Lecture G Flashcards Preview

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Flashcards in Lecture G Deck (92):
1

T/F

Energy from fat only available aerobically

T

2

Typical male has ?% fat

15-20

3

Athlete have ?% fat

3-5%

4

Typical female have what percentage fat

25-33%

5

Athlete female have ?% fat

7-10% fat

6

T/F

>90%. Of fat in body is in TAG form

T

7

Lipolysis is breakdown of

TAG

8

In fed state lipolysis

Decreases

9

During exercise lipolysis

Increases

10

Hormone sensitive lipase is controlled primarily

Via phosphorylation /dephosphorylation

11

T/F

At rest HSL is unphosphorylated/inactive

T

12

Lipids in adipocytes are surrounded by

Perilipins

13

Perilipins inhibit

Lipolysis

14

Phosphorylation of HSL and perilipins

Increase activation of HSL
Prevent perilipin inhibition of lipolysis

15

Lipolysis regulated by how many hormones and how many NT?

Regulated by 1 hormone and 2 NT

16

NTs that regulate lipolysis

Epinephrine
Norepinephrine

17

Hormone that regulate lipolysis

Insulin

18

Functions of epinephrine and norepinephrine

Binds to B adrenergic receptor on fat cells and activates lipolysis

19

Function of insulin on lipolysis

Binds to insulin receptor
Increases glucose transport into fat cells
Activates enzymes that decrease lipolysis

20

What determines Fat mobilization

Balance between b-adrenergic and alpha 2 adrenergic catecholamine binding

21

T/F

--balance between β-adrenergic and alpha 2 adrenergic catecholamine binding is altered in obese individuals

T

22

Growth hormone secreted from

Anterior pituitary

23

Cortisol is secreted from

Adrenal cortex

24

GH and cortisol are secreted in response to

Exercise and stress

25

GH and cortisol may interfere with ability of insulin to

Inhibit lipolysis

26

Function of Adenosine

Activates the inhibitory G protein
Thus inhibits lipolysis

27

Function of Estrogen

Very moderate inhibition of lipolysis

28

Key regulatory mechanism in lipolysis

Phosphorylation of HSL

29

T/F

There is no perilipin in skeletal muscle

T

30

Fate of fA and glycerol,

Formation of fatty acyl CoA
Formation of Glycerol 3-phosphate
Triacylglycerol synthesis

31

TAG synthesis

3 Fatty acyl CoA + 1 glycerol-3-p

32

Esterification

Alcohol + acid ---> Ester

33

During exercise esterification

Decreases

34

During exercise lipolysis

Increases

35

During exercise lipolysis increases results in

Increased FFA in blood

36

What is the primary source of blood FA used for energy by tissue including skeletal muscle

Adipose tissue

37

Carrier protein for transferring FFA from adipose tissue to muscle

Albumin

38

Major site of LCFA oxidation

Skeletal muscle

39

Sourced of FA

Albumin bound FFA
Hydrolysis of VLDL

40

Capillaries in skeletal muscle have -------to release FA from the lipoprotein

Lipoprotein lipase

41

FA must get into ----and -----for beta oxidation to occur

Muscle fiber
Mitochondrial matrix

42

Beta oxidation

Breakdown of FA 2C by 2C to generate acetyl CoA

43

In skeletal muscle there are 2 FA binding protein

FABPpm (FA binding protein , plasma membrane

FAT/CD36 ( FA translocase )

44

High fat diets induce which FA binding protein

Both binding proteins

45

Endurance training induces which binding protein

FABPpm only in males

46

Mitochondrial inner membrane impermeable to

CoA

47

Only FA attached to ----- can cross membrane to enter matrix

Carnitine

48

Carnitine deficiency

Muscle weakness
Poor exercise tolerance
Inability to oxidize FA for energy

49

supplementation: does carnitine improve endurance by improving ability to
oxidize fatty acids? (does it spare glycogen?)

No probably not

50

Beta oxidation happens in

Mitochondrial matrix

51

What happens in beta, oxidation

Repeated cycles of 4 steps, removing 2 carbons at a time until all carbons are acetyl CoA

52

Oxidation of unsaturated fattyacid
18:1

Oleic

53

Oxidation of unsaturated fattyacid

18:2

Linoleic

54

Oxidation of unsaturated fattyacid

18:3 (n6)

Gamma linoleic

55

Oxidation of unsaturated fattyacid

18:3 (n3)

Alpha linoleic

56

Oxidation of unsaturated fattyacid

20:4 (n6)

Arachidonic

57

Usually PUFA have double bonds

Between C9 and C10

58

Formation of ketone bodies is due to

Accumulation of acetyl CoA

59

Increased ketone body formation occurs when

Fatty acyl CoA transport into liver mitochondria accelerated
Beta-oxidation increased
Generation of acetyl CoA exceeds capacity of citric acid cycle to oxidize it

60

T/F
Skeletal muscle, heart and brain can use ketone bodies for energy

T

61

T/F

Typically brain is glucose only, but under severe conditions, brain can use 3-hydroxybutyrate and acetoacetate

T

62

Acetyl CoA oxidized in

TCA cycle

63

Sources of lipid used to fuel exercise

1. adipose stores
2. Intramuscular triacylglycerol
3. Fatty acids from VLDL

64

Exercise effect on esterification

Decreased esterification so more FA released to blood

65

Blood levels of FFA

initially increases UPTAKE of FFA by exercising muscles, so FFA in blood fall
--Adipose tissue lipolysis eventually increases, releasing more FFA into blood,
until it’s release exceeds rate of uptake, and FFA INCREASE

66

T/F

During intense exercise, rate of lipolysis reduced

T

Pay attention : INTENSE

67

During intense exercise, rate of lipolysis reduced why?

Unclear
Maybe due to lactate accumulation, lactate increases esterification

Reduced blood flow to adipose tissue ( due to increased blood flow to working muscles)

68

Lactate-----esterification

Increases

69

Is Fat better fuel for exercising muscle or CHO?

CHO

70

Why CHO is better fuel for exercising muscles ?

1. can generate acetyl CoA for CAC at much higher rate than FA from TAG
2. more ATP per unit of oxygen
3. CHO can generate ATP in absence of oxygen

71

T/F
CHO can generate acetyl CoA for CAC at much higher rate than FA from TAG

T

72

T/F

Fat gives more ATP per unit of oxygen

F

CHO gives more ATP per unit of oxygen

73

T/F

CHO can generate ATP only in presence of oxygen

F

CHO can generate ATP in absence of oxygen

74

T/F

Resting muscle uses fat as its primary fuel

T

75

T/F

When CHO oxidation increases, fat oxidation decreases

T

76

CHO used as precursor for FA synthesis via

Melonyl CoA

77

Glucose to pyruvate

Glycolysis

78

Pyruvate to acetyl CoA

pyruvate dehydrogenase

79

Acetyl CoA combines with OAA to form

Citrate

80

T/F

In well-nourished, RER increases as exercise intensity increases

T

81

Crossover point

exercise intensity beyond which energy produced by CHO oxidation exceeds lipid:

82

Any exercise beyond crossover point reply more and more on

CHO

83

Beyond 90% VO2 max, essentially entirely

CHO

84

T?F
high fat diet alters metabolism during exercise

T

85

Metabolic differences between MCT and LCFA:

no TAG synthesis
no packaging in chylomicrons
directly from gut into blood
enter cells and into mitochondria without carnitine transport
MCT oxidation not depressed by CHO through malonyl CoA mechanism

86

does MCT spare muscle glycogen or blood glucose use

No

87

If during prolonged, submaximal exercise, no glucose ingested:
What happens to level of glucose and RER

RER will decline
After 1 hr , blood glucose declines

88

If glucose consumed during prolonged exercise, what happens to level of glucose and RER

Blood glucose better maintained,
RER decline attenuated
Increase insulin levels
Decrease FFA level
Increase in CHO oxidation
CHO promotes its own oxidation at expense of fat

89

T/F

Training increase fat oxidation and decrease CHO oxidation

T

90

T/F

Training increases IMTG and the ability to oxidize IMTG

T

91

T/F

Trained muscles have higher LPL activity (increased ability to use VLDL

T

92

T/F
Overweight/obese individuals: reduced ability to release and oxidize
FFA during exercise

T
decreased sensitivity
catecholamines? Like insulin resistance?)