Lecture G Flashcards
(92 cards)
1
Q
T/F
Energy from fat only available aerobically
A
T
2
Q
Typical male has ?% fat
A
15-20
3
Q
Athlete have ?% fat
A
3-5%
4
Q
Typical female have what percentage fat
A
25-33%
5
Q
Athlete female have ?% fat
A
7-10% fat
6
Q
T/F
> 90%. Of fat in body is in TAG form
A
T
7
Q
Lipolysis is breakdown of
A
TAG
8
Q
In fed state lipolysis
A
Decreases
9
Q
During exercise lipolysis
A
Increases
10
Q
Hormone sensitive lipase is controlled primarily
A
Via phosphorylation /dephosphorylation
11
Q
T/F
At rest HSL is unphosphorylated/inactive
A
T
12
Q
Lipids in adipocytes are surrounded by
A
Perilipins
13
Q
Perilipins inhibit
A
Lipolysis
14
Q
Phosphorylation of HSL and perilipins
A
Increase activation of HSL
Prevent perilipin inhibition of lipolysis
15
Q
Lipolysis regulated by how many hormones and how many NT?
A
Regulated by 1 hormone and 2 NT
16
Q
NTs that regulate lipolysis
A
Epinephrine
Norepinephrine
17
Q
Hormone that regulate lipolysis
A
Insulin
18
Q
Functions of epinephrine and norepinephrine
A
Binds to B adrenergic receptor on fat cells and activates lipolysis
19
Q
Function of insulin on lipolysis
A
Binds to insulin receptor
Increases glucose transport into fat cells
Activates enzymes that decrease lipolysis
20
Q
What determines Fat mobilization
A
Balance between b-adrenergic and alpha 2 adrenergic catecholamine binding
21
Q
T/F
–balance between β-adrenergic and alpha 2 adrenergic catecholamine binding is altered in obese individuals
A
T
22
Q
Growth hormone secreted from
A
Anterior pituitary
23
Q
Cortisol is secreted from
A
Adrenal cortex
24
Q
GH and cortisol are secreted in response to
A
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?)
