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Physiology > MID SEM 1 > Flashcards

MID SEM 1 Flashcards

1
Q

What is the myofibril diameter?

A

1-2 micrometres

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2
Q

Where are nuclei in healthy muscle fibres located?

A

Periphery

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3
Q

What is the role of titin?

A

Provide elasticity and stabilise myosin

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4
Q

What does nebulin do?

A

Stabilise actin

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5
Q

What does calcium do to start the cross bridge cycle?

A

Binds to troponin on actin and allows tropomyosin to be released so that myosin can bind to actin

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6
Q

What direction do fibres insert onto the tendon? Why?

A

Obliquely, increase number of fibres packed in and muscle CSA

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7
Q

What is force directionally proportional to?

A

CSA

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8
Q

What is the length tension relationship?

A

At optimum muscle length, we get maximum force, if a muscle is shortened or lengthened excessively the overlap of thick and thin filaments is changed so there cannot be maximum force

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9
Q

What happens when there is zero load?

A

Maximum velocity

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10
Q

What happens when there is maximum load?

A

Zero velocity (isometric)

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11
Q

What is the equation for power?

A

Power = load x velocity

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12
Q

What is DHP?

A

Receptor on t-tubule that senses voltage different and allows RyR to open and calcium outflow from SR

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13
Q

What is a motor unit?

A

An alpha motor neuron and all of the muscle fibres it innervates

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14
Q

What are the fibre types?

A

Slow: type I, oxidative, fatigue resistant, high mitochondria and calcium, low glycogen
Fast: type IIB, fatigue susceptible, glycolytic, low mitochondria and calcium
Partially Fast: type IIA, partially fatigue resistant, glycolytic and oxidative, high mitochondria and glycogen

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15
Q

What is hennemans size principle?

A

Small, slow motor units will be recruited first and as the task intensity increases the larger, faster motor units will be recruited

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16
Q

What do golgi tendon organs do?

A

Sense forces developed by fibre, located in tendons of muscle in series

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17
Q

What do muscle spindles do?

A

Sense lengths of muscle fibres, located in muscle belly in parallel

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18
Q

What is alpha gamma coactivation?

A

Muscle spindle stretches and sends afferent signal to CNS, CNS sends efferent signal to extrafusal fibres to make them contract, gamma motor neurons signal for ends of intrafusal fibres to contract to maintain the length of the muscle spindle

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19
Q

What type of action is knee jerk?

A

Monosynaptic, involves reciprocal inhibition of hamstrings, flexion of quads

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20
Q

What is a flexion reflex?

A

Polysynaptic reflex pathway causing limbs to be pulled away from stimuli, involves neural inputs to both limbs for balance, pulling away etc.

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21
Q

What are the ATP dependent processes in contracting skeletal muscle?

A

Crossbridge (60%)
Calcium reuptake to SR
Sarcolemmal excitability

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22
Q

How can fats be broken down?

A

Only through oxidation

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23
Q

What does phosphocreatine do?

A

Converts ADP to ATP

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24
Q

What does adenolyte kinase do?

A

Converts 2ADP to AMP & ATP

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25
Q

What is power?

A

The rate of ATP generation

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26
Q

What energy source has the greatest power output? What has the greatest capacity?

A

PCr has greatest power output but lowest capacity. Glucose and FFA have a lower power output but greater capacity

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27
Q

What is athletes hitting a wall?

A

Switching from CHO to FFA for energy. FFA don’t give off as much power so athletes cannot exercise at same level

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28
Q

What energy sources are used at different stages of exercise?

A

PCr used initially - don’t have enough oxygen and metabolic inertia.

As time progresses more FFA used.

As intensity increases more CHO used.

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29
Q

Where are triglycerides stored, what is their benefit?

A

Muscle - high energy content

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30
Q

What is the maximal level of FFA oxidation?

A

60-65% VO2 max

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31
Q

What are the main factors influencing fuel choice?

A

Duration and intensity of exercise

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32
Q

What fuel is used more in hot conditions?

A

CHO

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33
Q

Which gender burns more fat, why?

A

Females, circulating oestrogen

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34
Q

What is the role of CAMKII?

A

Influence SERCA and RyR

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35
Q

When does CAMKII increase?

A

Exercise

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36
Q

What activates AMPK?

A

High AMP, low glycogen

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37
Q

How does AMPK act?

A

Stimulates brain to eat more, stops energy consuming process - maintains brain glucose and restores fuel sources

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38
Q

What is the action of ROS?

A

At low concentrations acts as a signalling molecule for kinases and phosphatase activity, at high concentrations damages the SR

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39
Q

What is the role of IGF-1?

A

Increase mTOR - hypertrophy

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40
Q

When does mTOR increase?

A

After exercise

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41
Q

What is insulin?

A

Anabolic hormone, increases muscle glucose uptake, activates glycogen synthase, inhibits liver glucose production and lipolysis

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42
Q

What is glucagon?

A

Catabolic hormone, stimulates liver glycogenolysis, increases gluconeogenic enzymes, stimulates lipolysis, mobilise glucose

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43
Q

What happens to glucagon and insulin levels during exercise?

A

Insulin decreases, glucagon increases

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44
Q

Why is the insulin response blocked during exercise?

A

Sympathetic activity

45
Q

What does exercise do to insulin sensitivity?

A

Increases it - less insulin needed to lower blood glucose levels - muscles more sensitive to insulin

46
Q

What protein do insulin and exercise pathways converge onto and what does this cause?

A

RAB binding protein modulators - causes GLUT4 to move to the membrane and increase glucose uptake

47
Q

What does training do in regards to glucose uptake?

A

Increase GLUT4 to membrane, increase hexokinase, increase glycogen synthase, oxidative capacity increases, vasodilation/ increased blood flow

48
Q

What does adrenaline do?

A

Increase glycogenolysis, liver glucose output and lipolysis

49
Q

What happens to adrenaline levels during exercise?

A

Increase (increase due to decreased fluid and glucose and increased temp)

50
Q

What do cortisol and growth hormone do?

A

Decrease muscle glucose uptake, increase gluconeogenesis, proteolysis and lipolysis - try to spare glucose for brain

51
Q

When so cortisol and growth hormone levels rise?

A

During exercise

52
Q

What are myokines?

A

Muscle cytokines - have effects on brain, liver and adipose tissue

53
Q

What factors regulate muscle glycogenolysis?

A

Calcium and Pi: activate glycogen phosphorylase

Adrenaline: activates beta receptors and stimulates glycogen breakdown

54
Q

Do trained subjects have higher resting muscle glycogen?

A

Yes - less glycogen breakdown at a given power output, lower adrenaline, better ATP regulation

55
Q

What does hexokinase do?

A

Converts glucose to G6P - most goes to glycolysis during exercise

56
Q

Why is glucose delivery increased during exercise?

A
  • Increased GLUT4 to membrane
  • Increased blood flow
  • Increased hexokinase activity
  • More glycogen in muscle
57
Q

What things increase GLUT4 translocation to the membrane?

A

CAMK, PKC, AMPK

58
Q

What does the liver do as exercise intensity increases?

A

Increase glucose output

59
Q

What does adrenaline do to glucose output?

A

Stimulates glucose output

60
Q

What does PDH do and what happens to levels as intensity increases?

A

Pyruvate dehydrogenase. As intensity increases - more PDH - more CHO breakdown

61
Q

What happens when you exercise below the lactate threshold?

A

Stable lactate level

62
Q

What does the lactate threshold determine?

A

How hard you can work without feeling uncomfortable

63
Q

What happens with increased oxidative capacity?

A

Less lactate produced - more oxidation of pyruvate

64
Q

What happens if LDH enzymes have a greater affinity for lactate?

A

More lactate to pyruvate conversion

65
Q

What does adrenaline do to lactate?

A

More adrenaline - more glycogen breakdown - more lactate

66
Q

What happens to lactate levels after training?

A

Lower

  • Less glycogen breakdown, less lactate
  • Less adrenaline
  • More MCT1 receptors to facilitate lactate uptake
67
Q

What do ATGL, HSL & MGL do?

A

ATGL- tri to diglyceride
HSL- di to mono
MGL- mono to FFA

68
Q

What mediates adipose tissue lipolysis?

A

ATGL, HSL

69
Q

What does adrenaline do to HSL?

A

Increases it - increase lipolysis

70
Q

What is the role of albumin?

A

Transport FFA (hydrophobic) through plasma (hydrophilic)

71
Q

What does caffeine do to fuel choice?

A

More FFA oxidation

72
Q

What does AMPK do to HSL?

A

Inhibits it - inhibiting lipolysis - unusual because usually it wants to increase fuel utilization

73
Q

What do carnitine and CPT do?

A

CPT binds FFA and carnitine so FFA (long chain) can be taken up by the mitochondria

74
Q

What are the transporters for FFA uptake?

A
  • Simple diffusion
  • CD36 and FABP enhance diffusion
  • CD36 and FABP facilitate uptake
  • FA uptake via FATP
  • Long chain FA uptake via FATP
75
Q

What influences the ability to oxidise FA?

A

Number of mitochondria and presence of HAD (involved in first step of FA oxidation)

76
Q

What happens to levels of carnitine as exercise continues?

A

Fall - bind to acetyl coA to stop overwhelming the krebs cycle - acetylcarnitine (high glucose breakdown at high intensity - high acetyl carnititne - low FA oxidation)

77
Q

What happens to mitochondria, CPT and HAD with training?

A

Increase - more FFA oxidation, less FFA stored as adipose tissue

78
Q

Why does FFA oxidation decrease at high intensity exercise?

A
  • Low adipose tissue blood flow, FFA not release
  • Glycolytic flux inhibits CPT
  • Low carnitine
79
Q

What are the RER values for CHO and FAO?

A

CHO - 1

FAO - 0.7

80
Q

What is the alanine glucose cycle?

A

Alanine converted to glucose in liver - transported in blood to muscle - converted to pyruvate then alanine - back to liver through blood

81
Q

What does more CO2 in the breath mean?

A

More oxidation

82
Q

Pyruvate + glutamate?

A

Alpha ketoglutarate + alanine

83
Q

Why is more leucine oxidised than phenylalanine?

A

More in the body

84
Q

When are amino acids used for fuel?

A

Only if beta blockers are in place causing reduced FFA availability and glycogen utilisation

85
Q

How much do proteins contribute to overall energy expenditure?

A

12% at 25% of muscle efficiency

86
Q

What type of exercise has the greatest effect on weight loss?

A

Vigorous intensity and high duration

87
Q

What is the oxygen deficit likely due to?

A

Metabolic inertia: lag in mitochondrial respiration

Lag in oxygen transport

88
Q

What is usually the max intensity of exercise where oxygen uptake stops increasing?

A

250 watts

89
Q

Why does VO2 drift increase?

A

Muscles need more oxygen, recruitment of inefficient type II fibres, less efficient oxidative phosphorylation (more oxygen required for same amount of ATP), increased temp, adrenaline and cateocholamines

90
Q

What is EPOC?

A

Excess post exercise oxygen consumption. Occurs to resyntheise ATP, CP, myoglobin oxygen, elevated HR, VE, Temp, hormones, and switch to ffa metabolism, mitochondrial uncoupling, glycogen resynthesis

91
Q

How does CP resynthesis occur?

A

Rapidly, oxygen dependent, occurs more quickly if muscle oxidative capacity is greater

92
Q

Does lactate increase VO2?

A

No - but oxygen is needed for oxidation of lactate

93
Q

What happens to LDH after training?

A

More LDH with affinity for lactate- more lactate to pyruvate conversion - less lactate build up

94
Q

What enhances lactate removal?

A

Active recovery below lactate threshold

95
Q

What is hyperaemia?

A

Increased muscle blood flow: metabolic vasodilators, conductive vasodilation, functional sympatholysis, muscle pump

96
Q

What happens to the mixed venous oxygen content during exercise?

A

Becomes similar to the muscle oxygen content because the muscles are receiving a lot of the CO

97
Q

What is CV drift?

A

Increase in HR and drop in SV - trying to maintain CO

98
Q

What is the increase in HR due to during exercise?

A

Early - withdrawal of vagus nerve

Late - sympathetic activity

99
Q

What are the cardiac changes to trained people?

A
  • Increased blood volume
  • Increased heart size
  • Increased capillary density and recruitment
100
Q

What happens to ventilation during exercise?

A

Rapid increase when starting exercise, slow adjustment then levelling off - when exercise stops there is a rapid decline and then a slow decline to baseline

101
Q

What is the major driver of ventilation?

A

CO2

102
Q

What is EIAH?

A

Exercise induced arterial hypoxemia - low blood oxygen content due to diffusion limitation, inadequate compensatory ventilation and oxygen dissociation curve shifting to the right (CO2, pH, 2-3 DPG)

103
Q

When does the diaphragm fatigue?

A

During extremely high intensity exercise

104
Q

What do resp muscles do to maintain oxygen supply during exercise?

A

Cause vasoconstriction to skeletal muscles by signalling through chemoreflexes - group IV afferents

105
Q

What is ventilation controlled by?

A

Resp neurons in the hindbrain (medulla)

106
Q

What is exercise hyperpnea?

A

Increased breathing - affected by many factors but NOT OXYGEN

107
Q

What happens to ventilation after training?

A

Less ventilation - less oxygen needed for work

108
Q

What happens to potassium levels after training?

A

More Na/K pumps so less potassium released

Physiology (12 decks)

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