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Movement and Musculoskeletal Biology Emily > 019 control of fuel selection in muscles > Flashcards

019 control of fuel selection in muscles Flashcards

1
Q

what are the 2 types of muscle fibres?

A

type 1 (slow twitch) and type 2 (fast twitch)

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2
Q

what is the myosin ATPases like in type 1 and 2 muscle fibres?

A

-type 1 = slow
- type 2 = fast

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3
Q

what is the oxidative capacity like in type 1 and 2 muscle fibres?

A
  • type 1 = high
  • type 2 = low
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4
Q

what is the glycolytic capacity like in type 1 and 2 muscle fibres?

A
  • type 1 = moderate
  • type 2 = high
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5
Q

what fuel do type 1 and 2 muscle fibres mostly use?

A
  • type 1 = more TAG
  • type 2 = more glycogen
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6
Q

how fatigueable are type 1 and 2 muscle fibres?

A

type 1 = resistant to fatigue
- type 2 = easily exhausted

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7
Q

whats the mitochondria amount in type 1 and 2 muscle?

A
  • type 1 = mitochondria rich
  • type 2 = mitochondria poor
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8
Q

what is the blood supply like for type 1 and 2 muscle fibres?

A
  • type 1 = good blood supply
  • type 2 = moderate blood supply
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9
Q

what type of exercises do type 1 and 2 muscle fibres work best at?

A
  • type 1 = aerobic, longer periods of time, low-moderate intensity e.g. marathon
  • type 2 = anaerobic, short duration, high intensity e.g. sprint
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10
Q

what are the 5 different sources of fuel for muscles?

A
  • muscle and liver glycogen
  • plasma glucose
  • muscle and adipose TAG
  • plasma lipoproteins
  • ketone bodies
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11
Q

describe the usage of the fuel of glycogen

A
  • both muscle and liver glycogen may be used in fasting or exercise, esp high intensity
  • exhaustion during exercise is often due to depletion of muscle glycogen
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12
Q

describe the usage of the fuel plasma glucose

A
  • uptake increases during the fed state, exercise and after exercise (to replace glycogen store) and because of insulin release
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13
Q

describe the usage of the fuel TAG

A
  • usage increases during fasting and exercise, esp low intensity
  • type 1 muscle fibres store more TAG and athletes tend to store more TAG
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14
Q

describe the usage of the fuel plasma lipoproteins

A
  • muscle secretes lipoprotein lipase during fasting and after exercise replenishes TAG store
  • too slow to use during exercise
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15
Q

describe the usage of the fuel ketone bodies

A
  • not usually used in exercise but may during very prolonged exercise or very prolonged fasting
  • depends on liver supply
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16
Q

what are the 5 different ways to produce ATP?

A
  • adenylate kinase
  • creatine kinase
  • glycolysis
  • FA oxidation
  • The citric acid cycle and the electron transport chain
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17
Q

how does ATP amount effect muscle/exercise

A
  • intensity and duration of muscle exertion is limited to how quickly ATP can be regenerated and for how long
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18
Q

describe ATP production with adenylate kinase

A
  • can regenerate ATP from ADP almost immediately, and increases AMP (typically very low)
  • AMP is a sensitive indicator of cell energy status
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19
Q

describe ATP production with creatine kinase

A
  • phosphocreatine can maintain ATP for first 5s of maximal exertion
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20
Q

describe ATP production with glycolysis

A
  • not limited by O2
  • once stimulated, provides ATP rapidly
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21
Q

describe ATP production with FA oxidation

A
  • supplies lots of ATP, but slowly and relies on O2
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22
Q

describe ATP production with the citric acid cycle and the electron transport chain

A
  • responsible for the majority of ATP production from fuels, relies on O2
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23
Q

describe muscle metabolism in fed state

A
  • insulin stimulates an increase in glucose uptake
  • glycogenesis and glycolysis increase
  • FA oxidation is inhibited
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24
Q

describe the liver metabolism in fed state

A

-can sense high glucose and uptake increases
- use for synthesis of glycogen / TAG

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25
Q

describe pancreas metabolism in fed state

A
  • Beta cells can sense high glucose, and uptake increases
  • insulin release is stimulated
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26
Q

describe adipose tissue metabolism in fed state

A
  • insulin favours lipogenesis and inhibits lipolysis
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27
Q

describe muscle metabolism in fasting state

A
  • decrease in insulin causes a decrease in glucose uptake
  • fatty acid oxidation increases
  • amino acids may be released
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28
Q

describe liver metabolism in fasting state

A
  • can sense low glucose
  • glycogen stores break down and release glucose
  • gluconeogenesis
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29
Q

describe pancreas metabolism in fasting state

A
  • Beta cells can sense low glucose, so uptake decreases
  • low insulin favours release of fatty acids
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30
Q

describe adipose tissue metabolism in fasting state

A
  • decreased insulin favours fatty acid release
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31
Q

describe the muscle metabolism during exercise

A
  • glycogenolysis and glucose uptake increase
  • uptake of fatty acids and breakdown of TAG increase
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32
Q

describe the liver metabolism during exercise

A
  • adrenaline stimulates glycogenolysis, and glucose is released
  • lactate released by muscle converted back to glucose
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33
Q

describe the adipose tissue metabolism during exercise

A
  • adrenaline favours release of fatty acids (replace what the muscle is taking up)
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34
Q

describe what is happening in terms of fuels, ATP and muscle fibres during high intensity exercise

A
  • require high rate of ATP replenishment
  • glycolysis is the pathway best for this, doesn’t rely on oxygen
  • type 2 fibres recruited (best at glycolysis)
  • in 5 secs before glycolysis can be increased, stores of phosphocreatine are used to replenish ATP via creatine kinase
  • Adenylate kinase replenishes ATP using ADP
  • the AMP produced is an allosteric effector for several enzymes
35
Q

describe how adenylate kinase increases ATP production

A

2ADP —> ATP + AMP
- helps to maintain the ATP : ADP ratio

36
Q

which has the greatest chnge from rest to after exercise, ATP, ADP, AMP?

A

AMP has a huge increase after exercise due to adenylate kinase ATP production
- therefore AMP is a sensitive indicator of the cells energy status
- AMP is an important allosteric effector

37
Q

how does phosphocreatine increase ATP?

A

creatine phosphate + ADP + H+ —->(using creatine kinase) Creatine + ATP

38
Q

when is phosphocreatine used as an energy store (usually)?

A

replenishes ATP in the first 5s of high intensity exercise = before metabolic pathways can respond

39
Q

what happens to the pH of muscles during anaerobic exercise and what effect does this have on the phosphocreatine ATP reaction?

A
  • pH decreases due to anaerobic glycolysis producing lactic acid
  • favours forward reaction = more ATP produced
40
Q

what happens after exercise has finished in terms of adenylate kinase and phosphocreatine?

A
  • after exercise has finished, adenylate kinase works to convert AMP to ADP
  • so the ADP can be converted to ATP and then the reverse reaction can occur to replenish phosphocreatine from ATP (to use in oxidative phosphorylation)
41
Q

what is the breakdown of the muscle glycogen stimulated by?

A
  • the activation of glycogen phosphorylase
42
Q

How does muscle contraction cause an increased uptake of glucose?

A
  • the contraction causes translocation of GLUT4 glucose transporters to the membrane
43
Q

what is the role of glycogen phosphorylase and what is it activated by?

A
  • converts glycogen to glucose-6-P (which can be used in glycolysis)
  • activated by AMP, adrenaline and Calcium, phosphorylase kinase
44
Q

what is the role of hexokinase?

A
  • convert glucose to glucose-6-P which can be used in glycolysis
45
Q

what does phopshorylase kinase activate?

A
  • glycogen phosphorylase which converts glycogen to glucose 6-P
46
Q

what activates phosphorylase kinase in the muscle?

A
  • Calcium
  • phosphorylation
  • adrenaline
47
Q

what activates phosphorylase kinase in the liver?

A
  • glucagon
  • adrenaline
  • calcium
48
Q

what 4 enzymes/things regulate glycolysis?

A
  • hexokinase
  • phosphofructokinase-1
  • pyruvate kinase
  • fatty acid oxidation
49
Q

how does hexokinase regulate glycolysis (what activates and inhibits it)?

A
  • glucose 6-P inhibits hexokinase (product inhibition)
  • inhibition is relieved as the rate of glycolysis is increased (uses up glucose 6-P)
50
Q

how does phosphofructokinase-1 regulate glycolysis (what activates and inhibits it)?

A
  • activated by the increase in AMP
  • any fructose 6-P buildup is converted to F2,6-bisP, also activates it
  • substrate = ATP
  • but high ATP = inhibits enzyme
  • when ATP is high and phosphocreatine is high, inhibition of PFK-1 stops glycolysis
  • citrate from fatty acid oxidation also inhibits PFK-1
51
Q

what is the role of phosphofructokinase-1?

A
  • convert fructose 6-P to fructose 1,6-bisP in glycolysis
52
Q

how does pyruvate kinase regulate glycolysis (what is it activated by)?

A
  • activated by the increase of AMP and buildup of F1,6 bisP
53
Q

what is the role of pyruvate kinase?

A
  • convert phosphoenolpyruvate into pyruvate during glycolysis
54
Q

what 2 enzymes does phosphofructokinase regulate?

A
  • hexokinase and pyruvate kinase
55
Q

how does ATP affect the activity of phosphofructokinase?

A
  • ATP is a substrate for PFK-1
  • but high ATP = inhibits PFK-1
  • graph is a hill curve
56
Q

what 2 things inhibit PFK-1 enough to shut down glycolysis?

A
  • high ATP and high phosphocreatine
  • both inhibit PFK-1 which stops glycolysis
57
Q

how does fatty acid oxidation regulate glycolysis?

A

fatty acid oxidation slows down the rate of glycolysis, causing glycogen to last longer
- it also inhibits PFK-1 (citrate inhibits it)

58
Q

what metabolic pathway is more suitable for low-moderate intensity exercise?

A

fatty acid oxidation
- glucose is not used at it is a more precious fuel as it has so many uses

59
Q

how is fatty acid oxidation regulated?

A
  • in terms of supply only, not within the pathway itself
60
Q

during low-moderate intensity exercise, how is the release of stored fatty acids (lipolysis of TAG) changed?

A
  • it is increased
  • both from adipose tissue and intramuscular TAG droplets
61
Q

during low-moderate intensity exercise, how is uptake of fatty acids into muscle mitochondria changed?

A
  • increased uptake
62
Q

during exercise, what stimulates the release of fatty acids?

A
  • adrenaline
63
Q

in fed state, what is happening to TAG molecules?

A
  • perilipin shields/blocks TAG from hormone-sensitive lipase, stimulated by insulin
  • so this promotes storage of TAGs
64
Q

in exercise/fasting, what is happening to TAG molecules?

A
  • adrenaline and low insulin stimulates hormone-sensitive lipase to be phosphorylated/activated
  • perilipin is also phosphorylated and is moved off the surface of TAG
  • now HSL can facilitate maximal lipolysis and release fatty acids
65
Q

why cant fatty acids go into cells as they are?

A
  • they can be toxic to cell
  • could act as a detergent and damage cell
  • so needs to be modified first
66
Q

how are fatty acids modified to enter cells?

A
  • they are esterified to fatty acyl CoA
  • CoASH + fatty acid —> (fatty acyl CoA synthase) (enzyme) —> fatty acyl CoA
67
Q

what is the role of fatty acyl CoA synthetase and how does it work?

A
  • convert CoASH + fatty acid —> fatty acyl CoA
  • converts ATP to AMP + P-P
  • pyrophosphatase then breaks down P-P into Pi + Pi
  • this step is reversible, so can only produce AMP, not ATP
68
Q

how do fatty acyl CoA enter mitochondria?

A
  1. CPT1 on outer mitochondrial membrane converts fatty acyl CoA into fatty acyl carnitine
  2. fatty acyl carnitine can then cross the outer mitochondrial membrane
  3. CACT then transports fatty acyl carnitine through the inner mitochondrial membrane into the mitochondrial matrix
  4. CPT2 then reconverts fatty acyl carnitine back into fatty acyl CoA
69
Q

what compound regulates/inhibits CPT1/entry of fatty acids?

A
  • malonyl CoA inhibits CPT1
  • malonyl CoA is regulated by acetyl CoA carboxylase
70
Q

what regulates malonyl CoA?

A
  • acetyl CoA carboxylase
  • converts acetyl CoA to malonyl CoA which inhibits CPT1
71
Q

what activates acetyl CoA carboxylase and what effect does that have?

A
  • fed state = citrate (fatty acid oxidation) activates acetyl CoA = converts acyl CoA into malonyl CoA = inhibits CPT1
72
Q

what inhibits acetyl CoA carboxylase and what effect does that have?

A
  • fasting state = fatty acids inhibit acetyl CoA
  • so no malonyl CoA is produced, so CPT1 is activated
73
Q

where does acetyl CoA come from?

A
  • produced from fatty acid oxidation (using fatty acids as fuels)
74
Q

how does a build up of acetyl CoA (fatty acid oxidation)affect glucose metabolism?

A
  1. Acetyl CoA inhibits pyruvate kinase in glycolysis
  2. large amounts of acetyl CoA cause citrate to enter the cytoplasm
  3. citrate inhibits pyruvate kinase and phosphofructokinase-1 in glycolysis
  4. inhibition of PFK-1 causes an accumulation of Glucose 6-P, which inhibits glycogen phosphorylase (which breaks down glycogen into glucose for glycolysis)
75
Q

why is it useful that acetyl CoA decreases the rate that glycogen is used up/glycolysis?

A
  • it delayes exhaustion
76
Q

what are respiratory quotients?

A

gives ratio of CO2 produced to O2 used
- number between 0-1
- smaller the number = more O2 used than CO2 given out

77
Q

what are the respiratory quotients for carbohydrates, protein and fat?

A
  • carbohydrate = 1
  • protein = 0.8
  • fat = 0.7
  • the lower the RQ, the more fat used
78
Q

how do you work out % of energy derived from a fuel?

A

RQ - fat RQ / the fuel you have RQ - fat RQ x100

79
Q

how does the % of fat used change from fed to fasted?

A
  • more fat used when fasting
80
Q

how does the % of fat used change from someone untrained to trained athletically?

A
  • increased fat use in trained people
81
Q

how does anaerobic exercise (e.g. sprinting, weight lifting…) affect the body?

A
  • size of type 2 fibres increase
  • increased muscle bulk
  • increased strength
  • increased glycogen storage
82
Q

how does aerobic exercise (e.g. marathon running) effect the body?

A
  • changes are more varied, more holistic, increasing stamina
  • increase in glycogen synthase activity
  • increase in glycogen store
  • increase density of capillaries in muscles
  • increased expression of fatty acid transport proteins
  • AMPK activity increases = increased capacity to oxidize fats
  • size and number of mitochondria increases
  • increased activity of the citric acid cycle and fatty acid oxidation
83
Q

what are the overall effects on the body from muscle training?

A
  • increase capacity to oxidize fatty acids and spare glycogen
  • however, all these changes are temporary and reversible = if you stop training that muscle, it will go back to how it was before

Movement and Musculoskeletal Biology Emily (23 decks)

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