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EXCI 445 > Chapter 3- Fuel for Muscle and Exercise Metabolism > Flashcards

Chapter 3- Fuel for Muscle and Exercise Metabolism Flashcards

1
Q

what provides energy for muscle contraction?

A

the breakdown of ATP into inorganic phosphate and ADP

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2
Q

what are type I fibers ?

A

slow-acting, more myoglobin therefore more capacity for oxidative metabolism

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3
Q

what are type II fibers

A

fast-acting, fewer mitochondria and capillary supply, fatigue rapidly

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4
Q

what are the three things contained in skeletal muscle

A

75% water
20% protein (myosin, actin, tropomyosin)
5% salts and substances

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5
Q

the hydrolysis of ATP yields how many kJ? kcal ?

A

31 kJ or 7 kcal

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6
Q

what is the formula of ATP hydrolysis ?

A

ATP + H2O=> ADP+ Pi + H+

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7
Q

what are the three mechanisms involved in resynthesis of ATP

A

PCr hydrolysis
glycolysis
TCA cycle

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8
Q

what is the resting concentration of ATP in muscle? what does this imply

A

4-5 mmol/kg ww muscle (only enough energy for a few seconds)

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9
Q

when does PCr hydrolysis begin ? what is its purpose

A

at immediate onset of contraction to buffer ADP accumulation after you use up the initial quantity of ATP in muscle. this prevents rapid acidification of the muscle and therefore premature fatigue

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10
Q

how much is [PCr] in sarcoplasm compared to ATP

A

3-4x

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11
Q

why can’t we rely only on PCr hydrolysis ?

A

rate of PCr hydrolysis declines after only a few seconds of maximal force contraction

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12
Q

where does PCr hydrolysis occur

A

the sarcoplasm

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13
Q

how does glucose uptake from blood happen? with help from what ?

A

GLUT4 transporter

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14
Q

what occurs to prevent the loss of glucose from the cell after it passes through the transporter in the muscle ?

A

an irreversible phosphorylation catalyzed by hexokinase.

glucose + ATP => ADP+ glucose-6-phosphate

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15
Q

why is the transformation of glucose into glucose-6-phosphate irreversible in the muscle and not the liver?

A

because skeletal muscles lack the enzyme glucose-6-phosphatase, but the liver does not

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16
Q

how does one control the production of glucose-6-phosphate in the skeletal muscle ?

A

by negative feedback on hexokinase

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17
Q

how does one break down muscle glycogen in order to utilize it ? (formula)

A

glycogen phosphorylase breaks off glucose molecule from glycogen

glycogen + Pi => glucose-1-phosphate + glycogen shorter by one glucose

then, glucose-1-phosphate has the Pi placed on a different carbon to become glucose-6-phosphate with phosphoglucomutase

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18
Q

what is the amount of ATP used in glycogen breakdown ?

A

none

you use an inorganic phosphate to bind to glucose so no ATP needed

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19
Q

what does phosphoglucomutase do

A

in glycogen breakdown, glucose-1-phosphate has the Pi placed on a different carbon to become glucose-6-phosphate

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20
Q

what are the two sources for glycolysis

A

glucose and glycogen

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21
Q

what is the main step between glucose/glycogen and pyruvate in glycolysis ?

A

fructose-1,6-bisphosphate is cleaved by aldolase into 2 glyceraldehyde-3-phosphate

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22
Q

when pyruvate is produced, what are the two pathways for it ?

A

either it becomes lactate or acetyl CoA

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23
Q

how does pyruvate become lactate

A

with lactate dehydrogenase

pyruvate+ NADH => lactate+ NAD+

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24
Q

how does pyruvate become acetyl coA

A

with pyruvate dehydrogenase

pyruvate+ CoA + NAD+ => Acetyl CoA + NADH

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25
Q

in glycolysis from glucose, what is the total ATP produced ? the net ATP produced ?

A

total ATP = 4 (2 from each glyceraldehyde-3-phosphate)

net = 4-2 = 2

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26
Q

in glycolysis from glycogen, what is the total ATP produced ? the net ATP produced ?

A

total ATP = 4

net= 4-1 = 3

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27
Q

what happens if glycolysis is too fast?

A

availability of NAD+ (necessary cofactor) becomes the limiting factor, and the reaction is limited at the 2 3C chain split (stays at glyceraldehyde 3-phosphate)

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28
Q

how can one regenerate the NAD+ in muscle ?

A

reduction of pyruvate to lactate

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29
Q

when does lactate formation occur ?

A

always, it’s just that it accumulates in heavy exercise

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30
Q

how does the body deal with lactic acid accumulation ?

A

lactate brought to liver and converted back to glucose in the Cori Cycle

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31
Q

what does the Cori Cycle do

A

lactate brought to liver and converted back to glucose

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32
Q

what is the main goal of the Cori Cycle

A

gluconeogenesis

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33
Q

in resting state, how many ATP and lactate are needed in the Cori Cycle to produce 1 glucose ?

A

2 lactate and 6 ATP

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34
Q

where is the Cori Cycle taking place ? why

A

the liver because lactate can only go to pyruvate and therefore glucose in the liver

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35
Q

what does TCA cycle stand for

A

tricarboxylic acid cycle (Krebs)

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36
Q

what are the two main sources of energy for the TCA cycle

A

fats and carbs

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37
Q

where does the TCA cycle occur ?

A

in the mitochondrion

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38
Q

where does glycolysis occur ?

A

cytoplasm/sarcoplasm

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39
Q

how does a pyruvate get into the TCA cycle ?

A

it has to first go to the mitochondrion from the cytoplasm

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40
Q

what are the two nutrients needed in enzymatic reactions ?

A

NADH and FADH2

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41
Q

what and where is the electron transport chain

A

creates a proton gradient across inner membrane and mitochondrial matrix

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42
Q

what does oxygen do in the ETC

A

removes electrons from the chain

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43
Q

how much ATP is made from ETC ?

A

38 ATP

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44
Q

after how long is glycogen depleted in exercise ?

A

1-2 h

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45
Q

what determines the sustainability of an exercise ?

A

glycogen stores

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46
Q

what is the enzyme responsible for lipolysis

?

A

hormone-sensitive lipase

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47
Q

what are the 5 hormones that stimulate HSL ?

A 
epinephrine
norepinephrine
glucagon 
cortisol 
growth hormone
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48
Q

what inhibits HSL ?

A

insulin

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49
Q

what does HSL do ?

A

breaks down triacylglycerol into glycerol and 3 FA which go into the blood

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50
Q

break down the source of the 38 ATP from the complete oxidation of one glucose molecule

A

from glycolysis:
2 + 6 (from NADH)

from TCA:
24 (from NADH) + 4 (from FADH2) + 2 (from GTP)

therefore 38 in total

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51
Q

how do fatty acids enter the mitochondria ?

A

< or = to 12 carbons without membrane transporter

> or = to 14 carbons with membrane transporter

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52
Q

why does insulin inhibit HSL ?

A

bc it promotes TG synthesis

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53
Q

during prolonged moderate exercise, what is the rate of lipolysis and the rate of entry of FA into circulation like ?

A

adipose tissue blood flow increases

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54
Q

during intense exercise, what is the rate of lipolysis and the rate of entry of FA into circulation like ?

A

SNS vasoconstriction causes fall in adipose tissue blood flow, meaning accumulation of FA in adipose tissue

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55
Q

the concentration of what limits fat mobilization during intense exercise

A

lactate because a high amount promotes re-esterification (more TG) and therefore limits entry of FA into bloodstream

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56
Q

what happens to glycerol once it’s in the circulation ?

A

taken up by liver or converted into glucose

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57
Q

what happens to FA once they are in circulation ?

A

loosely bounded with albumin for the most part

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58
Q

what is uptake of FA by muscle related to directly ?

A

the plasma FA concentration

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59
Q

how do long chain (= or > 14 carbon) FFA get into the mitochondria for oxidation ?

A

via the carnitine shuttle

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60
Q

what is the carnitine shuttle ?

A

two forms of carnitine-acyl-transferase in the mitochondrial membrane of the muscle. CAT-I outside membrane, CAT-II on inner surface.

FFA becomes FA-CoA or acyl-CoA with acyl-CoA synthetase
then, at the outer membrane, acyl-CoA releases its CoA and binds to carnitine (fatty acyl-carnitine + free CoA) which transports it across membrane in carnitine transporter.. then in the mitochondrion, carnitine is removed and fatty acyl-CoA is reformed

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61
Q

what is the main rate-limiting step in utilization of FFA for energy ?

A

carnitine shuttle

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62
Q

beta-oxidation cleaves how many carbons at a time? what does this imply for the beta oxidation of a 16 carbon FA ?

A

2 carbons at a time

for a 16C- cleave 7 times

63
Q

what is CAT I (carnitine acyl-transferase) inhibited by ?

A

malonyl CoA

64
Q

what does malonyl CoA do ?

A

promote TG formation in cell and therefore inhibits CAT I

65
Q

what does beta-oxidation achieve ?

A

breakdown of carbons in order to create acetyl CoA to be used in TCA

66
Q

what are ketones ?

A

by-products of incomplete fat catabolism

67
Q

what are 3 examples of ketones ?

A

acetone
acetoacetate
beta or 3-hydroxybutyrate

68
Q

what do ketones consist of

A

2 acetyl CoA form acetoacetate which then can transform reversibly or irreversibly into other ketones

69
Q

what ketone reaction is irreversible

A

acetoacetate to acetone

70
Q

what is ketosis ?

A

elevated concentration of ketone bodies (>3mg/dL)

71
Q

what is ketoacidosis ?

A

concentration of ketones > 90 mg/dL

overwhelms normal compensatory mechanisms

72
Q

in a type I diabetic, what will be the concentration of ketones ?

A

90 mg/dL

73
Q

in a healthy person, what will be the concentration of ketones ?

A

<3 mg/dL

74
Q

when would a ketogenic diet be suggested ?

A

pediatric epilepsy

75
Q

what 2 normal compensatory mechanisms do we have for ketosis ?

A

bicarbonate buffering

and respiratory compensation

76
Q

usually, proteins contribute to how much of energy provision ?

A

5%

77
Q

when do proteins contribute more to energy ?

A

starvation or depletion of glycogen stores

78
Q

what are the two things that happen before a protein can be oxidized ?

A

transamination (removal of NH2 group, transfer it to a ketoacid to form a different amino acid)

deamination (formation of ammonia)

remaining molecule can enter TCA

79
Q

how many amino acids can be oxidized to significant amounts ?

A

6

80
Q

what are the 6 amino acids that can be oxidized to significant amounts ?

A 
leucine
isoleucine
valine
asparagine
aspartate
glutamate
81
Q

how is energy extracted from protein amino acids ?

A

after it is digested and absorbed into liver, it can be synthesized into proteins or released into blood for cellular uptake

82
Q

if there is excess protein consumption, what happens ?

A

used for energy, and the extra is converted into fatty acids for storage as TG

83
Q

why is it untrue that more protein= more muscle ?

A

because extra protein will turn into TG in storage

84
Q

what are the two kinds of amino acids in terms of structure ?

A

glucogenic and ketogenic

85
Q

give 5 examples of glucogenic a.a

A 
alanine
glycine
serine
cysteine
tryptophan
86
Q

give 2 examples of ketogenic a.a

A

lysine, leucine

87
Q

what happens to the carbon skeletons of glucogenic a.a ?

A

turn into pyruvate, which will then either go to gluconeogenesis in the liver or become acetyl coA and to into TCA

88
Q

what happens to the carbon skeletons of ketogenic a.a ?

A

turn into acetyl coA and then either become FFA, ketones, or go into TCA

89
Q

in the process of deamination in the liver, what happens to the NH3 (ammonia) ?

A

becomes urea and excreted by kidneys in urine

90
Q

what is gluconeogenesis ?

A

formation of glucose from non carb sources such as protein

91
Q

how do CHO intake impact protein metabolism

A

low CHO = high protein metabolism

92
Q

at 60% VO2max what is one’s main source of energy at the onset of workout ?

A

ATP and PCr

93
Q

at 60% VO2max what is one’s main source of energy at 5-10 s of workout ?

A

glycolysis

94
Q

at 60% VO2max what is one’s main source of energy after a few minutes ?

A

glycogen stores

95
Q

at 60% VO2max what is one’s main source of energy at 30 min ?

A

glycogen but starting to metabolize fat

96
Q

at 60% VO2max what is one’s main source of energy at 45 min ?

A

glycogen and fat

97
Q

how much glycogen is stored in liver and muscle and blood

A

liver: 100g
muscle: 300g
blood: 0.9g/L or 5 mmol/L

98
Q

where is fat stored ?

A

in white adipose tissue and also intramuscularly

99
Q

where is fat found in muscle ?

A

dispersed along muscle fibers, close to mitochondria within fibers

100
Q

what supports the view that intramuscular fat could be a good source of energy during prolonged exercise ?

A

decrease of intramuscular triglyceride post-exercise

101
Q

which fibers contain more intramuscular triglyceride ?

A

type I

102
Q

which nutrient is the best at energy storage ?

A

fat

103
Q

what is the drawback to fat as fuel ?

A

slow, takes more time to tap into it as source of fuel

104
Q

1g fat, carb, protein= ? kcal

A

1 g fat= 9 kcal
1 g carb = 4 kcal
1 g protein = 4 kcal

105
Q

why are carbs not as efficient in storage ?

A

1g carb stored with 3g water, less efficient and can be overloaded with water

106
Q

how much exercise time can blood, muscle, and liver CHO provide ?

A

2 hrs

107
Q

how much exercise time can fat provide ?

A

> 80 hrs but you need to know how to utilize it

108
Q

how much exercise time can protein provide ?

A

30 hours but rarely used (only in dire situations)

109
Q

what is the limitation to fat as fuel in high intensity exercise ?

A

can’t maintain exercise at an intensity higher than 60% VO2max

110
Q

what are 4 intramuscular factors that regulate mobilization of fuels

A

ATP/ADP
Pi
AMP
Ca2+

111
Q

how does ATP regulate fuel mobilization

A

decline in ATP cellular concentration means parallel increases in ADP and AMP, directly stimulate anaerobic and oxidative resynthesis

112
Q

what is the rate-limiting step in glycolysis ?

A

conversion of fructose-6-phosphate to fructose-1,6-diphosphate by phosphofructokinase (PFK)

113
Q

what is the rate-limiting step in glycogen breakdown to prepare for glycolysis ?

A

glycogen phosphorylase concentration who converts glycogen to glucose-1-phosphate

114
Q

what is the rate-limiting step in carb oxidation

A

from pyruvate to acetyl coA by pyruvate dehydrogenase

115
Q

what is the rate limiting step in the TCA cycle ?

A

citrate synthase concentration

116
Q

what controls glycogen phosphorylase in the rate-limiting step of glycogen breakdown

A

glycogen breaking down to glucose-1-phosphate

+ AMP, Pi, Ca2+, epinephrine
- ATP

117
Q

what controls phosphofructokinase in the rate-limiting step of glycolysis

A

fructose-6-phosphate going to fructose-1,6-diphosphate

+ ADP, AMP, Pi, NH4+
- ATP, H+

118
Q

what controls pyruvate dehydrogenase in rate limiting step of carb oxydation

A

pyruvate goes to acetyl coa

+ Ca2+, ADP, CoA, NAD+
- ATP, NADH

119
Q

what controls citrate synthase in rate limiting step of TCA ?

A

+ ADP, NAD+

- ATP, NADH

120
Q

which hormone is anabolic ?

A

insulin

121
Q

which hormones are catabolic ?

A

all those we’ve learned except insulin

122
Q

glucagon: how is it stimulated and what does it do

A

stimulated by fall in blood glucose

stimulates gluconeogenesis and liver glycogen breakdown

123
Q

epinephrine: how is it stimulated and what does it do

A

stimulated by stress and fall in blood glucose

stimulates glycogen breakdown and lipolysis

124
Q

norepinephrine: how is it stimulated and what does it do

A

stimulated by stress, fall in blood glucose and BP

stimulates glycogen breakdown and lipolysis

125
Q

cortisol: how is it stimulated and what does it do

A

stimulated by stress, ACTH, interleukin-6

stimulates protein breakdown, lipolysis, gluconeogenesis

126
Q

growth hormone: how is it stimulated and what does it do

A

stimulated by stress

stimulates lipolysis

127
Q

interleukin-6: how is it stimulated and what does it do

A

stimulated by Ca2+ and decreased glycogen

stimulates glycogen breakdown, cortisol secretion, lipolysis

128
Q

insulin : how is it stimulated and what does it do

A

stimulated by rise in blood glucose and amino acid
stimulates uptake of blood glucose and amino acids
inhibits lipolysis and protein breakdown

129
Q

why does Ca2+ cause positive feedback for energy ?

A

stimulates GLUT4 translocation and therefore glucose uptake

130
Q

in exercise, what is enhanced in order for cells to take in glucose ?

A

GLUT4

131
Q

how is insulin enhanced in exercise ?

A

it’s not

132
Q

what promotes GLUT4 translocation

A

Ca2+ increase due to exercise

133
Q

what mostly promotes GLUT4 at rest ? in exercise

A

at rest: insulin

in exercise : Ca2+

134
Q

how does epinephrine and glucagon act upon a cell to activate HSL ?

A

bind to membrane, release adenylate cyclase and enzyme cascade, covalent activation leads to hormone activation

135
Q

what role does cortisol have in lipolysis ?

A

increases effectiveness of catecholamines

136
Q

if you stop exercising, does lipolysis stop right away

A

no

137
Q

what is fatigue ?

A

inability to maintain work at a given force/power output

138
Q

what will the rates of anaerobic ATP resynthesis be like from PCr hydrolysis over time ?

A

at first, strong

then, declines abruptly until there is almost none at 20-30s

139
Q

what will the rates of anaerobic ATP resynthesis be like from glycolysis over time ?

A

slowly increase until a drop at 20-30s

140
Q

in a graph with x=time and y=g glycogen/kg muscle, how will the slope vary with varying %VO2max

A

at 120%VO2max, extremely sharp drop in slope
then less and less sharp drop
30% VO2max depletion much slower, since there is also fat oxidation that supplies energy

141
Q

in a graph with x=time and y=g glycogen/kg muscle, what are the two things we can look at with varying %VO2max

A

the slope of decline in glycogen and also the duration of the exercise
30%Vo2max able to last longer and with less of a decline in glycogen bc there is also fat utilization

142
Q

why is there a drop in plasma FA at 30 min of exercise ?

A

fatty acid oxidation takes time, usually starts at 30 min after prolonged exercise, therefore will use up plasma FA until lipolysis comes through at 30 min

143
Q

when does peak uptake of glucose occur regardless of exercise intensity ?

A

90 min

144
Q

how can one increase the utilization of glucose depending on the intensity of the workout ?

A

increase intensity and you’ll uptake more glucose

145
Q

as duration of exercise increases, which fuel utilization will increase the most ?

A

fat

146
Q

as duration of exercise increases, which fuel utilization will decrease the most ?

A

muscle glycogen

147
Q

what is a way of replenishing glycogen stores ?

A

sports drinks

148
Q

in resting post-absorptive state, glucose release is enough only for what ?

A

CHO demands of CNS

149
Q

energy going to CNS in post absorptive state is what%

A

70% CHO from liver glycogen

30% from gluconeogenesis

150
Q

in exercise, rate of hepatic glucose release related to what

A

exercise intensity (contribute to 90% CHO)

151
Q

in trained athletes, how will hormone concentrations change during exercise ?

A

they will have an attenuated response

152
Q

what will happen to intramuscular triglyceride content in trained athletes ?

A

increase concentration due to better fat utilization

153
Q

how will rate of lactate accumulation change in trained athletes ?

A

decrease

154
Q

how will rate of muscle glycogen and glucose change in trained athletes ?

A

decrease

EXCI 445 (13 decks)

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