetylcholine mimic but with much slower hydrolysis, and they cause sustained contracting leading to paralysis
(Lecture 3, Slide 26)

64
Q

What is an example of a depolarising NMJ blocker?

A

Suxamethonium
(Lecture 3, Slide 26)

65
Q

What are non-polarising NMJ blockers?

A

Competitive inhibitors of nicotinic acetylcholine receptors, work by blocking acetylcholine binding
(Lecture 3, Slide 26)

66
Q

What is an example of a non-depolarising NMJ blocker?

A

Answers include:
Atracurium
Tubocurarine
(Lecture 3, Slide 26)

67
Q

What does botulinum toxin A (botox) do)

A

It inhibits acetylcholine release causing flaccid paralysis, and can be used to cause local muscle paralysis to treat excessive sweating or facial wrinkle formation
(Lecture 3, Slide 26)

68
Q

What does dantrolene do?

A

It inhibits sarcoplasmic reticulum release of Ca2+ ions
(Lecture 3, Slide 26)

69
Q

What 2 things can dantrolene be used to treat?

A

Muscle spasticity or malignant hyperthermia
(Lecture 3, Slide 26)

70
Q

What is malignant hyperthermia?

A

A genetic mutation that can cause sarcoplasmic reticulum Ca2+ ion release when exposed to some anaesthetics or suxamethonium
(Lecture 3, Slide 26)

71
Q

What 3 things does exercise decrease in skeletal muscle?

A

ATP
Phosphocreatine
Oxygen
(Lecture 3, Slide 27)

72
Q

How do the cardiovascular and respiratory systems respond to increased demands of skeletal muscle during exercise?

A

Oxygen is supplied from the lungs to skeletal muscle via increased blood flow
Temperature is regulated by increased peripheral blood flow (to supply the oxygen) and sweating (to cool the body down as increased blood flow increased body temp)
(Lecture 3, Slide 27)

73
Q

What does exercise training do to skeletal muscles?

A

Increase size of muscle fibres and ATP production
(Lecture 3, Slide 28)

74
Q

What does low-intensity exercise training do to skeletal muscles?

A

It increases the amount of mitochondria and capillaries present
(Lecture 3, Slide 28)

75
Q

What does endurance training do to skeletal muscles?

A

It converts fast-glycolytic fibres into fast-oxidative-glycolytic fibres (Type IIb > Type IIa)
(Lecture 3, Slide 28)

76
Q

What 3 things does high-intensity (“Strength training”) do to skeletal muscles?

A

Increase diameter of fast-twitch fibres
Increase expression of glycolytic enzymes
Greater synchronisation of motor unit recruitment
(Lecture 3, Slide 28)

77
Q

Why does exercise training increase cardiac output and increases vasoconstriction in abdominal organs and kidneys?

A

As brain “exercise centres” signal parasympathetic output to the heart decrease whereas sympathetic output to the heart increases
(Lecture 3, Slide 30)

78
Q

Why does local blood flow in the muscle increase due to exercise training?

A

Contracting skeletal muscles lead to local chemical changes leading to more dilated muscle arterioles, leading to an increase in local blood flow
(Lecture 3, Slide 30)

79
Q

How much fold does the total blood flow increase during exercise?

A

3 - 4x
(Lecture 3, Slide 32)

80
Q

How much does heart rate and stroke volume and therefore cardiac output increase during exercise?

A

Heart rate = 1.8x
Stroke Volume = 1.2x
Cardiac output = 1.8*1.2 = 2.2x
(Lecture 3, Slide 33)

81
Q

How much does cardiac output and total peripheral resistance and therefore mean arterial pressure increase during exercise?

A

Cardiac output = 2.2x
Total peripheral resistance = 0.6x
Mean arterial pressure = 2.2*0.6 = 1.2x
(Lecture 3, Slide 33)

82
Q

What is Vo2 max?

A

The maximal amount of O2 a person can consume
(Lecture 3, Slide 35)

83
Q

How do you calculate Vo2 max?

A

(Arterial - venous O2 content) * CO
(Lecture 3, Slide 35)

84
Q

Does mitochondria affect Vo2 max?

A

No
(Lecture 3, Slide 35)

85
Q

What does mitochondria increase by up to 300%?

A

Endurance
(Lecture 3, Slide 35)

BM213: Introduction to Pharmacology (15 decks)

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