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?

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?

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?

25
what is generated as a byproduct of aerobic metabolism?
water (H2O)
26
how long must an event last for for it to be classed as endurance?
8min-10h
27
do endurance athletes have more efficient glycolysis of lipolysis systems?
lipolysis
28
true or false - endurance athletes could theoretically exercise forever given unlimited O2 & FFA?
true
29
in what time frame are glycogen stores used up in endurance events?
1-1.5h
30
which fibre type changes to benefit endurance events in trained athletes?
type II fibres - they take on characteristics like type I fibres to facilitate more aerobic metabolism
31
do endurance athletes use all CHO, FFA or a combination of both as fuel?
combination
32
can training enhance aerobic energy pathways such as the krebs cycle and ETC?
yes
33
list two physiological changes in endurance training that increase aerobic capacity
increased mitochondrial density, increased capillary density
34
list 3 points related to easy-moderate endurance exercise
- 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
list two reason FFA release to bloodstream is reduced in moderate-high endurance exercise
1. accumulation of H+ inhibits lipolysis 2. blood flow to adipose tissue reduces (redirected to skeletal muscle)
36
list two causes of fatigue in endurance athletes
1. ATP synthesis reduces in skeletal muscles 2. hepatic glycogen stores deplete
37
list two limitations of aerobic metabolism, especially as endurance exercise duration increases
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
does amount of energy demand met by aerobic metabolism increase or decrease with exercise duration?
increase
39
what energy source is most important for games players?
muscle glycogen
40
does aerobic contribution to energy increase or decrease with cumulative sprints?
increase
41
how many minutes of recovery are required to restore pre-10s sprint levels of PCr?
5mins
42
list four reasons the increase in BLa levels slow throughout a game?
- 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
what is a good target for pre-game glycogen stores to prevent early fatigue?
45mmol/khww
44
list two reasons for temporary fatigue in games
1. muscle ion homeostasis disrupted 2. impaired excitation of sarcolemma
45
do type I or II fibres have larger net glycogen storage capacity?
type II