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Nutrition & Metabolism > W2 - Chapter 3 - Fuel Sources for Muscle & Exercise Metabolism > Flashcards

W2 - Chapter 3 - Fuel Sources for Muscle & Exercise Metabolism Flashcards

1
Q

What surrounds the myofibrils of a muscle?

A

Sarcoplasmic reticulum

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2
Q

How is energy stored in the sarcoplasm?

A

Triacylglycerol droplets

Glycogen

PCr

small pool of aa

ATP

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3
Q

What are myofibrils composed of?

A

Thick + thin filaments

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4
Q

What ATPase in the muscle breaks ATP down?

A

Myosin ATPase

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5
Q

G-actin

A

Its monomers are polymerised into long strands of fibrous actin (F-actin)

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6
Q

F-actin

A

2 F-actin strands twist together to form thin filament backbone.

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7
Q

What spirals around the F-actin chains?

A

Rod-shaped tropomyosin molecules

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8
Q

3 sub units of troponin

A

Troponin - I

Troponin - T

Troponin - C

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9
Q

What does Troponin - I bind to?

A

Actin

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10
Q

What does Troponin - T bind to?

A

Tropomyosin

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11
Q

What does Troponin - C bind to?

A

Ca2+

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12
Q

Define a sarcomere

A

Smallest contractile unit of a muscle fibre + is the region between 2 z-lines.

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13
Q

What happens when there’s a sufficient amount of Ca2+ + ATP present in the muscle?

A

Actomyosin is formed

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14
Q

When does sliding of the filaments in the muscle happen?

A

When myosin heads form cross-bridges w/ active sites of actin.

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15
Q

What happens in the muscle without Ca2+

A

Tropomyosin blocks myosin binding sites on actin.

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16
Q

How is Ca2+ released from the sarcoplasmic reticulum and into the sarcoplasm of a muscle?

A

AP along sarcolemma + down T-tubules

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17
Q

What does Ca2+ do once released into the sarcoplasm of a muscle?

A

Bind to troponin = change shape = tropomyosin moves away from myosin binding sites.

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18
Q

How is muscle excitation initiated?

A

By arrival of a nerve impulse at muscle membrane via motor end plate.

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19
Q

What do the activated/cocked myosin heads do?

A

Bind to actin

Myosin head then changes to a bent shape = head pulls on thin filament = slides towards centre of sarcomere.

== Power stroke

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20
Q

What also happens during the power stroke?

A

ADP + Pi are released from myosin head.

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21
Q

What happens when a new ATP binds to the myosin head at the ATPase activity site?

A

Myosin cross-bridge detaches from actin.

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22
Q

Energy released per mole of PCr

A

43kJ/mol

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23
Q

What does it mean that PCr has a higher free energy of hydrolysis than ATP?

A

Its P is donated directly to ADP.

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24
Q

When is PCr broken down?

A

When ATP content ⬇️

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25
Q

What is an additional pathway to regenerate ATP when ATP + PCr stores are depleted?

A

Kinase reaction

– ONLY important during high intensity exercise.

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26
Q

When can the total adenylate pool decline rapidly?

A

If AMP conc. of cell ⬆️ during muscle force generation

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27
Q

What is the principal reason for why the total adenylate pool declines rapidly when AMP conc of cell ⬆️ during muscle force generation?

A

By deamination of AMP to IMP

ALSO, by dephospho rylation of AMP –> adenosine.

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28
Q

When does the deamination of AMP to IMP occur?

A

Under low ATP:ADP

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29
Q

When is adenine nucleotide loss important to muscle function?

A

During cond of metabolic crisis

i.e max exercise or later stages of prolonged submax exercise when glycogen stores become depleted.

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30
Q

What carries glucose across cell membrane?

A

Transporter protein - GLUT4

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31
Q

What happens once the glucose molecule has been transported into the muscle cell?

A
  1. Irreversibly phosphorylated

2. Catalyzed by hexokinase

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32
Q

What does attaching a P group to glucose to prod G-6-P mean?

A

Now trapped in cell

33
Q

Do the liver + skeletal muscle contain the G-6-P enzyme?

A

No, just liver.

34
Q

When is hexokinase inhibited?

A

By accumulation of G-6-P

35
Q

What enzyme helps conversion of glucose-1-phosphate to G-6-P?

A

Phosphoglucomutase

36
Q

IN MITOCHONDRIA

Reaction for pyruvate to Acetyl-CoA

A

Pyruvate + CoA + NAD+ – (Pyruvate dehydrogenase) –> AcetylCoA

37
Q

What does insulin promote in regards to fat?

A

Triacylglycerol synthesis

38
Q

What does insulin inhibit in regards to fat?

39
Q

When does adipose tissue bf increase?

A

During prolonged exercise at around 50% of vo2 Max

40
Q

What does sympathetic vasoconstriction during intense exercise cause?

A

⬇️ in adipose tissue bf = accumulation of FA w/in adipose tissue + limits entry of FFAs + glycerol into circulation.

41
Q

Where is glycerol readily soluble?

42
Q

What can happen to the glycerol in the plasma?

A

Taken up into the liver + phosphorylated to G-3-P

43
Q

What can glycerol-3-phosphate be used for in the liver?

A

To form triacylglycerol

OR

oxidised to dihydroxyacetone P

44
Q

What can happen to dihydroxyacetone P

A

Enter glycolytic pathway

OR

be converted to glucose

45
Q

How are most FAs in plasma transported?

A

Loosely bound to albumin

46
Q

What is the uptake of FA by muscle directly related to?

A

Plasma FA conc

47
Q

What must FFAs do to be taken up by muscle?

A

Dissociate from albumin

Then pass through:

  • Endothelial lining of capillary
  • Interstitial fluid
  • Sarcolemma
48
Q

What happens to the FA-albumin complex at the endothelial lining of the blood capillary?

A

Binds to albumin-binding proteins (ABPs)

= allow FAs to be released from albumin = facilities entry into muscle

49
Q

When will FA uptake into muscle only occur?

A

IF ICF FFA conc is less than that in the true aqueous solution in ECF

50
Q

How is the low intracellular FFA conc maintained?

A

By the cytoplasmic FA-binding protein

51
Q

Where does beta-oxidation of FAs occur?

A

Mitochondria

52
Q

What does beta-oxidation of FAs do?

A

Removes 2-C units from FA chain in the form of ACoA.

– ACoA can then enter TCA cycle.

53
Q

How are the fatty ACoA molecules in the muscle sarcoplasm transported into the mitochondria?

A

w/ carnitine.

54
Q

Where is carnitine synthesised?

55
Q

Where is carnitine usually abundant?

A

Tissues that are able to oxidise FAs

56
Q

What enzyme regulates the transport of FA by carnitine?

A

Carnitine acyl-transferase (CAT)

57
Q

What are the forms of CAT found in the muscle?

A

CAT-I

CAT-II

58
Q

CAT-I in the muscle

Where is it located?

What does it do?

A

Outer surface of membrane

Generates acyl-carnitine

59
Q

CAT-II in the muscle

Where is it located?

What does it do?

A

Inner surface of inner mitochondrial membrane

Regenerates ACoA + free carnitine

60
Q

What are CAT-I and CAT-II also referred to as?

A

Carnitine palmitoyl transferase I + II

CPT 1 + CPT 2

61
Q

Why has carnitine been promoted as a dietary supplement?

A

Weight loss by ⬆️ fat oxidation

⬆️ endurance exercise by promoting fat use = sparing limited glycogen stores.

62
Q

What must happen before aa can be oxidised?

A

Removal of amino group

63
Q

Activators of liver glycogen to plasma glucose

A

Glucagon

Epinephrine

Norepinephrine

64
Q

Inhibitors of liver glycogen to plasma glucose

65
Q

Activators of muscle glycogen to glucose-1-phosphate

A

AMP

Pi

Ca2+

Epinephrine

66
Q

Inhibitors of muscle glycogen to glucose-1-phosphate

67
Q

Activators of muscle protein to aa

68
Q

Inhibitors of muscle protein to aa

69
Q

Activators of pyruvate to ACoA

A

Ca2+

ADP

CoA

NAD+

70
Q

Activators of adipose tissue + muscle triacylglycerol to FAs

A

Epinephrine

Glucagon

Cortisol

71
Q

Inhibitors of adipose tissue + muscle triacylglycerol —> FAs

72
Q

What are the catecholamines?

A

Epinephrine

Norepinephrine

73
Q

Where is insulin secreted from?

A

Beta cells of pancreatic islets

74
Q

Where is glucagon secreted from?

A

Alpha cells of pancreatic islets

75
Q

Where is epinephrine secreted from?

A

Adrenal medulla

76
Q

Where is norepinephrine secreted from?

A

Sympathetic nerve endings

77
Q

Where is cortisol secreted from?

A

Adrenal cortex

78
Q

Where is the growth hormone secreted from?

A

Anterior pituitary gland

79
Q

Metabolic changes in response to endurance training

A

⬆️ fat oxidation

⬇️ muscle glucose + glycogen use

Small ⬆️ in circulating hormones

⬆️ FFA transporters in muscle membrane

⬇️ Lactate accumulation

Nutrition & Metabolism (17 decks)

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