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Physiology > MID SEM 2 > Flashcards

MID SEM 2 Flashcards

1
Q

Limiting factors on VO2 max?

A

Genetics & Training

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2
Q

Endurance Athletes VO2 max?

A

80-90mL/kg

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3
Q

Untrained Person VO2 max?

A

40-50mL/kg

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4
Q

Percentage heritability/training of VO2 max?

A

Genes: 51%
Training: 49%

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5
Q

Limitations to VO2 max?

A 
Lung capacity
Haemoglobin
CO max
Capillary density
Mitochondrial capacity
Availability of substrates
CNS -motivation
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6
Q

Leg or arm has higher oxidative capacity?

A

Leg - used for walking all the time - generally more trained than arms

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7
Q

What determines O2 availability?

A

Haemoglobin
CO
Oxygen content

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8
Q

Muscle diffusion capacity?

A

The ability of oxygen to get from the erythrocytes to muscle mitochondria

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9
Q

What is muscle diffusion capacity dependent on?

A

Distance
Number of mitochondria
How easy oxygen is to unload
capillaries

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10
Q

What is convection?

A

The movement of heat from the body to the surroundings through movement

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11
Q

What is exertional heat stroke?

A

Overworking in hot environment, heat stress, break down of muscles due to high temps

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12
Q

What are the mechanisms of heat loss as temperature increases?

A

At lower temperatures most heat loss occurs through conduction and convection and as temperatures increase more heat is lost through sweating

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13
Q

Components of sweat

A

Sodium

Chloride

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14
Q

Sweating action of trained people?

A

Lower sweat sodium, better able to maintain plasma sodium due to aldosterone action - higher plasma volume

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15
Q

Plasma constituents

A

sodium and chloride

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16
Q

Muscle constituents

A

potassium and some magnesium

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17
Q

Blood supply priorities during exercise

A

Muscle>brain>skin

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18
Q

Effects of pre cooling?

A
  • increased performance time

- core temp does not increase as rapidly

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19
Q

Effects of pre heating?

A

Higher RPE
Reduced performance time/power output
Rapid increase in core temp

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20
Q

Effects of exercising in hot environment?

A
  • higher RPE
  • less voluntary muscle activation
  • reduced cerebral blood flow
  • hyperprolactinaemia
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21
Q

Hyperprolactinaemia

A

Hormone released from the pituitary - reflects changes in the brain associated with fatigue

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22
Q

Heat acclimatisation

A

lowers heart rate and rise in core temp during exercise

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23
Q

Physiological and Metabolic adaptations to heat acclimatisation?

A
  • increased blood volume
  • reduced heart rate
  • lower core and skin temp
  • increased sweat rate and earlier onset (more sensitive)
  • more dilute sweat
  • reduced muscle glycogen use
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24
Q

What does fluid ingestion do to CV drift?

A

Blunts it. By increasing fluid ingestion you increase blood volume and prevent drop in SV and increase in HR - CO maintained

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25
Q

Benefits of Fluid Ingestion

A
  • increased blood volume
  • decreased heart rate
  • decreased SV and CO
  • decreased core temp
  • decreased plasma sodium and osmolarity
  • decreased glycogen use
  • increased exercise performance
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26
Q

What is associated with cramping?

A

Dehydration and sodium loss

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27
Q

Muscle Fatigue

A

Force loss during a sustained maximum voluntary contraction, a loss of maximal or potential performance, failure to maintain the required or expected force

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28
Q

What does the rate of fatigue depend on?

A
  • muscle used
  • intensity of exercise
  • type of contraction
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29
Q

Central site of fatigue?

A

Brain and spinal cord

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30
Q

Peripheral site of fatigue?

A

Peripheral nerves and muscle

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31
Q

What is central fatigue?

A

emotional and psychological factors that influence our motivation to perform a task - works by impairing transmission and recruitment for contraction

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32
Q

What is peripheral fatigue?

A

neural, mechanical or biochemical factors which are not operating in a way that allows us to sustain force

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33
Q

Mechanisms of peripheral fatigue - neural?

A

Insufficient neurotransmitters-AP unable to be generated or threshold not reached

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34
Q

Mechanisms of peripheral fatigue -biochemical?

A

Potassium build up in t-tubules - impairment of sodium/potassium pump

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35
Q

Mechanisms of peripheral fatigue -mechanical?

A
  • ATP reduction due to reduced action of myosin ATPase
  • build up of magnesium which blocks calcium binding to troponin and opening of RyR to let calcium out of SR
  • lactate and H+, pH drop that decreases troponin sensitivity for calcium
  • Pi accumulates and decreases muscle force (10mM Pi - decreases muscle force by 30%)
  • PCr loss - loss of energy store
  • ADP accumulation
  • ROS - damages SR causing calcium efflux problems
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36
Q

High Frequency Fatigue

A

Fast onset and fast recovery, electrical stimulation of the muscle after work will give the same level of force, likely caused by t-tubule conduction failure

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37
Q

Metabolic Fatigue

A

Slow onset, slow recovery, acidosis and PCr depletion

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38
Q

What level does ATP drop to following exercise?

A

60% of pre work level

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39
Q

Resting muscle pH?

A

7.0-7.4

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40
Q

What is McArdles Disease?

A

Inability to break down glycogen (no glycogen phosphorylase) so don’t produce lactate or H+ but fatigue more easily than normal people

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41
Q

Effects of caffeine on muscles?

A

Further open up calcium channels allowing more calcium efflux and a greater force of contraction

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42
Q

Effects of fentanyl?

A

Blocks muscle feedback, athlete starts out at higher power output, but declines more than control group and does not have a very high end burst

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43
Q

Glycogen influence on power output?

A

High glycogen = longer time to fatigue

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44
Q

What does taking bicarbonate do?

A

Exercise increases the acidity in the body, so taking bicarbonate will facilitate the removal of hydrogen from muscle so the body can exercise for longer without getting to a critical acid level

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45
Q

How much power output is accounted for by cytochrome oxidase?

A

81%

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46
Q

How much power output is accounted for by VO2 max

A

49%

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47
Q

Fluid and CHO performance improvement?

A

6% each, and have an additive effect (12%)

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48
Q

What happens at the costumere?

A

force is transmitted

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49
Q

Components of the dystroglycan complex?

A

Alpha dystroglycan
Beta dystroglycan
Laminin

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50
Q

Components of the dystrophin glycoprotein complex (DGC)?

A

Dystroglycan complex

Dystrophin

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51
Q

Dystrophin Structure

A
  • 4 hinge repeats: flexibility
  • 24 spectrin like repeats:stable
  • 2 actin binding domains (n-terminal CH1,CH2) and (central: 11,12,13,15,17)
  • 1 cysteine rich domain: attaches to dystroglycan complex
  • 1 C-terminal: attaches to dystrobrevin and syntrophin
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52
Q

What happens when dystrohpin is partially/completely missing?

A

Partial: Beckers muscular dystrophy
Completely: Duchennes muscular dystrophy

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53
Q

What are the components of laminin and what happens if laminin is missing/damaged?

A

Alpha, gamma and beta chains

Congenital muscular dystrophy (missing alpha chain-merosin)-immature fibres and connective tissue

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54
Q

What is alpha dystroglycan?

A

Site for glycosylation

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55
Q

What is beta dystroglycan?

A

link between ECM and cytoskeleton

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56
Q

Function of dystroglycan complex?

A

Joins ECM (basal lamina) to plasma membrane

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57
Q

Function of the DGC?

A

Link ECM to f-actin cytoskeleton, stabilises sarcolemma, forms costameres, mechanical link between sarcomeres

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58
Q

Components of the sarcoglycan complex?

A

alpha, beta, delta and gamma sarcoglycans and sarcospan

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59
Q

Function of Sarcoglycan complex?

A

mediate interactions along the ECM, stabilise DGC at sarcolemma

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60
Q

What happens when a sarcoglycan subunit is damaged/missing?

A

Limb girdle muscluar dystrophy

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61
Q

Function of the vinculin-talin-integrin complex?

A

Formation of focal adhesions (cell membranes binding), force transducer

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62
Q

What is integrin?

A

Alpha and beta subunits - alpha 7B, beta 1D - regulates intracellular organisation

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63
Q

What is talin?

A

Talin 1 & 2(most common form), interacts with beta 1D integrin, vinculin and actin to form link

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64
Q

What is vinculin?

A

linkage of integrin to actin - metavinculin is muscle specific splice version

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65
Q

What happens when integrin is missing?

A

Congenital muscular dystrophy - mutations in alpha7

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66
Q

What happens when talin 1 is missing?

A

Progressive Myopathy

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67
Q

What happens when talin 2 is missing?

A

Myopathy with central nuclei

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68
Q

What happens when vinculin is missing?

A

Idiopathic dilated cardiomyopathy

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69
Q

What happens when talin 1&2 are missing?

A

Severe defects in myoblast fusion and sarcomere assembly

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70
Q

What is desmin?

A

Intermediate type II filament
Links myofibres at z-disc
Essential for maintenance of myofibril integrity (not required for normal muscle development)

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71
Q

Loss of desmin?

A

Desminopathy - misalignment of sarcomeres, disorganisation of fibres and cell death

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72
Q

What is plectin?

A

500kDa
In almost all mammalian cells
Links actin, microtubules and intermediate filaments
12 isoforms - 1f, 1d, 1b, 1

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73
Q

Plectin 1 and 1f?

A

Costameres

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74
Q

Plectin 1d?

A

Z-disc

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75
Q

Plectin 1b?

A

mitochondria

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76
Q

What happens with plectin mutation?

A

EBS- blistering, muscle weakness and dystrophy

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77
Q

What is titin?

A

Biggest protein
At Z and M lines
Prevents over stretching of muscle fibres

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78
Q

What happens with titin mutation?

A

Titinopathy/tibial muscular dystrophy - restricted to lower leg muscles, interrupt normal muscle contractions

79
Q

Gastrulation and germ layers

A

Ectoderm: skin and nervous system
Endoderm: internal organs
Mesoderm: muscle and notchord

80
Q

What muscles do somites generate?

A

All muscles from the neck down as well as the tongue - not extra-occular and jaw muscles

81
Q

Myogenesis steps

A 
Embryonic stem cell
muscle progenitor cell
myoblast
myotube
mature muscle fibre
82
Q

Which intermediate in myogenesis is committed to becoming muscle?

A

Myoblast

83
Q

What can MPCs form?

A

MPCs are totipotent but can only form mesodermal tissues

84
Q

What do pax3 and pax7 do?

A

Specify differentiation of ESC to MPC

85
Q

What happens if you lose pax3?

A

No limb muscle development

86
Q

What happens if you lose pax7?

A

Lack of adult satellite cells

87
Q

What happens if you lose pax7 and pax3?

A

Complete lack of musculature

88
Q

What is unique about MRFs?

A

They can cause non-muscle tissue to become muscle

89
Q

What are the types of MRFs (myogenin regulatory factors)?

A

MyoD
Myf5
Myogenin
MRF4

90
Q

What are the primary MRFs?

A

MyoD/Myf5 - expressed early, promote expression of myogenin and beginning of differentiation

91
Q

What happens if you remove either MyoD or Myf5 or both?

A

Either - normal

Both - no skeletal muscle

92
Q

What are the secondary MRFs?

A

Myogenin and MRF4 - expressed during differentiation and promote further differentiation

93
Q

What are MEF2 and SRF?

A

Transcription factors that are not MRFs - will not make muscle if expressed in non-muscle tissue, can’t initiate myogenesis on their own

94
Q

What are the growth factors and how do they influence proliferation and differentiation?

A 
IGF-1: increase P, increase D
LIF, IL6: increase P, same D
FBF, HGF: increase P, decrease D
Insulin, IGF-2: same P, increase D
TBF-B1: decrease P, increase D
95
Q

What is the role of myostatin?

A

Regulate the balance between differentiation and proliferation

96
Q

Micro RNA families?

A

miR-1/206 & miR-133

97
Q

Function of miR-1/206?

A

Enhance myoblast differentiation - blocks follistatin which is blocking myostatin which causes differentiation

98
Q

Function of miR-133?

A

Drive myoblast proliferation - blocks SRF which is causing differentiation

99
Q

What happens if there is an over expression of follistatin?

A

Uncontrolled proliferation - massive muscle size

100
Q

What are satellite cells?

A

Adult stem cells capable of resythesising muscle for repair, located between muscle fibre and basal lamina, close to blood vessels

101
Q

What do satellite cells express?

A

Pax3, pax7, CD34

102
Q

What are the theories of satellite cell renewal?

A
  1. satellite cell proliferates and one goes back to repopulate the niche
  2. cell divides to form one new proliferative cell and one cell that stays behind to repopulate the niche
103
Q

Is pax3 or pax7 required for satellite cells?

A

Pax7 required for development and maintenance, pax3 only expressed in diaphragm and body wall muscles

104
Q

Function of HGF?

A

Post natal myogenesis: released from damaged muscles and activated satellite cells

105
Q

What happens when young muscles are transported into an old body?

A

They lose regenerative capacity

106
Q

What happens to the old muscles when a young and old mouse are connected?

A

They gain regenerative capacity

107
Q

Sources of adult stem cells?

A

Mesangioblasts, bone marrow, AC133, pericytes, muscle derived stem cells and side population cells

108
Q

Actions of mesangioblasts?

A

Blood derived, differentiate to mesodermal tissues

109
Q

Action of pericytes?

A

Blood derived, beneath basal lamina of small blood vessels, suitable for IV delivery

110
Q

Action of AC133+ cells?

A

blood and skeletal muscle derived, can form myogenic cells, 1% of mono nucleated cells

111
Q

Action of Bone marrow?

A

circulating myogenic precursor cells, inject into muscle

112
Q

Action of muscle derived stem cells?

A

In interstitial space, positive for CD34, regenerate skeletal muscle when delivered into muscle or vasculature

113
Q

Action of side population cells?

A

efflux Hoechst (DNA binding dye), skeletal muscle, dont express satellite markers, located outside muscle fibres, injected - have potential

114
Q

Myoblast Transplant

A
  • poor survival in vivo
  • limited migration from injection site
  • no paritcipation in long term regeneration
115
Q

Satellite cell Transplant

A

delivered direct to muscle, poor contribution when no damaged muscle, poor survival in vivo, need multiple injections

116
Q

Myofibre Transplant

A

protects against age related muscle degeneration

117
Q

Mesangioblast Transplant

A

can be delivered systemically, difficult to purify, improves dystrophy effects

118
Q

How much muscle wasting do ICU patients have in 10 days?

A

20% of CSA

119
Q

How much protein is synthesised/broken down each day?

A

300g of each process

120
Q

What is 3-methylhistidine?

A

component of myosin and actin, can indicate protein breakdown but also arises from other tissues

121
Q

What is autophagy?

A

Breakdown and recycling of damaged glycogen, organelles and protein

122
Q

What percentage of autophagy do mTOR and Fox03 regulate?

A

mTOR - inhibits 10%

Fox03 - promotes 50%

123
Q

What is ubiquitin activated by?

A

E1/E2 ligases

124
Q

What are the muscle specific E3 ligases?

A

MURF-1

Astrogin-1/MAFbx

125
Q

What happens to autophagy when there is an increase in insulin?

A

Causes increase in AKT - phosphorylates FOXO - stops increase in muscle specific E3 ligases - reduces protein breakdown and boosts protein synthesis

126
Q

What does Astrogin-1/MAFbx do?

A
  • Reduces MyoD (reduces proliferation)

- Blocks elF3-F and S6K1 (stop formation of pre-initiation complex) and mTOR (stop protein synthesis)

127
Q

What do caspases 3 & 9 do?

A

Cause apoptosis/programmed cell death

128
Q

What does caspase 1 do?

A

Regulates inflammation

129
Q

What is protein breakdown/synthesis dependent on?

A

Exercise, food intake, hormones and inflammation

130
Q

What has higher FSR?

A

Mitochondria>myofibrilar

131
Q

During exercise, what happens to mTOR and AMPK?

A

AMPK: increases
mTOR: decreases

132
Q

What does rapamycin do during exercise?

A

Blocks mTOR

133
Q

Rate of sarcopenia?

A

8-10% per decade

134
Q

What happens to protein processes in the elderly?

A

Reduce protein synthesis rate, protein intake and protein synthesis response to exercise

135
Q

What does cancer mean for protein synthesis?

A

Protein synthesis after food intake is blunted

136
Q

Does CHO affect protein synthesis?

A

No (breakdown>synthesis)

137
Q

How do essential AAs stimulate protein synthesis?

A

Signal through mTORC1

138
Q

How much protein is needed to maximally stimulate synthesis?

A

25g

139
Q

What is the effect of AA infusion?

A

Increases muscle protein synthesis but effect is short lived

140
Q

How much protein does milk have and how much of this is whey?

A

3%, 20% of this is whey - better because it contains more leucine and moves into circulation more quickly

141
Q

Pathway of leucine affect?

A

leucine:leucyltRNA synthase- GTP-mTOR-protein synthesis

142
Q

What does increasing the leucine in the diet do?

A

Increases protein synthesis and turnover

143
Q

What is the protein RDI?

A

1.2-1.7/g/kg/day

144
Q

What does increased protein during weight loss do?

A

Reduced muscle mass loss

145
Q

Are the elderly affected by protein/leucine supplements in addition to exercise?

A

No - no affect in increasing muscle size and strength

146
Q

What does glycine supplementation do?

A

Reduces tumour growth and muscle loss

147
Q

What does glycine supplementation decrease?

A

atrogin-1 mRNA expression- reduce protein breakdown by maintaining protein synthesis machinery

148
Q

What does inflammation cause?

A

Heat, swelling, pain, loss of function, redness

149
Q

What does mechanical stress (exercise) lead to?

A

Release of immune cells from muscle and circulation - tissue cross talk - communication for muscle repair

150
Q

What happens if tissue repair is not properly regulated?

A

Chronic inflammation

151
Q

When does immune cell involvement occur?

A

0-14 days after stress

152
Q

Sepsis/exercise upregulated cytokines?

A

Sepsis: TNF and IL-6
Exercise: IL-6

153
Q

What does the amount of IL-6 released depend on?

A

Duration and intensity of exercise and number of muscles recruited

154
Q

What do myokines promote?

A

Hypertrophy and satellite cell activation

155
Q

JAK/STAT Pathway

A
  • IL-6 TO GP130
  • Phosphorylate JAK
  • Phosphorylate STAT3
  • STAT3 dimerise
  • STAT3 translocate to nucleus
  • Transcription factors: hypertrophy, angiogenesis, survival
156
Q

When are STAT3 and STAT5 phosphorylated?

A

STAT3- following resistance exercise

STAT5- following aerobic exercise (due to growth hormone)

157
Q

Do recurrent bouts of exercise lead to IL-6 increase?

A

No

158
Q

Does inflammation level change with training?

A

No - inflammation always occurs. Plasma and muscle IL-6 levels are always increased following exercise

159
Q

Who has a greater macrophage response following exercise?

A

Young people

160
Q

Who has higher plasma IL-6 levels?

A

Older people

161
Q

Who has higher muscle IL-6 levels?

A

Older people

162
Q

Do men or women have higher neutrophils following exercise?

A

Women

163
Q

What are the effects of anti-inflammatory drugs?

A
  • Blunt IL-6 rise
  • Reduce protein synthesis
  • Blunt IL-10 (due to bunting IL-6)
  • Reduce satellite cell production and activation
164
Q

How do blood volume and red cell mass increase VO2?

A
  • Blood volume- allows higher SV and CO - not as effective in trained people as they already have an increased blood volume
  • Red Cell Mass- altitude training and pumping blood with RBC increases the arterial O2 carrying capacity so there is greater delivery and VO2 max
165
Q

What happens when you sweat for a long time?

A

Begin to lose ions due to massive water loss

166
Q

Why does heat stress increase glycogen utilisation?

A

More blood lactate and glycogen usage due to increased temp increasing plasma adrenaline driving glycogen breakdown

167
Q

How does the CNS contribute to central fatigue?

A
  • reduced drive of motor neurone
  • impaired spinal cord transmission
  • neuromuscular transmission failure
  • recruitment of motor units
  • reduced motor unit firing frequency
  • inhibitory input from muscle afferents
168
Q

What happens to relaxation during fatigue?

A
  • Extended rate of relaxation

- Due to a decreased rate of cross bridge detachment and calcium reuptake to SR

169
Q

Why does high intensity resistance training result in acidosis?

A

Fast twitch fibres with less mitochondria used, greater accumulation of protons causing acidosis

170
Q

How does lactate delay fatigue onset?

A

By resetting the sodium potassium pumps

171
Q

What alters calcium sensitivity?

A

Sarcomere length, light chain phosphorylation, pH, Pi and temp

172
Q

Having more of which fibres improves performance time?

A

slow twitch

173
Q

What does nNOS do?

A

Produces NO during muscle contrition to facilitate vasodilation

174
Q

Which complex requires post-translational modifications for proper function?

A

Dystroglycan complex

175
Q

4 Main roles of Titin

A
  • provide a structural framework
  • centre thick filament within sarcomere
  • act as a molecular spring
  • signalling mediator
176
Q

Criteria for ideal stem cell to treat muscle wasting?

A
  • immunoprivilleged
  • systemically deliverable
  • expandable in vitro and don’t lose stem cell properties
  • survive, proliferate and migrate in host muscle
  • differentiate into muscle fibres
  • repopulate satellite cell pool
  • capable of expressing muscle genes
  • improve muscle strength and quality of life
177
Q

How much of total protein breakdown does ubiquitin system account for?

A

80%

178
Q

What do calpains do?

A

Initiate degradation of myofibrilar proteins

179
Q

What fibre type does S6K1 have most effect on after exercise?

A

Type 2

180
Q

What are the liver and gut protein turnovers per day?

A

liver 12%

gut mucosa 500%

181
Q

What contributes most to total body protein turnover?

A

Muscle

182
Q

What type of exercise stimulates protein synthesis?

A

Resistance, endurance doesn’t affect basal protein levels

183
Q

For how long after exercise are protein synthesis levels increased?

A

up to 48 hours

184
Q

What are the two steps of translation initiation?

A
  • Binding of initiation complex to mRNA

- Binding of first tRNA to ribosomal subunit (if these don’t occur translation and protein synthesis won’t occur)

185
Q

When do transcription and translation occur and what are they mediated by?

A

Translation: resistance exercise, mTOR, proteins-myofibrils
Transcription: endurance exercise, mitochondria, promotes protein synthesis

186
Q

What does S6K1 do?

A

Activates assembly pre-initiation complex

187
Q

What is the function of dystrophin?

A

Signalling and force transmission

188
Q

What is the role of AKT?

A

Inhibits FOXO (phosphorylates it and makes it move to cytosol), promotes mTOR pathway

189
Q

mTOR Pathway

A

IGFs-AKT-mTOR-S6K1-Protein Synthesis

190
Q

What are caspases and calpains activated by?

A

Caspases: calcium and ROS
Calpains: caclium

191
Q

How is mTOR blocked during exercise?

A

AMPK-TSC1 (blocked by AMPK - cannot activate mTOR) - mTOR

192
Q

What is the effect of endurance/resistance exercise on protein synthesis?

A

Untrained:

  • Myofirbril R>E (no effect)
  • Mitochondrial E>R

Trained:

  • Myofibril R>E
  • Mitochondira E>R (no effect)
193
Q

Whole body protein equation

A

Breakdown + intake = synthesis + oxidation

194
Q

Do trained or untrained people have higher anabolism?

A

Trained

Physiology (12 decks)

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