Energy metabolism 2 Flashcards

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1
Q

What does Pyruvate dehydrogenase (PDH) do?

A

Enzyme that convers pyruvate to Acetyl-CoA

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2
Q

PDH is rate-limiting for.. A
And the B step in mito’s
Makes up the balance between C and D metabolism and is E

A

A- Rate limiting for CHO oxidation
B- Key enzyme
C- First step in mito’s
D- Balance between aerobic (ox phos) and anaerobic metabolism (substrate phosphorylation)
E- Irreversible

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3
Q

PDH is controlled by two enzymes, namely..

A
  1. PDK (pyruvate dehydrogenase kinase): inactivates PDH when there is plenty of energy
  2. PDP (Pyruvate dehydrogenase phosphatase): activates PDH bc of Calcium
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4
Q

What is a crucial difference in the oxidation of fat vs CH?

A

FA can be present inside muscle cells, but majority in adipose tissue.
> Can enter muscle cell: fatty acyl-CoA enters mito.

> oxidation/utilization fat ALWAYS takes place in mito, it is ALWAYS aerobic.
= crucial difference CH and Fat

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5
Q

What is the rate-limiting step for entrance in mito’s?

A

 CPT-1

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6
Q

What is a key hormone that activates lipolysis?

A

Andrenaline

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7
Q

What determines the dominant pathway (CH vs fat)?

A

being fasted or not
Nutrient sensing and signalling regulate substrate selection during fasting and feeding

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8
Q

What happens in more detail during fasting/feeding with the CH/fat pathways?

A

During fasting: lot of FA available. High rate of beta-oxidation, lot of acetyl-CoA (or: acyl-CoA?).
Accumulates: feed-back inhibition. PDH shuts down it activity. High fat oxidation will limit/reduce activity of glycolytic system.

During feeding: Lots of Ch, acetyl-CoA. Can be converted to mal-CoA: inhibitor CPT1. Lot of Ch metabolism, inhibition of fat oxidation.

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9
Q

CPT-1: rate-limiting enzyme, C stands for X

A

Carnitine

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10
Q

What can cause an increase in FFA due to increased lipolysis, besides adrenaline?

A

Elevation glucagon, GH, cortisol

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11
Q

What can inhibit lipolysis?

A
  • lactate accumulation
  • increase insulin after CH intake
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12
Q

AMPK: activated as soon as the ratio between X is going up (stress/exercise).

A

AMP/ATP

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13
Q

When AMPK is activated, it inhibits X. This is involved in …. and it means that …. is no longer ….

A

Inhibits ACC1 = involved conversion acetyl-CoA to malonyl-CoA. Means that fat oxidation is no longer inhibited.

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14
Q

What are factors that influence substrate utilization?

A

> Substrate availability
Activity of rate-limiting enzymes
Local factors, such as..

o Oxygen availability; Muscle fiber composition
o Previous exercise and diet
o Type, intensity and duration of exercise
o Drugs; Exercise training
o Levels of plasma hormone

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15
Q

What happens when the endurance athlete ‘hits a wall’?

A
  • Muscle glycogen depletion (fat oxidation can only meet energy 50-60% VO2max)
  • hepatic glycogen depletion (hypoglycaemia)

Switch to only fat oxidation

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16
Q

With intermittent HI exercise (such as soccer), X contribution will decrease and glycogen stores will be depleted more and more but PCR and aerobic stays roughly the same (with enough rest)

A

anaerobic glycolysis

 With repeated sprint: mainly PCr and aerobic contributions: anaerobic glycolysis rapidly decreases