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Sport and Exercise Nutrition > Fat > Flashcards

Fat Flashcards

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1
Q

What is the structure of a fatty acid?

A

Hydrocarbon chain

Carboxyl group

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2
Q

How is a triglyceride formed?

A

Fatty acid bonds covalently with a glycerol element

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3
Q

What type of reaction occurs to join a fatty acid with glycerol?

A

Esterification reaction

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4
Q

How are fatty acids mobilised for oxidation?

A

In the tissue and muscle, hormone-sensitive lipase is sensitive to alterations in adrenaline, which activate and liberate fatty acids
In the blood, lipoprotein lipase in capillary walls can be activated and liberate fatty acids
Fatty acids are transported in the blood to the muscle to be used by mitochondria to produce ATP and CO2
GLycerol can be kept to create more TAG or transferred to the liver

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5
Q

How are fatty acids transported into the mitochondria?

A

Fatty acids move from the vascular space into the interstitial space via diffusion
Fatty acids move from the interstitial space into the sarcolemma via CD36
Binds to binding protein by muscle fatty acid-binding proteins (FABPc)
Fatty acids combine with CoA to form fatty-acyl-CoA via the action of acyl-CoA synthase
Fatty-acyl-CoA moves across the outer mitochondrial membrane via CPT1 whereby it combines with carnitine to from acyl-carnitine
Acyl-carnitine move across the inner mitochondrial membrane via CPT1 whereby it combines with CoA to form fatty-acyl-CoA

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6
Q

How are fatty acids transported in the blood?

A

Bound to albumin

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7
Q

By what process are fatty acids oxidised?

A

Fatty-acyl-CoA via B oxidation leads to acetyl-CoA (precursor to TCA cycle)

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8
Q

What protein converts pyruvate to acetyl-CoA?

A

Pyruvate dehydrogenase complex

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9
Q

The effect of exercise on substrate oxidation?

A

We change substrate oxidation dependent on exercise intensity
Fat oxidation predominates at ar lower exercise intensities and rest
As intensity increases, CHO contribution begins to predominate

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10
Q

What exercise intensity does fat oxidation predominate carbohydrate oxidation?

A

Lower exercise intensity
Rest
60-65%

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11
Q

What is the consequence of fat oxidation?

A

High muscle glycogen utilisation
Limited muscle glycogen stores
Fatigue

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12
Q

Why is fat oxidation limited at high exercise intensities?

A

Slow mobilisation of fatty acids from adipose tissue/skeletal muscle
Transport of fatty acids into the muscle cell
Transport of fatty acid into the membrane
Oxidation of fatty acids in B-oxidation

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13
Q

What can slow mobilisation of fatty acids from adipose tissue/skeletal muscle to limit fat oxidation at high exercise intensities?

A

Limitation of hormone-sensitive lipase

Reduced blood flow

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14
Q

What can limit the transport of fatty acids into the muscle cell that limit fat oxidation at high exercise intensities?

A

Reductions in CD36 translocation to the membrane

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15
Q

What limits the transport of fatty acid across the membrane that will limit fat oxidation at high exercise intensities?

A

CPT1

Carnitine availability

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16
Q

What are the adaptations to fat oxidation from training? (Talanian et al. 2017; Tunstall et al. 2002)

A

The shift from CHO oxidation to fat oxidation
Talanian et al. 2017 - in pre-trained state fat oxidation increases over-exercise, but training elevates fat oxidation at all time points
Tunstall et al. 2002 - post-training fat oxidation is increased

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17
Q

How are fatty acids converted to ketones?

A

Via acetyl CoA

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18
Q

What are the two main ketones used for energy-transport into tissues?

A

Acetoacetate

B-hydroxybuterate

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19
Q

Define ketosis?

A

Serum (ketone) 1-3mmol/l

Low insulin and glucose

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20
Q

What fuel does the brain predominantly rely on?

A

Glucose

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21
Q

How do ketones reach the brain and what are they used for?

A

Ketones can cross the blood-brain barrier and used as a fuel source

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22
Q

What ketone cannot be converted back into acetyl CoA?

A

Acetone

23
Q

Overview of low carbohydrate, high-fat diets for exercise performance?

A

Increase fat oxidation during exercise
This metabolic adaption occurs;
- in as little as 5 days
- even when muscle glycogen is restored and CHO is available
No performance benefit and performance of high-intensity exercise may be impaired

24
Q

Why is it that despite sparing muscle glycogen we do not observe an increase in exercise performance with a high-fat diet?

A

Using fat is less economical
The Randle Cycle
Transcriptional regulation

25
Q

Is using fat is less economical - oxygen utilisation, substrate oxidation and exercise economy? (Krogh & Lindhard 1920; Burke et al. 2017)

A

Oxygen utilisation doesn’t change as a consequence of training
Oxygen utilisation is higher in low CHO, high data diets from every time point
Fat oxidation is higher in the low CHO, high fat diet
Oxidation of fats produces more FADH2 than CHO, so for the same amount of ATP you consume more O2 when fat is the main fuel source (exercise economy is impaired)

26
Q

What complex transports NADH?

A

Complex 1

27
Q

What complex transports FADH2?

A

Complex 2

28
Q

How many ATPs does one NADH yield?

A

2.5 ATPs

29
Q

How many ATPs does one FADH2 yield?

A

1.5 ATPs

30
Q

How do high-fat diets influence The Randle Cycle (1964)

A

High fat -> elevated FFA concentration in blood -> entres muscle -> increase fatty-acyl-CoA -> increase B-oxidation -> increase acetyl-CoA -> entres TCA cycle -> increase citrate
Acetyl-CoA and citrate slows down CHO metabolism

31
Q

How does acetyl-CoA slow down CHO metabolism?

A

Inhibits pyruvate dehydrogenase thought the stimulation of pyruvate dehydrogenase kinase

32
Q

How does citrate slow down CHO metabolism?

A

Diffuses across the mitochondrial membrane and inhibits phosphofructose-kinase (glycolysis rate-limiting step)

33
Q

What does PPAR-delta stand for?

A

Peroxisome-proliferator activated receptor delta

34
Q

What are transcriptional factors?

A

Proteins that can elicit increases in the expression of a variety of genes

35
Q

What is the role of PPAR-delta?

A

A transcriptional factor for PDK4 which deactivates PDH, slows down CHO metabolism
When activated it induces increases in expression of CD36, CPT1 and FABP?

36
Q

What does FABP stand for?

A

Fatty acid-binding protein

37
Q

What is a key regulator of fat metabolism?

A

Fatty acid-binding protein

38
Q

The relationship between fatty acids and PPAR-delta?

A

Fatty acid upregulates PPAR-delta

39
Q

What is the the role of Fat-P1?

A

Protein involved in binding fatty acids on the skeletal muscle membrane

40
Q

What how does PPAR-delta deactivate pyruvate dehydrogenase?

A

PPAR-delta increases PDK4 levels
PDK4 phosphorylates PDH and render it inactive
PDK4 can also be stimulated by excess acetyl CoA, NADH and reduced pyruvate

41
Q

Overview of high fat/ketogenic diets and biochemistry?

A

Increased fat availability increases fat oxidation and expression of key regulatory proteins (CPT1 and CD36)
Fat oxidation requires more oxygen, therefore, exercise is less economic
Increases fat oxidation results in inhibition of PDH and PDK

42
Q

What is the ratio to NADH/FADH2 when oxidising is purely glucose within skeletal muscle?

A

5:1

43
Q

What is the ratio to NADH/FADH2 when oxidising is purely fat within skeletal muscle?

A

2:1

44
Q

Explain to an athlete how a ketogenic diet might affect oxygen utilisation at a given power output during a 50km time trial?

A

CHO = 5:1 = 14 ATP
Fat = 2:1 = 6.5 ATP
The ketogenic diet is a less economical pathway in terms of ATP production, therefore, would require more oxygen at a given power output if you are relying purely on fat metabolism

45
Q

Explain how a ketogenic diet might affect performance during the time trial?

A

As the ketogenic diet is less economical, you require more oxygen at a given power output during a time trial, so your VO2 would be higher relative to VO2 max and therefore, would cause a performance deficit and limits use of CHO stores
If you go to a sprint as you’re already in a high VO2, you would want to switch substrate to CHO, however, this can not be achieved due to the high acetyl-CoA which inhibits PDH through the activation of PDK, therefore, you cannot convert pyruvate to acetyl-CoA which limits CHO metabolism

46
Q

Compared to a ketogenic diet, how would ketone-salts influence exercise economy?

A

Ketones yield 2 acetyl-CoA
Yields 10 ATP
Exercise economy is better than a ketogenic diet but worse than a CHO diet

47
Q

Compared to a ketogenic diet, how would ketone-salts influence exercise performance?

A

It is more economical and VO2 is less than a ketogenic diet

However, if you want to increase power output, there is still inhibition of PDH

48
Q

Could a ketogenic diet be effective for other sports?

A

Ultramarathon

49
Q

True or false?

Beta oxidation occurs in the mitochondria

A

TRUE

50
Q

True or false?

Fat is transported across the membrane by transport protein CD36?

A

TRUE

51
Q

True or false?

Free fatty acids are transported by the protein albumin?

A

TRUE

52
Q

True or false?

Lipolysis is stimulated by insulin?

A

FALSE

53
Q

Which compound is required for fatty acids transport into muscle mitochondrial?

A

Carnitine

Sport and Exercise Nutrition (9 decks)

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