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HL22015 physiology > All of it > Flashcards

All of it Flashcards

1
Q

What was seen in starving populations in eastern europe during WWI?

A

Amenorrhea (lack of menstruation)

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2
Q

When was the first large cross-sectional study examining reproductive health in female athletes?

A

60s

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3
Q

What were the 3 answers given as a result of the 1962 study on reproductive health in female athletes?

A

favourable change, no change, unfavourable change

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4
Q

What was the conclusion of the 1962 study?

A

“We may find menstrual disorders that may be associated with too much sports activities”

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5
Q

What is menarche?

A

The onset of menses

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6
Q

What is menses?

A

Blood being discharged from the uterus at menstruation (period)

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7
Q

What did the results of the 1993 study show regarding age at menarche in athletes vs non athletes?

A

The age at menarche of athletes was generally higher than non athletes

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8
Q

What is secondary amenorrhoea?

A

An interruption to menses after they have already occured

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9
Q

What was observed in the 1978 study regarding secondary amenorrhoea and training mileage?

A

The incidence of secondary amenorrhoea increased with the weekly training mileage done by the participants

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10
Q

What are the three components of the female athlete triad?

A

Disordered eating, Amenorrhea, Osteoporosis

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11
Q

What is osteoporosis?

A

premature bone loss/inadequate bone formation

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12
Q

Conditions of 1985 study regarding female athletes menstruation?

A

28 untrained women
8 wks training
4mls up to 10 mls per day run
3.5 daily moderate intensity sorts
weight maintenance (-1kg) and weight loss (-4kg) groups

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13
Q

What were the results of the 1985 study regarding exercise effect on menstrution?

A

Higher % of menstrual abnormalities compared to control

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14
Q

What happened to the menstrual cycles of the 28 subjects in the 1985 study 6 months after the study?

A

All the participants cycles had returned to normal

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15
Q

What is energy availability?

A

The amount of energy that is left over excluding physical activity

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16
Q

Energy availability formula?

A

Energy availability = energy intake – exercise energy expenditure

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17
Q

Why is energy availability normalised to fat free mass (the weight of fat is removed)?

A

Fat is metabolically inert–> doesn’t use up much energy

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18
Q

What is the energy availability target for physically active women per day?

A

45 kcal·kgFFM-1·d-1

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19
Q

When does luteinizing hormone spike in concentration during the menstrual cycle?

A

ovulation (day 14)

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20
Q

What does luteinizing hormone affect?

A

Progesterone and oestrogen release

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21
Q

Effect of reduced energy availability on LH pulse frequency?

A

Lower energy availability means a reduced LH pulse frequency by 23%

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22
Q

Effect of exercise on LH pulse frequency?

A

Not much

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23
Q

Effect of decreased energy availability on markers of bone breakdown?

A

Increase in markers of bone breakdown

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24
Q

Effect of decreased energy availability on markers of bone formation?

A

Decrease in markers of bone breakdown

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25
Q

Inflammation definition?

A

a defensive process that a living body initiates against local tissue damage

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26
Q

What can cause inflammation?

A

Physical agents, chemical agents, biological agents

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27
Q

What are the stages of inflammation?

A

Onset of inflammation, onset of resolution and resolution

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28
Q

What happens in the onset of inflammation?

A

Identification of damage, production of proinflammatory mediators, vasodilation and recruitment of white blood cells

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29
Q

Cytokines present in early inflammation?

A

TNF-alpa, IL1

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30
Q

Cytokines present in resolution of inflammation?

A

IL-10

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31
Q

What occurs during the onset of resolution of inflammation?

A

down regulation of pro-inflammatory signals, up regulation of anti-inflammatory signals, destruction of infecte tissue, clotting factors

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32
Q

Role of clotting factors?

A

stop clotting

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33
Q

What occurs during the resolution of inflammation?

A

production of anti-inflammatory mediators, apoptosis of immune cells, vascular repair

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34
Q

Five cardinal signs of inflammation?

A

Redness, heat, swelling, pain, loss of function

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35
Q

Outcome of increased blood flow?

A

Redness and heat

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36
Q

Outcome of accumulation of fluid?

A

swelling

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37
Q

Outcome of release of nerve stimulating chemicals?

A

pain

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38
Q

What are the 5 stages of inflammaiton resolution?

A

Removal of dead cells, restoration of vascular integrity, regeneration of tissue, remission of fever and relief of pain

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39
Q

What are biomarkers used to assess inflammation?

A

Acute phase proteins, cytokines

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40
Q

Which proteins increase or decrease in blood acutely in response to inflammation?

A

Acute phase proteins

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41
Q

What is an example of an acute phase protein?

A

CRP (C-reactive protein)

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42
Q

What is the role of CRP?

A

Helps clear dead cells

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43
Q

Where is CRP synthesised?

A

Liver

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44
Q

What are cytokines?

A

Small (hormone like) acute phase proteins released by a variety of different cells

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45
Q

What does IL6 do in regards to CRP?

A

induces its release from the liver

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46
Q

Meaning of pleiotropic?

A

Affects many different cell types in different ways

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47
Q

Autocrine hormone?

A

Acts on the cell it was released from

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48
Q

Paracrine action?

A

Acts on a nearby cell

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49
Q

Endocrine action?

A

Acts on a distant cell

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50
Q

IL8 role?

A

Chemokine–> a chemical that promotes chemotaxis

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51
Q

TNF-alpha role?

A

A pro-inflammatory cytokine that “ramps up” local inflammatory responses

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52
Q

IL1 role?

A

Affects nearly every cell type in the body, in synergy with TNF-alpha

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53
Q

Which cytokines are generally considered inflammatory?

A

IL8, TNF-alpha, IL1

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54
Q

Role of IL1RA?

A

Inhibition of IL1, so anti-inflammatory

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55
Q

Which cells produce IL-10?

A

macrophages, dendritic cells, t and b cells

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56
Q

Which cytokines are released near the beginning of infection?

A

TNF-alpha, IL1, IL8

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57
Q

Which cytokine is released in the middle of an infection?

A

IL6

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58
Q

Which cytokines are released at the end of an infection?

A

IL-1RA, IL-10

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59
Q

What is a bimodal response?

A

An acute spike followed by sustained elevation above baseline

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60
Q

What was observed in regard to IL6 levels and exercise?

A

A spike after exercise, followed by a maintained heightened level after the initial spike

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61
Q

What was initially thought to be the source of IL6? (THIS IS WRONG)

A

immune cells

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62
Q

What is eccentric exercise?

A

Uses target muscles to control a weight as it moves in a downward motion

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63
Q

Why is eccentric exercise used to assess the effect of muscle damage?

A

Eccentric exercise causes a lot of muscle damage in unaccustomed muscle compared to accustomed muscle, so they can be compared

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64
Q

What was observed in the 1999 study regarding IL6 and muscle damage?

A

There was no difference in IL6 released by muscles even when there were differences in the amount of muscle damage, thus muscle damage doesnt affect IL6

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65
Q

What was observed in the 2000 study regarding the absence of muscle damage on IL6?

A

IL6 release increased during exercise in the absence of muscle damage (as the exercise was only concentric)

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66
Q

How did the 2000 study show IL6 is produced as a result of exercise?

A

Did a bike test where one leg was exercising and one wasnt–> exercising leg produced most of the IL6

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67
Q

What was observed regarding the amount of increase in IL6 production over the duration of extended exercise in the 2000 study?

A

Initial increase was modest, later increase was dramatic

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68
Q

What was observed regarding muscle glycogen content and IL6 release at the start of exercise?

A

Lower muscle glycogen content caused a higher increase in IL6 during exercise

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69
Q

What was observed regarding muscle glycogen content and IL6 release at the start of exercise?

A

The muscle glycogen content did not massively affect the amount of IL6 released

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70
Q

What was confirmed regarding muscle glycogen content and IL6 secretion in the 2004 study?

A

Higher IL6 secretion is associated with depleted muscle glycogen content

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71
Q

Which processes does IL6 stimulate?

A

glycolysis and lipolysis

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72
Q

What cytokines does IL6 stimulate the release of?

A

IL-1RA and IL10

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73
Q

What is a myokine?

A

A signalling cell that is released in response to muscle contraction

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74
Q

What is resistance exercise?

A

Any exercise that causes the muscle to contract against an external resistance with the primary aim of improving muscle strength

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75
Q

Three types of resistance exercise?

A

Concentric, eccentric, isometric

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76
Q

How do concentric exercises work?

A

They shorten the muscle

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77
Q

How do eccentric exercises work?

A

They lengthen the muscle

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78
Q

How do isometric exercises work?

A

They generate force without changing the length of the muscle

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79
Q

Issue with definition of resistance exercise?

A

“external resistance” is a relative term

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80
Q

What is strength?

A

Capacity to exert force under a set of biomechanical conditions

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81
Q

What is the short term effect of resistance training?

A

negative

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82
Q

Actual short term effects of resistance training?

A

Fatiguing, damaging

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83
Q

What is supercompensation?

A

An increase in capacity after a recovery from a resistance exercise

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84
Q

What is involution?

A

The returning to original capacity after a supercomposition if nothing is done to maintain it

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85
Q

What makes a muscle stronger?

A

size

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86
Q

What attaches a muscle to a bone?

A

A tendon

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87
Q

Name for a bundle of muscle fibres?

A

Fasiculus

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88
Q

How many myofibrils in a single muscle fibre?

A

roughly 2000

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89
Q

What makes up muscle fasicles?

A

Muscle fibres

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90
Q

How many myonuclei per muscle fibre?

A

200-300

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91
Q

What connects myosin to Z lines?

A

titin

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92
Q

Step 1 of muscle contraction?

A

AP arrives at neuromuscular junction

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93
Q

What happens after AP arrives at neuromuscular junction?

A

ACh is released

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94
Q

What happens as a result of ACh release in muscle?

A

Depolarization as a result of binding to receptors in myocyte membrane

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95
Q

What happens as a result of depolarisation?

A

Ca2+ is released inside the cell from the sarcoplasmic reticulum

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96
Q

What does Ca2+ bind to after being released?

A

Troponin

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97
Q

What happens as a result of Ca2+ binding to tropinin?

A

Troponin changes shape

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98
Q

What happens as a result of troponin changing shape?

A

Tropomyosin is moved from the active site of the actin filament

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99
Q

What happens after tropomyosin has moved from the actin filament’s active site?

A

Myosin attaches to actin, forming a cross bridge at a binding site?

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100
Q

What happens as a result of myosin forming a cross bridge?

A

ATP attached to the myosin head it broken down to release energy for a power stroke of the myosin filament

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101
Q

What happens as a result of a power stroke?

A

Z lines move together

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102
Q

What does it mean if Z lines have moved together?

A

Sarcomere length is reduced–> contracting

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103
Q

What happens after the Z lines have moved closer together?

A

A new ATP molecule binds to the myosin head

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104
Q

What happens as a result of a new ATP binding to the myosin head?

A

The head is released from the actin binding site

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105
Q

What happens if there is still calcium left in the cell once the myosin head has released?

A

It will attach to the next nearest actin filament binding site

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106
Q

What happens if there is no Ca2+ or ATP?

A

The process stops

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107
Q

What is hypertrophy?

A

Net muscle gain

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108
Q

What is atrophy?

A

Net muscle loss

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109
Q

What happens to muscle synthesis when amino acids are ingested?

A

The rate of muscle synthesis increases

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110
Q

What happens to the rate of muscle breakdown when AAs are ingested?

A

decreases

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111
Q

What happens to the rate of muscle synthesis a while after AA ingestion?

A

Decreases

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112
Q

What happens to the rate of muscle breakdown a while after AA ingestion?

A

Increases/ returns to original level

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113
Q

What happens to muscle breakdown if you do exercise a while after eating?

A

It increases higher than it would do if you hadn’t done exercise

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114
Q

What happens to muscle synthesis if you do exercise after eating?

A

It increases a lot

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115
Q

How does muscle synthesis increase after doing exercise?

A

The anabolic response is primed as a result of doing resistance exercise

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116
Q

How long is the anabolic response primed post exercise?

A

24-48 hrs

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117
Q

What happens to hypertrophy after the onset of training?

A

It is delayed

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118
Q

Why is hypertrophy delayed after training?

A

A lot of the muscle protein synthesis is repairing the muscles that were damaged as a result of the training, so it isnt “new” muscle

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119
Q

What happens to muscle synthesis as you train more?

A

There is less muscle damage, so more of the muscle synthesis is going to hypertrophy instead of repair

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120
Q

Why do muscles look larger after training even though they have been damaged?

A

Oedema induced muscle swelling

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121
Q

What is Oedema induced muscle swelling?

A

A swelling in response to the muscles being damaged

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122
Q

What happens as a result of Oedema induced muscle swelling?

A

The muscle size/cross sectional area is artificially increased

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123
Q

Why does hypertrophy slowly plateau as you train more?

A

The “priming effect” loses its potency so less hypertrophy occurs

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124
Q

What did the Damas 2017 study show about trained muscle hypertrophy effect in response to damage compared to non-trained muscle?

A

The initial increase in hypertrophy immediately post training for the trained muscle was the same as the untrained muscle (“priming effect”) however it dropped off over time a lot faster than the untrained muscle did

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125
Q

What is muscle fibre hypertrophy?

A

The muscle cells getting bigger

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126
Q

What is muscle fibre hyperplasia?

A

The amount of cells increasing

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127
Q

What increases post resistance training?

A

Fibre hypertrophy

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128
Q

How does myofiber hypertrophy happen?

A

myofibril splitting

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129
Q

What is a myofibril?

A

An organelle in a muscle cell

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130
Q

Role of myofibril?

A

produce contraction

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131
Q

Why is it a challenge to measure hyperplasia

A

Would have to chop leg in half, count number of cells, do exercise, chop leg in half and count cells again

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132
Q

When does hyperplasia definitely occur?

A

In utero (when foetus is growing)

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133
Q

At what point in utero does myofiber hyperplasia stop?

A

24 weeks (60-70% of mammalian gestation)

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134
Q

Is muscle fibre hyperplasia the cause of muscle hypertrophy?

A

NO

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135
Q

What factor other than muscle size can influence how much force a muscle will produce?

A

Neural factors–> how much of the action potentials are actually getting to the muscle to cause it to contract

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136
Q

What does each motor neuron axon join up with?

A

Muscle fibres

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137
Q

How many muscle fibres per axon?

A

multiple

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138
Q

How many axons per muscle fibre?

A

1

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139
Q

What makes up a motor unit?

A

The spinal cord, the motor neuron axon and the muscle fibres

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140
Q

How is motor unit size measured?

A

Fibres per unit

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141
Q

How many fibres per motor unit are there in the eye?

A

10 bc fine motor control is needed

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142
Q

How many fibres per motor unit are there in the hand?

A

300

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143
Q

How many fibres per motor unit are there in the gastrocnemius?

A

2000

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144
Q

What needs to happen for neuromuscular co-ordinaiton?

A

Agonist muscle must be maximally switched on at the right time, Support from appropriate synergistic ans stabiliser muscles, opposed by minimal antagonist activation

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145
Q

What can be increased regarding the motor unit to generate more force?

A

Motor unit firing frequency

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146
Q

How does resistance exercise affect motor units positively?

A

It allows us to increase firing frequency

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147
Q

Two types of motor units?

A

Type 1 and type 2

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148
Q

Type 1 motor unit?

A

Smaller, easier to switch on, less force

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149
Q

Type 2 motor unit?

A

Larger, harder to switch on, more force

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150
Q

What do type 2 fibres need to happen before they are recruited?

A

Type 1 fibres to be recruited, and a higher threshold of excitation than type 1

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151
Q

Use of type 1 fibres?

A

Lifting something light, clicking a button etc

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152
Q

How does resistance training positively impact the recruitment of motor units?

A

Reduces the electrical excitatory threshold required to switch on the type II motor units

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153
Q

What kind of runners have a higher proportion of type 1 muscle fibres?

A

Distance runners

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154
Q

Does weight load have an effect on muscle growth?

A

Sort of (maybe higher load better) but not 100% sure

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155
Q

What effect does exercise have on anabolic hormomes?

A

It increases the concentration of them

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156
Q

Examples of anabolic hormones?

A

insulin, growth hormone, testosterone

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157
Q

What happens to strength as a result of blocking testosterone?

A

Loss in strength

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158
Q

Why does leg press increase concentration of anabolic hormomes?

A

The muscles surrounding the gonads will spike testosterone and anabolic hormones if exercised

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159
Q

How many lines of defence are there in the immune system?

A

3

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160
Q

What are the components of the first line of defence?

A

Skin and mucous membranes (protective barrier)

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161
Q

What are the components of the second line of defence?

A

Macrophages, neutrophils, dendritic cells, NK cells

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162
Q

What do phagocytic cells do?

A

Eat other cells

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163
Q

What do cytotoxic cells do?

A

Secrete toxins that kill other cells

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164
Q

Which line of defence is specific?

A

The third line

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165
Q

Components of the third line of defence?

A

T cells, B cells (adaptive immune cells)

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166
Q

Which cells are cytotoxic?

A

NK cells and T cells

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167
Q

Which cells secrete antibodies?

A

Plasma cells

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168
Q

Where do immune cells start?

A

Bone marrow

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169
Q

What cell can differentiate into B cells, T cells and NK cells?

A

Common lymphoid progenitor cell

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170
Q

What cell can differentiate into platelets, erythrocytes, granulocytes and dendritic cells?

A

Common myeloid progenitor

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171
Q

What is the precursor cell to common lymphoid and myeloid progenitor cells?

A

Haematopoietic stem cell

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172
Q

What can monocytes differentiate into?

A

Macrophages

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173
Q

Which immune response occurs first in response to a pathogen?

A

Innate immune response

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174
Q

What are the four phases of an infection?

A

Establishment, inductive, effector, memory

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175
Q

How can immune memory capabilities be assessed?

A

T cell or B cell function

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176
Q

How are T cells used to measure memory capabilities?

A

Interferon-gamma production by T cells

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177
Q

How are B cells used to measure memory capabilities?

A

Antibody responses (IgG, IgA response)

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178
Q

How does a hematology blood analyzer work?

A

Each cell passes through a detector that has a light source, light is shone across the cell, the amount of light that passes around the cell to the forward scatter detector indicates the cell size

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179
Q

What tells you the size of a cell in a hematology blood analyze?

A

The amount of light going around the cell into the forward scatter detector

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180
Q

What tells you the granularity of the cell in a hematology blood analyzer?

A

The amount of light reflected off to the side into the side scatter detector

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181
Q

What are the characteristics of lymphocytes in a hematology blood analyzer?

A

Small (low FSC) and few granules (low SSC)

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182
Q

What are the characteristics of monocytes in a hematology blood analyzer?

A

Large with few granules

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183
Q

What are the characteristics of neutrophils in a hematology blood analyzer?

A

Large with many granules

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184
Q

What is done to immune cells before they are put into a hematology blood analyzer?

A

They are fluorescently labelled by attaching an antibody with a fluorescent tag

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185
Q

What are CD antigens?

A

Cluster of differentiation antigens–> antigens that are expressed on different immune cells and are used to identify them

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186
Q

Which CD does T cells express?

A

CD3

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187
Q

Which CD cells do B cells express?

A

CD19

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188
Q

Which CD do NK cells express?

A

CD56

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189
Q

Which CD do Th cells express?

A

CD4

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190
Q

Which CD do cytotoxic T cells express?

A

CD8

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191
Q

What does CD27 tell you?

A

The cells age

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192
Q

What does CD62L tell you?

A

The cells migration ability

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193
Q

What is interferon gamma a marker of?

A

Cytotoxicity

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194
Q

3 components of open window hypothesis?

A

Opportunistic infections follow acute strenuous exercise, changes to salivary IgA in the hrs post exercise, changes to immune cell frequency and functional capacity after acute strenuous exercise

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195
Q

What happens to the concentration of blood lymphocytes during exercise?

A

Increases

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196
Q

What happens to the concentration of salivary IgA during exercise?

A

It increases

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197
Q

What happens to the concentration of blood lymphocytes in the hours after exercise?

A

Drops significantly, below level before exercise

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198
Q

What happens to the concentration of salivary IgA in the hours after exercise?

A

Drops significantly, below level before exercise

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199
Q

1990 LA marathon study condition?

A

Compared runners who didn’t run LA marathon to those who did

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200
Q

Results of LA marathon study?

A

More runners (12.9%) became sick in the week after the race than those who didn’t run (2.2%)

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201
Q

What was the odds ratio of becoming sick after running a marathon compared to not running a marathon?

A

5.9*

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202
Q

Issues with LA marathon study?

A

The runners were at a mass participation event while the controls were not and this would have increased the likelyhood of getting an infection regardless of if they did exercise

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203
Q

How was the south africa run study better than the LA one?

A

The controls in the SA one lived with the runners, so the mass participation event aspect was nulified

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204
Q

What were the results of the SA study?

A

33.3% of runners got URTI symptoms compared to 15.3% of controls

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205
Q

What was observed regarding the majority of URTI symptoms in athletes?

A

Most of them are not of infectious origin (11/37 reported had a positive diagnosis)

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206
Q

What was observed regarding URTI symptoms and race time in the SA study?

A

People who ran a faster race were more likely to get URTI symptoms

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207
Q

What did the Mecca study observe?

A

The longer someone stayed there, the higher risk of URTI they had (URTI was not associated with age, sex, education or smoking)

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208
Q

What does the J shaped curve describe?

A

Those who undertake an excessive volume of exercises are at a greater risk of infection to those who are sedentary or moderate exercise. Those who are sedentary have a higher risk of infection than those who do a moderate amount of exercise

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209
Q

What did the Swedish study observe regarding the J shaped curve?

A

People who do higher amounts of physical activity have lower risk of infection compared to people doing medium or none–> contradicts J shaped curve

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210
Q

What was the makeup of the study done on mice to see the effect of exercise on immune response?

A

Mice were infected with influenza and the split into 3 groups: sedentary, moderate (20-30 mins) and prolonged (2.5 hrs)

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211
Q

What else could have caused the high intensity mice to die more?

A

The stress of having to do so much exercise

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212
Q

What was observed regarding morbidity in the infected mice that did different amounts of exercise?

A

The mice that had a prolonged bout of exercise had higher morbidity scores

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213
Q

What were the three groups of monkeys that had polio?

A

Forced swimming, kept in a cage, kept in water in a straitjacket

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214
Q

What is poliomyeltis?

A

An acute infection caused by poliovirus.

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215
Q

What was observed in the mice regarding survival?

A

30 mins per day exercise had 90% survival, sedentary control had ab 50% and prolonged exercise had ab 30%

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216
Q

Issues with the animal studies looking at effect of exercise on immune response?

A

They cant control for the stress response and other factors that arise in the animals as a result of the studies

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217
Q

Why is salivary IgA used to observe the effect of exercise on immune function?

A

obtaining it is non invasive

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218
Q

Why is IgA specifically looked at in saliva

A

It is the most abundant immunoglobulin in the body

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219
Q

Issues with the animal studies looking at effect of exercise on immune response?

A

They cant control for the stress response and other factors that arise in the animals as a result of the studies

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220
Q

Why is salivary IgA used to observe the effect of exercise on immune function?

A

It is non invasive

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221
Q

What was discovered regarding the Tomasi skiers IgA study?

A

Salivary IgA was reduced by 20% in cross country skiers after 2-3hrs of exercise

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222
Q

What was the conclusion of the skiing study?

A

A temporary antibody deficiency in saliva might lead to an increase in susceptibility to viral and bacterial infections following strenuous exercise

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223
Q

What was seen immediately post race in salivary IgA in the SA marathon study?

A

A sharp decrease in salivary IgA

224
Q

Was there a correlation between URTI symptoms and salivary IgA conc?

225
Q

What do most studies say about the effect of exercise on salivary IgA?

A

Exercise doesnt cause a decrease in IgA secretion

226
Q

What happens to the levels of salivary IgA levels in the absence of exercise?

A

It is very variable

227
Q

What are some factors that affect salivary IgA?

A

Diet, psychological stress, oral disease, menstrual cycle, medications, oral hygiene

228
Q

What is the blood immune response during exercise?

A

Increased levels of blood lymphocytes

229
Q

What is the blood immune response after exercise?

A

Decreased levels of blood lymphocytes (to lower levels than b4 exercise)

230
Q

Biphasic response of blood lymphocytes during and after exercise?

A

Increases during, sharply decreases after

231
Q

Which immune cell increases the most during exercise?

232
Q

Which immune cell increases by the lowest amount during exercise?

A

CD4+ T cells

233
Q

Which type of immune cells increase the most during exercise?

A

cells with the greatest cytotoxic potential

234
Q

What happens to immune cells a few hours post exercise?

A

They gradually increase again back to normal levels

235
Q

Which organs had an increase in immune cells migrating to it in exercised mice?

A

Lungs, peyers patches (gut) and bone marrow

236
Q

What are some non-infectious reasons that someone may have URTI symptoms?

A

Asthma, airway epithelial trauma due to increased ventilation or exposure to cold air, allergy

237
Q

What are some viral related causes that might not be to do with catching the virus while exercising?

A

It is possible that viruses can be reactivated in someone’s body–> epstein barr virus, herpes

238
Q

What did Pedersen et al show regarding the effect of exercise on tumors?

A

Exercise can lead to tumor suppression in rodents

239
Q

What were the conditions of the running wheel experiment done by Pedersen et al?

A

Two groups of mice, one had access to a running wheel, one didn’t. Both were administered tumor cells

240
Q

Tumor size results of running wheel experiment done by Pedersen?

A

Group without access to a wheel had larger tumors (statistically significant) than the group that did have a wheel

241
Q

Immune cell results of wheel experiment done by Pedersen et al?

A

More CD3, CD8, CD4 and NK cells in group that had wheel access

242
Q

How was the effect of stress controlled for in the wheel study?

A

Propranolol was administered

243
Q

Effect of propanolol?

A

Beta blocker so blocked the effect of stress hormones

244
Q

What happened to the tumor size of the exercised mice once the effect of adrenaline was blocked?

A

It increased to the same size as non-exercised animals

245
Q

How does physical activity reduce risk of cancer?

A

Every time someone exercises immune cells are mobilised into the blood where they can go to tissues where they are needed, such as tumors

246
Q

How can in vivo immune responses be assessed in humans?

A

Via vaccination

247
Q

Conditions of Eskola study in 1978?

A

4 athletes ran a marathon distance and were immediately given tetanus vaccine. Blood was taken 15 days later to assess immune response

248
Q

Results of Eskolas marathon study?

A

Showed that running for 2.5 hrs doesnt suppress antibody responses, might actually enhance responses

249
Q

Groups in Kate Edwards study?

A

Exercise group exercised their upper arm eccentrically (to increase heart rate and damage and inflame tissues where the muscle would be administered) and control group who did nothing. Half of each group receive the full dose while the other half received a half dose (creating 4 groups)

250
Q

Why were half doses of the vaccine given to participants in Edwards study?

A

To mimic what happens in older age–> older people don’t respond as well to vaccination

251
Q

Effects of exercise on full dose vaccine?

A

No benefits of exercise were observed for the full dose vaccine

252
Q

Effects of exercise on half dose vaccine?

A

Generally the exercise group responds better than the control group to the vaccine

253
Q

Why may exercise improve half dose vaccine response?

A

Increase in heart rate and thus blood flow to tissues

254
Q

Why would an increase in blood flow to tissues improve vaccine response?

A

better identification of antigens in vaccine, and increase in immune cell release into blood which would go to inflammation sites (i.e. where the vaccine is administered)

255
Q

How can inflammation increase vaccine response?

A

Inflammation attracts immune cells via the secretion of cytokines

256
Q

Which group could benefit from exercising before vaccination?

A

Older individuals

257
Q

What was the effect of a single bout of exercise in antibody responses in older adults?

A

No significant effect

258
Q

What is aging of the immune system known as?

A

Immunosenescence

259
Q

Where do T cells mature?

A

The thymus

260
Q

What are three components of the thymus?

A

Cortex, medulla, fat

261
Q

In which parts of the thymus do early T cells mature?

A

Cortex and medulla

262
Q

What happens to the size of the cortex and medulla of the thymus as you age from 18 ish?

A

They reduce

263
Q

What happens to the amount of fat in your thymus as you age?

A

It increases relatively and absolutely

264
Q

Where do stem cell progenitors arise from?

A

Bone marrow

265
Q

In what form do t cells enter the thymus?

A

Thymocytes or T cell precursors

266
Q

In what form do t cells leave the thymus?

A

Naive t cells

267
Q

Involution definition?

268
Q

What happens to the amount of naive t cells as you age?

269
Q

What happens to the amount of different memory t cells as you age?

A

Decreases (limited antigenic targets as you age)

270
Q

Which homing markers do naive t cells express?

A

CD62L, CCR7

271
Q

Which homing markers do senescent t cells not express?

A

CD62L, CCR7

272
Q

What are senescent t cells?

A

Older t cells

273
Q

Which differentiation markers do senescent t cells express?

A

CD57, KLRG1

274
Q

Which differentiation markers do naive t cells express?

A

CD27, CD28

275
Q

What was observed about the level of maintenance of naive CD8 t cells when aging in different fitness levels?

A

If VO2 max was higher, the maintenance of naive CD8 t cells in aging was better

276
Q

What generally happens to the amount of effector CD8 t cells as you age?

A

It increases

277
Q

What was seen regarding exercise effect on CD4 t cell count in older age?

A

More active people had more CD4 t cells when they are older

278
Q

Effect of exercise on amount of senescent t cells as you age?

A

More exercise generally leads to less of an accumulation of senescent t cells

279
Q

What effect did lifelong exercise have on the levels of IL6?

A

More exercise was correlated with lower levels of IL6

280
Q

What can IL7 do regarding muscle hypertrophy?

A

Promote it

281
Q

Effect of IL7 on immune cells?

A

naive t cells (CD4 and CD8) increase

282
Q

Effect of resistance exercise on IL7?

A

Increases it

283
Q

One possible mechanism behind exercise effect on senescent t cells?

A

Naive and senescent t cells in blood at rest, they are mobilized into the blood in response to exercise. Hours post exercise, the senescent cells are sent to the bone marrow where they receive pro apoptosis signals. This death creates space for new naive t cells to be produced

285
Q

How can energy balance be altered?

A

Changing energy intake or expenditure

286
Q

Positive energy balance?

A

More in than out

287
Q

Negative energy balance?

A

More out than in

288
Q

How to increase energy balance?

A

Increase intake/decrease expenditure

289
Q

How to decrease energy balance?

A

Decrease intake/increase expenditure

290
Q

What components of energy intake are there?

A

Carbs, fat, protein, alcohol

291
Q

Components of energy expenditure?

A

Resting metabolic rate (RMR), dietary induced thermogenesis (DIT), Physical activity energy expenditure (PAEE)

292
Q

What is RMR?

A

Resting metabolic rate–> the energy needed to keep us alive

293
Q

What is DIT?

A

Energy used to digest, absorb and metabolise the food we have eaten

294
Q

What is PAEE?

A

Energy used by muscles when they produce force

295
Q

Two main energy stores?

A

Carbs and fat

296
Q

Which energy store can store more energy (fat or carbs)?

297
Q

Where can fat be stored?

A

Blood, muscle and adipose tissue

298
Q

Where is the largest method of storing fat?

A

Adipose tissue

299
Q

How much fat (in kcal) can be stored?

300
Q

Where can carbohydrates be stored?

A

Blood, muscle, liver

301
Q

Where is the largest carbohydrate store?

302
Q

In what form is the largest carbohydrate store kept?

303
Q

What is the relationship between endurance training status and amount of muscle glycogen that someone can store?

A

More endurance trained means ability to store more muscle glycogen

304
Q

How much carbs can the body store?

305
Q

What is denovolipogenesis?

A

Conversion of non-fat sources to fat

306
Q

What happens if you have more than 3200kcal of carbs?

A

Denovolipogenesis

307
Q

What is leptin?

308
Q

Role of leptin?

A

Regulates appetite

309
Q

What is the result of someone with leptin deficiency?

A

They gain a lot of non-lean body mass

310
Q

What kind of tissue releases leptin?

A

Fat tissue

311
Q

What happens to leptin secretion as a result of an increase in fat?

A

The fat tissue releases more leptin

312
Q

Cause of leptin deficiency?

A

Mutation in gene sequence coding for the leptin protein

313
Q

Main issue with measuring energy intake?

A

Observation effect–> when you know someone is observing you you modify your behaviour,
reporting bias–>sometimes people underreport what they consume,
participant recall–> people forget what theyve eaten

314
Q

Which kind of sports have the highest energy intake?

A

Endurance (cross country skiing, triathlon) and large muscle mass (rugby, bodybuilding)

315
Q

What is the energy density of protein?

316
Q

What is the energy density of fat?

317
Q

What is the energy density of carbohydrates?

318
Q

What is the energy density of ethanol?

319
Q

Difference in energy balance in high or low fat diet?

A

High fat diet leads to more fat balance (high +ve) than low fat diet (-ve) , difference is >400g

320
Q

What is the difference in calories consumed between high and low fat diets (mass of food consumed is same)?

A

High fat diets have a higher energy intake than low fat diets as fats are more energy dense than carbs

321
Q

What is most of the difference in energy balance between high and low fat diets caused by?

A

Energy density

322
Q

Which macronutrient is the most satiating?

323
Q

What is a preload drink?

A

A drink drunk before a large intake of energy (a meal)

324
Q

What happens to energy intake of a meal as the protein content of the preload drunk before increases?

A

It decreases

325
Q

What is measured in direct calorimetry?

A

The heat produced by someone

326
Q

Issues with a direct calorimetry machine?

A

Need to be quite small (people cant move), very expensive

327
Q

What does indirect calorimetry measure?

A

Oxygen consumption and carbon dioxide production

328
Q

Ways to measure energy expenditure in free living conditionds?

A

Self report questionnaire, doubly labelled water, pedometers, accelerometers, accelerometry and heart rate combined (aciheart)

329
Q

Benefits of self report energy expenditure?

A

Easy to administer to a large group, low cost

330
Q

Issues of self report energy expenditure?

A

Reporting bias–> underreport intake and overreport exercise

331
Q

Benefits of doubly labelled water?

A

Precise and accurate

332
Q

Issues with doubly labelled water?

A

Expensive and technically challenging-> cannot be used on a large group

333
Q

What does the AciHeart measure?

A

Accelerometry and heart rate

334
Q

How does doubly labelled water work?

A

Ingest a dose of water with heavier H and O isotopes. O loss is steeper when measured as it is lost in CO2 and H20 whereas H is only lost in H2O. Difference between the two is the average CO2 produced over that time period

335
Q

Strengths of DLW?

A

Doesnt need to rely on accurate patient reporting

336
Q

Limitations of DLW?

A

Ratio of CO2 production to O2 consumption varied depending on diet of person, so O2 consumption isnt an exact measure it is inferred

337
Q

Issue with using DLW at high exercise intensities?

A

High exercise intensity results in acidosis (H+ production) which is buffered by bicarbonate system–> produces CO2 from non-metabolic processes

338
Q

Fuel source issue w/ DLW?

A

Can be oxidising things like lactate, ketone bodies, protein as well as Carbs and Fat

339
Q

Tissue specific measurement of substrate metabolism method?

A

Tracer based–> infuse a labeled form of glucose into a vein, ingest another form of carb–> measure exogenous carb oxidation

340
Q

What can be measured from tissue specific measurement of substrate metabolism?

A

Exogenous carb production

341
Q

Link between exercise intensity and fuel consumption?

A

At higher intensity exercises, carbohydrate fuels are used more than fats

342
Q

Effect of duration of exercise on fuel consumption?

A

Decrease in carb use and an increase in fat use

343
Q

Which metabolic fuels are blood based?

A

Plasma glucose, circulating FFA

344
Q

Contribution of muscle based fuels as exercise duration increases?

345
Q

Why does the contribution of muscle based fuels decrease as exercise duration increases?

A

Muscle fuels are depleted over the course of exercise so the longer it goes on the less readily available they are

346
Q

What effect on fuel use does ingesting Cho have?

A

Decrease fat oxidation and increase carb oxidation

347
Q

Which sex has the greater capacity for fat oxidation?

348
Q

Effect of VO2max on muscle glycogen storage?

A

Increases it

349
Q

Effect of a high carb diet on glycogen storage capacity?

A

Increases it

350
Q

What effect does a higher glycogen conc pre exercise have on glycogenolysis?

A

More glycogen at start of exercise = more glycogen is used

351
Q

What must be done to the triacyl glycerides in fat before they can be used as a fuel by muscle?

A

Hydrolysed

352
Q

Product of hydrolysis of triacylglycerides?

A

Glycerol and FAs

353
Q

Which transport protein allows FAs to get into muscle mitochondria?

354
Q

Which enzyme hydrolyses VLDLs and chylomicrons?

A

Lipoprotein lipase (LPL)

355
Q

What could limit NEFA availability?

A

Adipose tissue blood flow

356
Q

Transarcolemal meaning?

A

Transport across the muscle membrane

357
Q

What limits fat oxidation at high exercise intensities?

A

Transport into mitochondria

358
Q

What is fatigue?

A

The inability to maintain power output or force during repeated muscle contractions

359
Q

Which test could be done to assess exercise performance?

A

VO2max or VO2peak

360
Q

Which test could be done to assess exercise capacity?

A

Time to exhaustion

361
Q

What are the three exercise intensity domains?

A

Moderate, heavy, severe

362
Q

What level of exertion is moderate?

A

Anything below lactate threshold/gaseous exchange threshold

363
Q

When is lactate threshold reached?

A

When the production of lactate is occuring at a faster rate to the removal rate

364
Q

What intensity of exercise is heavy?

A

Between lactate threshold and critical power/critical speed

365
Q

What intensity exercise is severe?

A

Anything above critical power/critical speed

366
Q

How is critical power tested?

A

VO2max test, record highest power output (wattage) from that. Then have them do several time to exhaustion tests with the resistance of the bike being different %s (500, 100, 50 etc) of their VO2max test. Measure the time they can go until exhausiton against these different %s. Can plot a curve which will flatten (after going down). Flattened curve is intensity that the person can maintain for a long period of time

367
Q

What are the likely fatigue mechanisms for moderate exercise?

A

Hyperthermia, mental fatigue and muscle damage

368
Q

What are the likely fatigue mechanisms for heavy exercise?

A

Glycogen depletion and hyperthermia

369
Q

What are the likely fatigue mechanisms for severe exercise?

A

Depletion of finite energy stores (W’)

370
Q

Which three elements dictate performance velocity or power?

A

Performance VO2, Performance O2 deficit, Gross mechanical efficiency

371
Q

What can limit performance VO2?

A

Lactate threshold, capillary density

372
Q

What can limit lactate threshold directly?

A

Maximal oxygen consumption, aerobic enzyme activity, distribution of power output

373
Q

What can limit maximal oxygen consumption directly?

A

Muscle capillary density, stroke volume, max heart rate, hemoglobin content

374
Q

What directly influences performance O2 deficit?

A

Total buffering capacity and distribution of power output

375
Q

What is total buffering capacity?

A

How good our muscles are at buffering acidosis

376
Q

What is acidosis?

A

Acid build up in the muscles as a result of exercise

377
Q

What can affect performance O2 deficit and performance VO2?

A

Distribution of power output

378
Q

How can total buffering capacity be changed?

A

Training status and nutrition

379
Q

Which compound can improve total buffering capacity during exercise?

A

Sodium bicarbonate, NaHCO3

380
Q

Why can taking sodium bicarbonate help with high intensity exercise?

A

It can help with buffering of acidosis

381
Q

What can influence gross mechanical efficiency?

A

% slow twitch (type I) muscle fibres, anthropometry and elasticity

382
Q

Which type of muscle fibre is more efficient?

A

Slow twitch (type I)

383
Q

If two athletes were the same height but one had longer legs, which one would be more efficient?

A

One with longer legs

384
Q

Is it better to have stiffer or more relaxed tendons?

A

Stiffer as energy can be transferred more efficiently

385
Q

Which type of athlete has the highest VO2max?

386
Q

What sports do “endurance athletes do?

A

Cross country skiing, running

387
Q

Why do cross country skiers have a higher VO2 max than marathon runners?

A

They use both their arms and their legs

388
Q

Highest every VO2max?

A

93-95mL/kg/min

389
Q

Which type of marathon does VO2max correlate best with?

A

It correlated with normal marathon better than ultra marathon

390
Q

Why does VO2max correlate better with a normal marathon than an ultramarathon?

A

Ultramarathons have a slower pace and so are less reliant on VO2 for performance

391
Q

How does VO2max correlate with health?

A

It declines as you get older

392
Q

What age related issues can VO2max be used to predict?

A

Mortality and post surgery outcomes

393
Q

What is the Fick equation?

A

VO2 = Q (a-v O2diff)
Q is cardiac output
a-v O2diff is the muscle O2 extraction

394
Q

How is cardiac output measured?

A

Stroke volume * heart rate

395
Q

What is a-v O2diff in the fick equation?

A

The amount of oxygen in the artery going to the muscle minus the amount of oxygen in the vein leaving the muscle–> bigger means muscle is extracting more O2 from the blood

396
Q

In what ways can the a-v O2diff be limited?

A

Either a limitation in the limitation in the delivery of the oxygen to the muscle, or a limitation in the muscle itself and its ability to extract oxygen

397
Q

How is muscle VO2 measured?

A

Catheters are inserted into different blood vessels in the body.

398
Q

What are the main key steps in O2 transport?

A

Lungs, respiratory muscles, heart, muscle, mitochondria

400
Q

Arguments against lungs being a limiting factor in VO2max?

A

Alveolar area is v large, ventilation increases more than oxygen uptake, pp of oxygen in alveoli and arteries is maintained at VO2max

401
Q

Arguments in favour of lungs being a limiting factor in VO2max?

A

At normoxia, the oxygen saturation of haemoglobin declines as the intensity of exercise does, hypoventilation, mechanical constraints

402
Q

What is hyperoxia?

A

Atmospheric oxygen partial pressure is higher than usual

403
Q

What is normoxia?

A

Atmospheric oxygen partial pressure is the same as usual

404
Q

What is hypoxia?

A

Atmospheric oxygen partial pressure is lower than usual

405
Q

What is hypoventilation?

A

breathing that is too shallow

406
Q

How can hypoventilation be a limitation of VO2max?

A

Someone may have the capacity for a certain oxygen uptake but arent sensitive enough to the stimuli (exercise) to increase the ventilation rate

407
Q

What are the axis of a flow volume loop?

A

Flow rate in L/s on Y axis, volume in L on the x axis

408
Q

How to create a flow volume loop?

A

Maximal inspiration then forcefully expire all air in lungs as quickly and as hard as possible

409
Q

How can we test whether lung function is a limiting factor of VO2?

A

Changing density of inspired air

410
Q

What was observed as a result of changing the density of inspired air to see whether?

A

Less dense air overcomes the limitation of lungs reaching expiring capacity

411
Q

What is pulmonary oedema?

A

Swelling in the lungs

412
Q

How does pulmonary oedema negatively affect gas exchange in the lungs?

A

The swelling causes the interstitial space between the alveoli and capillary to increase thus gas exchange takes longer

413
Q

How can alveolar capillary diffusion limit VO2max?

A

Only one RBC can pass through a capillary at a time. In untrained this is 0.4-0.5s whereas in trained it is <0.4. Longer means more time to take oxygen to blood so lower VO2max

414
Q

Are lungs a limiting VO2max factor in untrained individuals?

A

Not a huge amount of evidence to support it

415
Q

Are lungs a limiting VO2max factor in trained individuals?

A

Some evidence that this may be true

416
Q

What is hyperpnea?

A

Increased ventilation

417
Q

What is the cost of exercise hyperpnea?

A

Respiratory muscles have a power output of around 50 watts

418
Q

WHat is unique about respiratory muscles?

A

They can produce a lot of force relative to their size

419
Q

What is proportional assisted ventlation?

A

Participant begins inhaling–> rest of air is forced into lungs via machine

420
Q

What is RPE?

A

Rating of perceived exertion

421
Q

What happens to leg RPE in unloaded (proportional assisted ventilation) condition?

A

It is a lot lower than load or control

422
Q

How to load inhalation?

A

Have the participant lift a small weight when they breathe in–> lungs and respiratory muscles have to work harder

423
Q

What is an MIP?

A

Maximum inspiratory mouth pressure test

424
Q

What does a MIP do?

A

Measures the pressure someone can generate at their mouth when they breathe in

425
Q

What happens to MIP following exercise?

A

It decreases

426
Q

Issue with doing an MIP after endurance exercise?

A

Athletes may be tired and so might not inspire as hard as they can

427
Q

What is a volitional measure?

A

Relating to someones will

428
Q

How is the diaphragm isolated when measuring its exertion?

A

Using a nasoesophageal catheter

429
Q

How does a nasoesophageal catheter work work?

A

It goes up the nose, down the throat and into the stomach where there is two pressure transducers, one in the stomach and one in the oesophagus. WHen diaphragm contracts it moves down which increases stomach pressure and decreases esophageal pressure

430
Q

What is the respiratory metaboreflex?

A

When respiratory muscles become fatigued, it sends a signal that changes blood flow to other muscles

431
Q

What is observed regarding leg blood flow when work of breathing is increased?

A

It decreases

432
Q

When using a nasoesophageal catheter, where are the pressure transducers?

A

Stomach and oesophagus

433
Q

What is observed regarding leg VO2 when work of breathing is increased?

A

It decreases

434
Q

How efficient is muscle O2 extraction?

435
Q

Why is muscle oxygen extraction unlikely to limit VO2max?

A

At high intensity exercise the difference in oxygen conc between the artery entering the muscle and the vein leaving the muscle is high meaning it is very efficient

436
Q

What explains most of the variance in VO2max between people?

A

Cardiac output

437
Q

What explains the early increase in VO2max with exercise training?

A

Plasma volume

438
Q

What is observed in the blood in the first week after beginning training?

A

Rapid increase in plasma volume

439
Q

How to artificially increase plasma volume?

A

Dextran infusion

440
Q

What is observed in the VO2max of people who have had their blood plasma volume artificially increased as a result of a dextran infusion?

A

An increase of ~4%

441
Q

How does dehydration affect performance?

A

It leads to a lower plasma volume which leads to lower blood flow and stroke volume

442
Q

In most people, what is the correlation between VO2max and performance time in a a marathon?

443
Q

In elite athletes, what is the correlation between VO2max and performance?

A

Not as strong as in the general population

444
Q

Why may the VO2max of elite athletes not perfectly correlate to performance?

A

other factors such as mechanical efficiency, running economy etc

445
Q

Which test could be better than VO2max for elite athetes?

A

Lactate threshold

446
Q

What was observed regarding time to fatigue differences at 70%VO2max in low, mixed and high CHO diets?

A

The low CHO diet performed the worst with around 1 hr, the high performed the best between 2 and 5 hrs

447
Q

Correlation between CHO content in diet and muscle glycogen levels?

A

Higher CHO content in diet means a higher muscle glycogen content

448
Q

What was observed when looking at the time when muscle glycogen depletion occurs in placebo and CHO-fed groups during exercise?

A

They reach muscle glycogen depletion at the same time (3hrs)

449
Q

Why could CHO-fed people exercise for longer than placebo despite reaching muscle glycogen depletion at the same time?

A

Taking on more CHO means it no longer becomes a reason for fatigue

450
Q

What role can muscle glycogen have other than a fuel?

A

A signalling molecule

451
Q

Subsarcolemmal region meaning?

A

Below the sarcolema

452
Q

Which type of muscle glycogen storage is most closely associated with fatigue?

A

Intramyofibrillar

453
Q

How does a lack of muscle glycogen affect calcium?

A

It affects its release rate

454
Q

Which out of glycogen, glucose, FAs can generate ATP the fastest?

455
Q

What is McArdles disease?

A

Lack of enzymes required to break down muscle glycogen

456
Q

Which fuel is more efficient, carbs or fats?

458
Q

What is known about the causal effect of diet on hard outcomes?

459
Q

Issues with non-randomised data?

A

It can be biased

460
Q

What is revesed causality?

A

Smthn ab a disease might cause someone to change their diet

461
Q

Example of reverse causality?

A

Obese people drink diet soft drinks–> diet soft drinks dont cause obesity its just that obese people drink them bc they want to lose weight

462
Q

What are confounding factors?

A

One factor directly causing the disease, and another cause

463
Q

Example of confounding factors?

A

Smoking–> causes cardiovascular disease, and changes in diet which in turn also cause cardiovascular disease

464
Q

How does randomisation minimise systemic bias?

A

It can minimise the effect of known and unknown confounding factors

465
Q

Example of long term study on diet effect on outcomes?

A

Mediterranean diet (oil, fish, vegetables and no red and processed meats) vs low fat diet (low fat dairy products, bread, potatoes, pasta) for 5 yrs

466
Q

Observations of Mediterranean diet vs low fat diet?

A

Mediterranean diet has a lower risk of getting a cardiovascular event compared to low fat diet

467
Q

What is metabolic health?

A

The ability to maintain metabolic control

468
Q

Maximal eating study?

A

Ate dominoes pizza until comfortably full vs eating until they physically couldnt eat anymore

469
Q

Results of maximal eating study?

A

1500kcal for normal, 3000 for maximal. 57g fat vs 113g. 187g Cho vs 367g

470
Q

What happens when double the amount of fat is eaten?

A

Fat levels in the blood don’t increase by 2* (triglyceride conc in blood increase was buffered)

471
Q

Why do fat levels in blood not increase by 2* when 2* the amount of fat is consumed?

A

Metabolite conc in the blood is buffered

472
Q

What is observed regarding insulin secretion in maximal eating group?

A

It is secreted more

473
Q

What is the oral glucose tolerance test?

A

drink w/ 75g of glucose

474
Q

What is an oral fat tolerance test?

A

Give people x amount of fat and observe the metabolism

475
Q

What is measured in oral glucose tolerance test?

A

Blood glucose response

476
Q

Association between metabolic control and cardiovascular mortality?

A

Better metabolic control = lower CVD mortality

477
Q

Healthy blood glucose cond 2 hrs post OGTT?

A

<7.8 mmol/L

478
Q

Prediabetic blood glucose cond 2 hrs post OGTT?

A

7.8-11 mmol/L

479
Q

Diabetic blood glucose cond 2 hrs post OGTT?

A

> 11 mmol/L

480
Q

Average triglyceride conc difference between sexes?

A

Women have a lower average triglyceride conc than men

481
Q

Issue with measuring conc of glucose?

A

Metabolism is dynamic so conc might be 5mmol/L, but there could be 130mg per min going in and out

482
Q

Where does glucose come from if we haven’t eaten a meal?

A

Liver–> breakdown of glycogen, and gluconeogenesis

483
Q

What is the main glucose consumer from the bood when resting?

484
Q

Causes of an abnormally high BGC?

A

Defective liver glycogen metabolism (too much) or defective glucose uptake in muscles (too little)

485
Q

Glycemia?

A

Blood glucose cond

486
Q

Effect of eating in blood?

A

Rise in BCG and lactate conc that reduces over time, and a suppression of circulating FAs

487
Q

Why does blood lactate conc increase after eating?

A

Glycolysis stimulated by insulin

488
Q

Why are circulated FAs suppressed after eating?

A

If FA conc remained high there would be competition for the muscle fuel uptake–> want muscle to take up glucose instead to buffer BGC

489
Q

Effect of insulin on FFAs?

A

Suppresses their availability-> inhibits adipose tissue lipolysis

490
Q

Effect of insulin on liver?

A

Suppresses liver glucose output

491
Q

Postprandial meaning?

A

After a meal

492
Q

What is glycaemic index?

A

A way to classify carbs

493
Q

How is glycaemic index calculated?

A

Give people 50g of available carbs, measure blood glucose conc over 2 hrs and calculate area under curve and compare this to a refernce

494
Q

What is the reference for a glycaemic index?

A

Pure glucose, white bread

495
Q

What if the area under the curve of a food is the same as glucose?

496
Q

What if the area under the curve of a food is half that of glucose?

497
Q

What are high GI foods?

498
Q

What are low GI foods?

499
Q

What GI is spaghetti regardless of wholemeal or white?

500
Q

What GI is bread regardless of wholemeal or white?

501
Q

Monosaccharides example?

A

Glucose, fructose, galactose

502
Q

Difference between sucrose and isomaltulose?

A

Bond between glucose and fructose is stronger isomaltulose

503
Q

Oligosaccharide example?

A

Maltodextrin

504
Q

Polysaccharides?

A

Amylopectin (starch) and amylose (starch)

505
Q

Benefits of isomaltulose over sucrose?

A

Lower GI (more slowly digested) and better for teeth as it isnt fermented in the mouth

506
Q

What is maltodextrin used ?

A

Sports nutrition products

507
Q

What is maltodextrin made up of?

A

8-12 glucose molecules

508
Q

Differences between amylopectin and amylose?

A

Amylopectin is branched, amylose is straight & Amylose has a lower GI as it takes longer to digest–> enzymes can only work on ends and in branch there is more ends

509
Q

How is area under curve counted for BGC?

A

Look at resting BGC, only count area that goes above it (incremental area under curve)

511
Q

Why do differences in GI arise?

A

Gross matrix structure (different sized oats–> smaller oats are ground up so increased SA so more digestion), cell wall present/absent

512
Q

Second meal effect?

A

Thing eaten can affect digestion of foods eaten after it

513
Q

What does a slower glucose appearance do to insulin response?

A

Reduces it

514
Q

How can foods with different exogenous glucose appearance rate result in similar blood glucose concentrations?

A

Foods that are digested faster (and so would cause a higher glucose appearance rate) cause a larger increase in insulin conc so the higher glucose conc is then buffered

515
Q

Why do rapidly and slightly slowly digestible starches result in a similar (moderate to high) glycaemic response?

A

Rapidly causes a high insulin response which cancels out the higher glucose and leads to a similar glycaemic response

516
Q

What kind of starch foods leads to a low glycaemic response?

A

Very slowly digestable starch

517
Q

Exercise interaction with GI?

A

Low GI combined with exercise can improve glucose control (via insulin)

518
Q

How to study positive energy balance effect on metabolic control?

A

Have one group who overate (150% of normal) and were sedentary while the other group overate but did enough exercise to offset the extra 50% calories

519
Q

Effect of flux on insulinemia independent of energy balance?

A

Exaggerated insulin response (bad as less sensitive to insulin) is only seen in non-exercise group even though both groups were eating 150% of what they normally would

520
Q

Effect of quantity of fat ingested on triglyceride response?

A

If a meal has more fat (and all else is equal) there is a higher plasma triglyceride concentration

521
Q

In the fasted state, where do triglycerides come from?

522
Q

How are triglycerides generally transported when fasted?

523
Q

What are VLDLs cleared by?

A

Adipose tissue and muscle

524
Q

What does adipose tissue and muscle have that allows them to digest lipids?

A

Lipoprotein lipase

525
Q

What does lipoprotein lipase break triglycerides into?

A

Non esterified fatty acids and glycerol

526
Q

Fate of fatty acids in adipose tissue?

527
Q

Fate of fatty acids in muscle?

528
Q

What kind of triglyceride enters circulation in the fed state?

A

Chylomicron triglycerides

529
Q

What competes for clearance with VLDL in the fed state?

A

Chylomicrons

530
Q

Which type of fat storage does LPL have the higher affinity for?

A

Chylomicrons so it will preferentially clear those

531
Q

What happens as a result of eating fats?

A

Increase in VLDL conc in blood

532
Q

Why does eating fat increase VLDL blood conc?

A

Chylomicrons are preferentially cleared

533
Q

Effect of insulin on VLDLs?

A

It directly suppresses the output of VLDL from the liver (reduced triglyceride appearance in circulation), also indirectly suppress VLDL appearance as it suppresses adipose tissue lipolysis (fewer FAs to incorporate in VLDLs)

534
Q

Effect of insulin on LPL in adipose tissue?

A

Stimulated it–> more storage

535
Q

Effect of insulin on LPL in muscle?

A

Inhibits it, so less oxidation

536
Q

Effect of high sugar diet on triglyceride clearance?

A

Can reduce triglyceride clearance so when eating fats the fats are cleared at a lower rate

537
Q

Clearance rate of fats on a lower carb diet compared to a higher carb diet?

A

Lower carb diet results in faster triglyceride clearance

538
Q

Effect of high carb diet on fatty acid fate?

A

High carb diet leads to a lower dietary fat oxidation

539
Q

Why should free sugars not exceed 5% of total dietary intake?

A

Free sugars can cause dental issues, and a higher energy intake

540
Q

Example of free sugar?

A

Sugar in apple juice is a free sugar, sugar in an apple is not (as matrix has been altered)

541
Q

Main difference in glucose and fructose metabolism in liver?

A

Fructose is two step metabolism, glucose is one step metabolism

542
Q

Glucose metabolism in liver?

A

Glucose–> glucose-6-phosphate–>G1P–>UDP glucose–> glycogen

543
Q

Why does fructose have a two step metabolism whereas glucose has a 1 step metabolism?

A

Fructose is not oxidised as fructose, it needs to be converted to other things before it can be used by peripheral tissues

544
Q

What can the liver convert fructose into?

A

Glucose, lactate or triglycerides

545
Q

What do high fructose diets increase the production of?

546
Q

What is denovolipogenesis?

A

The production of fats from non-fat sources

547
Q

Triglyceride response to glucose compared to fructose?

A

Fructose leads to a larger triglyceride response than the same amount of glucose

548
Q

VLDL and chylomicron response to glucose compared to fructose?

A

higher in response to fructose than glucose

549
Q

Why is the circulatory TAG response higher to fructose than glucose?

A

Fructose stimulates denovo lipogenesis

550
Q

How does fructose increase denovolipogenesis?

A

It can be the substrate and the signal, and it can saturate liver glycogen stores

551
Q

How is fructose the substrate for denovo lipogenesis?

A

It provides the fuel–> it can be converted into palmitate (fats)

552
Q

How is fructose the signal for denovo lipogenesis?

A

It stimulates glucose, AAs to be converted into fat

553
Q

How much fructose is converted to fat?

554
Q

More important role for fructose in denovo lipogenesis?

A

It is more important as a signal than as a substrate

555
Q

How does fructose saturating liver glycogen stores mean it can stimulate denovo lipogenesis?

A

Higher glycogen conc in the liver causes carbohydrates to be converted into fats instead of more glycogen

556
Q

Exercise effect on fructose denovolipogenesis?

A

Exercise reduces fructose induced de novo lipogenesis

HL22015 physiology (36 decks)

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