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Nutrition and Metabolism > Metabolism and Fatigue > Flashcards

Metabolism and Fatigue Flashcards

1
Q

What can creatine kinase tell you about muscle damage?

A

It’s presence can indicate muscle damage, but the amount does not relate to the amount of muscle damage

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2
Q

Why is energy not stored directly all as ATP?

A

too heavy and unstable of a molecule

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3
Q

Can you ever run out of ATP?

A

No. You always have atleast 50% of your ATP stores

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4
Q

How long does it take PCr to recover?

A

2 min for 80%,, 3-4 min for 100%

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5
Q

Why is glycogen more efficient to break down than glucose during glycolysis?

A

It is already partially oxidised.

  • Conversion of glycogen to g6p via glycogen phosphatase does not require ATP
  • Conversion of glucose to g6p via hexokinase does require ATP
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6
Q

What is the difference between lactate and lactic acid?

A

Lactic Acid does not accumulate, Lactate does. Lactate is made when Lactic acid dissociates from hydrogen ions

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7
Q

How may hydrogen ion accumulation associated with lactate accumulation contribute to fatigue?

A
  • Metabolic acidosis, inhibiting glycogen phosphorylase and PFK and thus glycolysis (but only in vitro, not in vivo)
  • Inhibition of calcium release and binding with troponin, impacting cross-bridge formation
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8
Q

How may inorganic phosphate contribute to fatigue?

A

-Accumulation impacts PCr breakdown by Creatine Kinase, also potential inhibition of calcium uptake to sarcoplasmic reticulum

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9
Q

What process can break down lipids for use in the Krebs Cycle and Oxidative phosphorylation to produce energy?

A

-Beta Oxidation

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10
Q

What is beta oxidation?

A

Conversion of fatty acids and glycerol into acetyl-CoA

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11
Q

What are the two ways lactate can be used as fuel?

A
  • Transported to and oxidised by other tissues, via intercellular lactate shuttling
  • Used as a gluconeogenic precursor by the liver
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12
Q

Explain intracellular lactate shuttling

A

Lactate Dehydrogenase converts lactic acid back into pyruvic acid, providing the necessary substrates to continue with aerobic glycolysis

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13
Q

What can we glean from high blood lactate concentration?

A

Either high lactate production, or poor lactate clearance, but not necessarily one or the other.

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14
Q

Summarise lipid oxidation briefly

A
  • Triacylglycerol is broken down into glycerol and 3 NEFA. Glycerol and NEFA are then converted into Acetyl CoA
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15
Q

Where is Vitamin B1 used metabolically, and where can you find it in diet?

A

Involved in krebs cycle, found in brown rice and wheat

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16
Q

Where is Vitamin B5 used metabolically, and where can you find it in diet?

A

Part of Acetyl CoA, comes from eggs and wheat

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17
Q

Where is Vitamin B2 used metabolically, and where can you find it in diet?

A

Part of FAD, Comes from Green Leaves and Dairy

18
Q

Where is Vitamin B6 used metabolically, and where can you find it in diet?

A

It is a coenzyme for glycogen phosphorylase. Found in Green Leaves, avocado, egg and banana

19
Q

Where is Vitamin B12 used metabolically, and where can you find it in diet?

A

Used in Krebs Cycle, comes from microbacteria or synthetic fortification

20
Q

What is the cause of fatigue in the oxidative system?

A
  • Muscle glycogen depletion
  • Liver Glycogen Depletion
  • Hypoglycemia
21
Q

What are the associated issues contributing to fatigue in the oxidative system?

A
  • Dehydration

- Reduced Central Drive

22
Q

Why does dehydration contribute to fatigue?

A

-Lower blood volume means heart has to work harder to deliver nutrients and oxygen to the muscle, and muscle does not receive them at a high enough rate

23
Q

Is glycogenin necessary for glycogen synthesis?

A

-Testoni et al 2017 found that glycogen synthesis can occur without glycogenin and may actually be increased, though also reducing mitochondrial oxidation

24
Q

DESCRIBE the steps of glycogen synthesis

A

Glucose to G6P to G1P to Uridine Disphosphate-Glucose (1 Glucosyl Unit).
Glycogenin makes a chain on itself, glycogen synthase continues it, glycogen branching enzyme makes branches. Initially made glycogen is called proglycogen, then gets converted to macroglycogen over time when enough glucosyl units have been added.

25
Q

What is the difference between proglycogen and macroglycogen?

A

Proglycogen: Low molecular weight, acid insoluble. Synthesised quickly.
-Macroglycogen: High molecular weight, acid soluble. Synthesised slowly.

26
Q

what are catecholamines?

A

Adrenal hormones

27
Q

What factors are muscle glycogen oxidation rates dictated by?

A
  • Exercise Intensity
  • Glycogen Availability
  • Exercise Duration
  • Blood Glucose Availability
  • Training Status
  • Sex
28
Q

How does exercise intensity affect glycogen oxidation rates?

A

-Catecholamine release increases glycogen oxidation

29
Q

How does glycogen availability impact its oxidation?

A

Autoregulation; Oxidation rate is high when storage is high, but is low when it is low.

30
Q

How does exercise duration impact glycogen oxidation rate?

A

Longer duration exercise is associated with increased NEFA utilisation

31
Q

How does blood glucose availability impact glycogen oxidation rates?

A

Higher blood glucose spares glycogen.

32
Q

How is glycogen oxidation during exercise impacted by sex?

A

Women use less glycogen than men, women have a lower adrenaline response so use less, but also have a higher insulin response to feeding so better recovery

33
Q

How much glycogen is there in various parts of the body, in grams?

A

250-500g in muscle
10-15g in systemic circulation
80-110g in liver
7.5g in kidneys, in fed state.

34
Q

What role do the kidneys have with reference to glucose in the fasted/starved state?

A

40% of gluconeogenesis in the fasted/starved state

35
Q

Why does fat use decrease at a high intensity?

A

-Reduced oxidation of all lipid sources due to reduced mobilisation of NEFA due to adrenaline secretion blocking bloodflow to fatty tissues, and limited mitochondrial NEFA uptake.

36
Q

Why dos fat use increase at long duration?

A
  • Glycogen depletion

- Elevated rate of lipid oxidation due to increased NEFA availability due to catecholamines increasing lipolysis

37
Q

What is lipid oxidation dictated by?

A
  • Exercise intensity
  • Exercise Duration
  • Sex
38
Q

What is central fatigue? General definition

A
  • A form of fatigue associated with:
  • changes in the synaptic concentration of neurotransmitters within the central nervous system
  • Affects exercise performance and muscle function
  • Can not be explained by peripheral factors that affect muscle function
39
Q

Explain central fatigue with reference to neurotransmitters

A

Increased serotonin near the end of prolonged exercise can influence arousal, lethargy and mood. Increasing brain concentrations has been found to induce fatigue.

40
Q

How does exercise increase serotonin?

A
  • Free tryptophan turns into serotonin (Not rate limited). Albumin is bound to serotonin. Exercise makes NEFA attach to albumin, freeing the tryptophan. The higher your blood NEFA, the more free tryptophan so more serotonin
41
Q

What is the case where having high blood NEFA will not necessarily increase your serotonin?

A

Large Neutron Amino Acids share the same transport pathway across the blood/brain barrier as tryptophan so if you have high LNAA, it will completely inhibit tryptophan transport, thus stopping serotonin production

42
Q

How can we delay central fatigue?

A
  • Reduce brain serotonin synthesis
  • Reduce the rate of muscle glycogen utilisation
  • Maintain euhydration?
  • Reduce the rate of intramuscular fat utilisation?
  • Increase pre-exercise muscle glycogen availability?
  • Increase muscle PCr?
  • Reduce metabolic acidosis?

Nutrition and Metabolism (5 decks)

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