Exercise and starvation Flashcards

1
Q

What does creatine/phosphocreatine act as a source for for the heart and muscles?

A
  • Source of phosphate groups
  • Can donate to ADP -> ATP
  • Reserve when ATP falls rapidly in exercise
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2
Q

What enzyme converts creatine to phsophocreatine?

A

Creatine kinase

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3
Q

What can creatine kinase be an important biomarker for identifying?

A

MI

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4
Q

What is creatinine?

A

Spontenously converesed from creatine

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5
Q

What is the amount of creatinine proportional to?

A

Muscle mass

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6
Q

What is creatinine excreted by?

A

Kidneys

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7
Q

When is ATP and creatinine consumed (what period of time)?

A

Within seconds of exercise

  • Used for short intense exertion
  • > Heavy lifting
  • > Sprinting
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8
Q

Why does intensity of exercise diminish over time?`

A

Creatinine and ATP are consumed rapidly

- Other pathways are required for longer exercise (which have a slower metabolism)

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9
Q

What does calcium (released from muscles) activate (what pathways)?

A
  • Glycogenolysis

- TCA cycle

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10
Q

What do Glucagon and epinephrine inhibit to stop fatty acid synthesis?

This occurs in intense aerobic exercise

A

Inhibit Acetyl-CoA Carboxylase (rate limiting step of fatty acid synthesis)

Acetyl CoA + CO2 -> Malonyl-CoA

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11
Q

What process does Malonyl-CoA inhibit?

A

B-oxidation

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12
Q

What vitamin is a cofactor for Acetyl-CoA carboxylase?

A

Biotin

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13
Q

Levels of what molecule fall in intense aerobic exercise, signalling a drop in fattyacid synthesis?

A

Malonyl-CoA

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14
Q

What molecule inhibits Carnitine Palmitoyl Transferase-1?

A

Malonyl-CoA

  • Less fatty acid degraded
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15
Q

What molecule is consumed in exercise which subsequently leads to muscle cramps?

A

NAD+ consumed

  • NAD+ generated in Pyruvate to lactate conversion
  • Increased lactate causes low pH and cramps
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16
Q

What organelle is more abundant in the muscles of distance runners?

A

Mitochondria

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17
Q

The presence of what chemical will cause NAD levels to increase (NADH to decrease)?

A

O2

- NADH can be converted to NAD in the ETC

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18
Q

What are the effects of insulin?

A
  • Glycogen synthesis
  • Increases glycolysis
  • Inhibits gluconeogenesis
  • Promotes glucose -> adipose tissue (used to form triglycerides)
  • Promotes uptake of amino acids by muscle
  • Stimulates protein synthesis / inhibits breakdown
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19
Q

What enzyme found in the liver and pancreas is induced by insulin?

A

Glucokinase (Glu -> G6P)

- ATP -> ADP

20
Q

What enzyme does insulin stimulate?

In regards to glucose/glycogen levels

A

Glycogen synthase

21
Q

What enzyme does glucagon (+epinephrine) stimulate?

In regards to glucose/glycogen levels

A

Glycogen phsophorylase (breaks down glycogen)

22
Q

What molecules/hormones stimulate acetyl-CoA carboxylase (fatty acid synthesis)?

A
  • Insulin

- Citrate

23
Q

What are the effects of glucagon?

A
  • Glycogen breakdown in liver
  • Inhibits fatty acid synthesis
  • Stimulates release of fatty acids from adipose tissue
  • Stimulates gluconeogenesis
24
Q

After how much time fasting will glycogen stores be exhausted roughly?

A

~ 24 hours

25
Q

What is glutamate and pyruvate converted into in the alanine cycle in muscles?

A
  • Alanine

- alpha-KG

26
Q

What substance does Glutmate require in the muscle cells to undergo the alanine cycle?

A

NH4+

27
Q

Where does alanine travel to to create glutamate and pyruvate?

A

The liver

- Also requires a-KG

28
Q

What is glutamate converted into in the liver?

A

NH4+

29
Q

Where does the pyruvate and subsequently glucose travel to to renter the alanine cycle?

A

Muscle tissue

30
Q

What molecule is involved in the cori cycle?

A

Lactate

31
Q

What 2 cycles maintain plasma blood sugar levels during starvation?

A
  • Cori cycle - Lactate

- Alanine cycle

32
Q

Describe the steps involved in glycerol becoming Dihydroxyacetone Phosphate?

A

Glycerol

- > Glycerol-3-Phosphate (enzyme: Glycerol Kinase
- > Dihydroxyacetone Phosphate
enzyme: G-3-P Dehydrogenase)

33
Q

What is the 3-carbon fatty acid that B-oxidation stops at?

A

Propionyl-CoA

34
Q

What is propionyl-CoA converted into to join the TCA cycle?

A

Succinyl-CoA

35
Q

What enzyme converts propionyl-CoA (3C FA) to Succinyl-CoA (TCA cycle or gluconeogenesis)?

A

Propionyl-CoA Carboxylase

36
Q

What vitamin acts as a cofactor for Propionyl-CoA carboxylase?

A

Biotin

37
Q

What causes oedema in Kwashiorkor?

A

Inadequate protein intake

- Hypoalbuminemia -> oedema

38
Q

What is the other malnutrition disease that has normal protein but insufficient total calories?

A

Marasmus

  • Muscle and fat wasting
  • No oedema
39
Q

Hypoglycemia and ketosis in a child, after an overnight fast is can be due to what group of diseases?

A

Glycogen storage diseases

40
Q

What enzyme is deficient in hereditray fructose intolerance?

A
  • Aldolase B
41
Q

When does hereditray fructose intolerance usually present?

A

After weaning from breast milk

42
Q

What is depleted and what can build-up in hereditray fructose intolerance?

A
  • F1P builds up
  • ATP depletes
  • Glucose depleted
43
Q

Disorders of what organelle create hypoketotic hypoglycemias?

A

Mitochondrial disorders

44
Q

Explain how a disorder in the mitochondria can create a hypoketotic hypoglycemia?

A
  • Loss of B-oxidation and gluconeogensis
  • FFA -> B-oxidation -> ketones (B-oxidation), cannot happen as mitochondria not functional
  • First step of gluconeogensis is pyruvate -> oxaloacetate, occurs in mitochondria also
  • Leads to hypoglycemia
45
Q

What are 2 disorders which cause hypoketotic hypoglycemia?

A
  • Carnitine deficiency

- MCAS deficiecy

46
Q

What are the findings in carnitine deficiency?

A
  • Hypoketosis
  • Hypoglycemia
  • Low serum carnitine
  • Low serum acylcarnitine
47
Q

What are the findings in MCAD deficiency?

A
  • Hypoketotic hypoglycemia
  • Medium chain acyl-CoA dehydrogenase
  • Dicarboxylic acids 6-10 carbons in urine
  • High acylcarnitine levels