LECTURE 5: lipid metabolism, aerobic metabolism, endurance athletes & games players Flashcards

1
Q

what attaches to TAG to activate them for storage & metabolism? what do they become?

A

acetyl CoA, fatty acyl CoA

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2
Q

what compounds are fatty acyl CoA broken into during beta oxidation?

A

groups of 2C acetyl groups attached to CoA

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3
Q

what is the purpose of beta oxidation?

A

breakdown of fatty acid chains of triglycerol to release energy for ATP resynthesis and acetyl CoA for krebs cycle

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4
Q

where does beta oxidation occur?

A

in the mitochondria

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5
Q

list four sources of acetyl

A

fatty acids (one for every 2 carbons), proteins (only little), ketone bodies, carbohydrates

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6
Q

what is lipolysis?

A

hydrolysis of triglycerides, “fat metabolism”

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7
Q

what protein transports FFA through blood?

A

albumin

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8
Q

what is lipolysis?

A

hydrolysis of triglycerides, “fat metabolism”, breakdown of TAG into 3 fatty acids + glycerol

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9
Q

which causes an uptick in lipolysis - higher FFA concentration or lower FFA concentration in the blood?

A

low FFA concentration. lipolysis is favoured when FFA is low

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10
Q

list 5 hormones stimulating and 1 hormone inhibiting lipolysis

A

adrenaline, noradrenaline, glucagon, cortisol, growth hormone stimulate, insulin inhibits

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11
Q

will fasted or non fasted athletes have a higher blood FFA concentration during exercise? why?

A

fasted, non-fasted athletes use blood glucose and ingested FFA, reducing lipolysis rates

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12
Q

what are typical blood FFA levels at rest and in exercise?

A

rest: 0.2-0.4mmol/L, exercise: 2.0mmol/L

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13
Q

what part of the mitochondria does the krebs cycle take place?

A

the matrix (inside both membranes)

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14
Q

where does the ETC take place?

A

intermembrane space (between two membranes)

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15
Q

true or false: krebs cycle begins within the first 2seconds of exercise?

A

true - to make up for the using up of intracellular ATP in 2seconds of exercise

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16
Q

list the 5 stages of the krebs cycle

A

1) acetyl CoA dissociates to form acetyl to enter krebs cycle
2) Acetyl (2C) + Oxaloacetate (4C) = Citrate (6C)
3) citrate is oxidised (e- removal) and loses 2C as CO2
4) step three turns citrate into Oxaloacetate (4C)
5) oxaloacetate binds with a new acetyl to enter another krebs cycle

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17
Q

how many ATP are generated in the krebs cycle and what other by products are produced?

A

2ATP, NADH, FADH2

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18
Q

what is the greatest number of ATP that can be generated in the ETC?

A

38 ATP

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19
Q

list the three aims of the krebs cycle

A

1) decarboxylation of acetyl groups (removing carbons)
2) complete oxidation of acetyl groups & resynthesise ATP
3) production of reduced electron carries/coenzymes (gained electrons)

20
Q

which is the definition of aerobic metabolism: the krebs cycle or the ETC?

A

ETC

21
Q

what is the main aim of the ETC?

A

transport of electrons from krebs cycle to ETC to generate ATP

22
Q

how many protein-lipid complexes make up the ETC?

A

4

23
Q

what is the basic principle of the ETC?

A

electrons jump from complex to complex, releasing energy each time

24
Q

what is the last recipient of e- in the ETC?

A

Oxygen

25
Q

what is generated as a byproduct of aerobic metabolism?

A

water (H2O)

26
Q

how long must an event last for for it to be classed as endurance?

A

8min-10h

27
Q

do endurance athletes have more efficient glycolysis of lipolysis systems?

A

lipolysis

28
Q

true or false - endurance athletes could theoretically exercise forever given unlimited O2 & FFA?

A

true

29
Q

in what time frame are glycogen stores used up in endurance events?

A

1-1.5h

30
Q

which fibre type changes to benefit endurance events in trained athletes?

A

type II fibres - they take on characteristics like type I fibres to facilitate more aerobic metabolism

31
Q

do endurance athletes use all CHO, FFA or a combination of both as fuel?

A

combination

32
Q

can training enhance aerobic energy pathways such as the krebs cycle and ETC?

A

yes

33
Q

list two physiological changes in endurance training that increase aerobic capacity

A

increased mitochondrial density, increased capillary density

34
Q

list 3 points related to easy-moderate endurance exercise

A
  • relies mostly on FFA, little on CHO,
  • high FFA uptake in skeletal muscle at beginning, followed by a catch up in lipolysis rates
  • FFA concentration increases over duration of exercise
35
Q

list two reason FFA release to bloodstream is reduced in moderate-high endurance exercise

A
  1. accumulation of H+ inhibits lipolysis
  2. blood flow to adipose tissue reduces (redirected to skeletal muscle)
36
Q

list two causes of fatigue in endurance athletes

A
  1. ATP synthesis reduces in skeletal muscles
  2. hepatic glycogen stores deplete
37
Q

list two limitations of aerobic metabolism, especially as endurance exercise duration increases

A
  1. supply of O2 to blood from lungs and ability of heart to pump O2 rich blood to circulation
  2. O2 extraction ability of skeletal muscle exceeding the O2 supply
38
Q

does amount of energy demand met by aerobic metabolism increase or decrease with exercise duration?

A

increase

39
Q

what energy source is most important for games players?

A

muscle glycogen

40
Q

does aerobic contribution to energy increase or decrease with cumulative sprints?

A

increase

41
Q

how many minutes of recovery are required to restore pre-10s sprint levels of PCr?

A

5mins

42
Q

list four reasons the increase in BLa levels slow throughout a game?

A
  • Insufficient recovery means Pi, H+ & La aren’t cleared and glycolysis is inhibited
  • accumulation of other inhibitors of glycolysis (eg ADP, NH4+) occurs in high intensity exercise
  • reduced neural drive
  • higher oxidative metabolism
43
Q

what is a good target for pre-game glycogen stores to prevent early fatigue?

A

45mmol/khww

44
Q

list two reasons for temporary fatigue in games

A
  1. muscle ion homeostasis disrupted
  2. impaired excitation of sarcolemma
45
Q

do type I or II fibres have larger net glycogen storage capacity?

A

type II