Metabolism Flashcards

1
Q

What are the four macromolecules?

A

carbohydrates, protein, lipids, nucleic acids

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2
Q

What is metabolism?

A

all the chemical reactions that occur in the body

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3
Q

What are the two principal forms of energy?

A

kinetic and potential

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4
Q

What is chemical energy?

A

potential energy stored in the bond of molecules

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5
Q

How is chemical energy released?

A

digestion of food converted to heat or mechanical energy

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6
Q

What is the human body’s main energy currency?

A

ATP

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7
Q

What is the term for the breakdown of ATP?

A

hydrolysis

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8
Q

Describe the makeup of ATP.

A

3 phosphate groups attached to adenine and 5 carbon sugar (ribose)

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9
Q

What enzyme catalyzes the breakdown of ATP?

A

ATPase

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10
Q

What is the main CHO for energy?

A

Glucose

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11
Q

What transport mechanism does glucose utilize?

A

facilitated diffusion

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12
Q

What is the typical glycogen value for a normally fed, untrained individual?

A

55-85 mmol/kg

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13
Q

What is the typical glycogen value for a normally fed, trained individual?

A

110-135 mmol/kg

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14
Q

What is the typical glycogen value for a well rested individual?

A

180 mmol/kg

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15
Q

What is the typical glycogen value for a CHO loaded individual?

A

220-240 mmol/kg

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16
Q

What nutrient is the most efficient due to its energy yield?

A

Glycogen

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17
Q

How can glycogen be metabolized?

A

both aerobically and anaerobically

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18
Q

Generally describe glycogen storage capacity.

A

it’s limited

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19
Q

What is the term given for glycogen synthesis?

A

Glycogenesis

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20
Q

What is the term given for glucose breakdown?

A

glycolysis

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21
Q

What is the term given to the process by which glycogen is broken down into G1P??

A

Glycogenolysis

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22
Q

Where can glycogenolysis occur?

A

liver or muscle

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23
Q

What is the term given to the process in which new glucose is formed from non-CHO sources?

A

Gluconeogenesis

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24
Q

Where does gluconeogenesis primarily occur?

A

liver

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25
Q

What does it signify when an enzyme has “kinase” in its name?

A

that it adds a phosphate

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26
Q

What does it signify when an enzyme has “phosphatase” in its name?

A

removes a phosphate

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27
Q

What does it signify when an enzyme has “phosphoylase” in its name?

A

splits a compound by adding a phosphate

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28
Q

How is CHO primarily stored?

A

in the form of glycogen

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29
Q

Glycogen breakdown begins by what event?

A

SNS/catecholemines releasing cAMP

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30
Q

cAMP binds to what enzyme for the first step of glycogen breakdown?

A

protein kinase A

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31
Q

What does protein kinase A do for the glycogen breakdown?

A

it adds a phosphate to glycogen synthase to inactivate it and phosphorylates phosphorylase kinase to activate which will activate glycogen phosphorylase for degradation to occur

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32
Q

What ion aids in glycogen breakdown and how?

A

Ca2+ phosphorylase activity

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33
Q

What stimulates glycogen synthesis?

A

insulin

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34
Q

By what mechanism does insulin start glycogenesis?

A

stimulates Protein phosphatase

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35
Q

What does Protein phosphatase do for glycogenesis?

A
  1. it removes a phosphate from glycogen synthase to activate it
  2. it inactivates phosphorylase kinase AND
  3. inactivates glycogen phosphorylase to pause glycogen degradation
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36
Q

True/False: Glycolysis requires oxygen.

A

false, can be anaerobic

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37
Q

What are the two main functions of glycolysis?

A

Produce ATP and pyruvate

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38
Q

Where does glycolysis occur?

A

in the cytosol of the muscle cell

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39
Q

What is glucose broken down into?

A

into 2 3-carbon pyruvates

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40
Q

Glycolysis is the only source of energy for what cell type?

A

RBCs

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41
Q

What is the first step of glycolysis?

A

Glucose enters the cell and in the presence of hexokinase becomes G6P and becomes trapped in cell.

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42
Q

What is the fate of G6P?

A

becomes pyruvate

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43
Q

What other reaction helps with glycolysis?

A

Glycogen -> G1P -> G6P

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44
Q

What are the three rate limiting enzymes for regulation of glycolysis?

A

hexokinase, phosphofructokinase, pyruvate kinase

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45
Q

Which enzyme catalyzes F6P -> F1,6 biphosphate?

A

PFK

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46
Q

What enzyme catalyzes phosphoenolpyruvate -> pyruvate?

A

Pyruvate kinase

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47
Q

What inhibits hexokinase?

A

G6P

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48
Q

What inhibits PFK?

A

ATP

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49
Q

What activates PFK?

A

AMP

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50
Q

What inhibits pyruvate kinase?

A

ATP and acetyl CoA

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51
Q

What activates pyruvate kinase?

A

AMP and F1,6BP

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52
Q

What other compounds are released during glycolysis?

A

NADH

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53
Q

How does NADH become?

A

NAD+ reacts with two H+ and it binds with one and accepts the electron from the other, reducing to NADH

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54
Q

What is the end results of glycolysis?

A

2 net ATP, 2 pyruvate, 2 NADH

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55
Q

What is the fate of pyruvate?

A

becomes lactate or is shuttled to the mitochondria for Krebs

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56
Q

What is the name of the similar enzyme to hexokinase that does the conversion of glucose to G6P in the liver?

A

glucokinase

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57
Q

Why does lactate form?

A

regenerate the NAD+ needed to continue oxidizing glucose

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58
Q

Lactate produces when there is a mismatch between what two things?

A

rate of pyruvate production and ability of PDH and mitochondrial shuttle systems to remove pyruvate and NADH

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59
Q

Lactate accumulation occurs when what events happen?

A

production exceeds clearance, insufficient O2 delivery, inadequate PDH activation

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60
Q

What are the three places lactate can be shuttled?

A

mitochondria, adjacent muscle fiber, and liver/heart/muscle cells

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61
Q

What ultimately happens to lactate?

A

is transported back to the liver for conversion back to pyruvate and then to glucose (via gluconeogenesis)

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62
Q

What is the fate of pyruvate?

A

form acetyl CoA

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63
Q

What enzyme catalyzes the oxidative decarboxylation of pyruvate?

A

pyruvate dehydrogenase

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64
Q

How many rounds of Krebs is in a cycle after glycolysis?

A

2 (1xpyruvate)

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65
Q

What is the relationship between exercise intensity and PDH activation?

A

Increases together (then stays stable)

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66
Q

What regulates PDH?

A

calcium, pyruvate, many other substrates and cofactors

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67
Q

Describe how the Kreb’s cycle works.

A

acetyl CoA combines with oxaloacetate to form citrate and as it converts back, it looses two CO2, releases 3 NADH, 1 FADH2, and converts one ADP to ATP

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68
Q

What is the end result of the Krebs cycle?

A

2 ATP, 6 NADH, 2 FADH2 (4 electrons each)

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69
Q

Describe how the Electron Transport chain works.

A

NADH and FADH2 turn back to their OG form (NAD+ and FAD+) and the H+ atoms are passed down the chain to form a proton concentration gradient to provide energy for ATP production, O2 serving as the final electron acceptor - forms water. As H+
ions flow down their gradient and back into the matrix, they pass through an enzyme called ATP synthase, which harnesses the flow of protons to synthesize ATP.

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70
Q

What happens if O2 is not available for the ETC?

A

if oxygen isn’t there to accept electrons, the electron transport chain will stop running, and ATP will no longer be produced

71
Q

How many H+ pass through ETC for 1 ATP?

A

4

72
Q

How much ATP is formed from NADH?

A

2.5

73
Q

How much ATP is formed from FADH2?

A

1.5 ATP

74
Q

What is the end result of one glucose molecule?

A

10 NADH, 10 H, 2 FADH2, and 4 ATP = 32 ATP

75
Q

Name some inhibiting factors that control glucose oxidation.

A

glucagon (inhibits PFK), citrate (inhibits PFK), ATP (inhibits PFK and Pyruvate kinase), NADH (inhibits citrate formation and pyruvate dehydrogenase)

76
Q

Name some stimulating factors that control glucose oxidation.

A

ADP (stimulates PFK)

77
Q

What is the relationship between exercise intensity and energy source?

A

higher intensities rely more on muscle glycogen

78
Q

What is the primary fuel source during high-intensity (85% VO2max) exercise?

A

muscle glycogen

79
Q

What is the primary CHO fuel source that becomes most important after 3-4 hours of moderate-intensity (~70% VO2max) exercise?

A

blood glucose

80
Q

What energy substrate is primarily utilized during rest-light to moderate intensity?

A

fats

81
Q

In a person with a mixed diet, what is the approximate duration for exercise?

A

~ 180 mins

82
Q

In a person with a carbohydrate diet, what is the approximate duration for exercise?

A

~240 mins

83
Q

In a carbohydrate deficient diet, what is the approximate duration for exercise?

A

~90 mins, doesn’t sustain as well

84
Q

What effect does eating before exercise have on exercise?

A

eating increases insulin which decreases blood glucose levels and if too close to exercise can lead to hypoglycemia

85
Q

What effect does CHO feeding during prolonged exercises have?

A

Can prolong and extend ability to sustain exercise

86
Q

For adequate glycogen resynthesis, when should CHOs be taken in?

A

as close to after as possible

87
Q

What is the relationship between glucose uptake and glycogen use during exercise?

A

linear increase : greater intensity = greater post-exercise glucose uptake

88
Q

What are the types of lipids?

A

fatty acids, triglycerides, and phospholipids

89
Q

Which lipid(s) are high density energy store?

A

Fatty acids, TG (FA form TG)

90
Q

Phospholipids contain precursors of many biologically active substances such as what?

A

prostaglandins, thromboxane, inositol triphosphate (IP3)

91
Q

What do phospholipids do?

A

modulate the activities of membrane enzymes and transporters

92
Q

What lipid soluble/derived substance controls fluidity and protein function?

A

cholesterol

93
Q

What can cholesterol be synthesized from?

A

acetyl coA

94
Q

Describe the structure of TGs.

A

glycerol backbone with 3 long chain FAs

95
Q

What are the three common FA in humans?

A

Stearic acid, oleic acid, and palmitic acid

96
Q

Which FA is 18C and unsaturated?

A

oleic acid (olive oil, nuts)

97
Q

Which FA is 18C and saturated?

A

stearic acid

98
Q

Which FA is 16C and saturated?

A

palmitic acid (fried foods, bad saturated fat)

99
Q

What does TG break down into?

A

a Monoglyceride and 2 fatty acids

100
Q

What catalyzes the breakdown of TG?

A

lipases

101
Q

What does cholesterol ester break down into?

A

Chol and Fatty acid

102
Q

What catalyzes the breakdown of cholesterol ester?

A

cholesterol ester hydrolase

103
Q

What does phospholipids break down into?

A

lysolecithin and fatty acid

104
Q

What catalyzes the breakdown of phospholipids?

A

phospholipase A2

105
Q

Describe the lipid transport from the GI tract.

A

Bile salts dissolve the broken down lipids which allow them to enter the epithelial cells of the SI, next they re-esterfy into OG state where PL form a chylomicron around Chol E and TG for exocytosis into the blood via lymph duct

106
Q

What happens next for lipid transport once the chylomicron enters the blood?

A

broken down into chylomicron remnants and FFA in the presence of Lipoprotein Lipase and enter adipose or muscle tissue

107
Q

What happens to the chylomicron remnants in lipid transport?

A

GO back to the liver into remnant receptors via LPL and Apo E

108
Q

What happens to the FFAs in adipose in lipid transport?

A

Go back to the liver directly

109
Q

_ transports FFA from the liver to adipose and muscle.

A

VLDLs

110
Q

In the presence of IDL, what happens to the transport of a lipid?

A

can wither be directly recycled to liver via Apo E OR in the presence of LPL become an LDL and go to muscle tissues, or do back to the liver via Apo B

111
Q

What is needed for activation of LPL?

A

Apoprotein C

112
Q

Chylomicrons obtain apoproteins C an E by transfer from what?

A

HDL

113
Q

The majority of fat is stored where?

A

in TG in subcutaneous adipose tissue and skeletal muscle (as IMTG)

114
Q

What must occur for TG to be metabolized?

A

lipolysis (TG - > glycerol + FFAs)

115
Q

True/False: Fat has the highest energy value of the fuel types.

A

True

116
Q

True/False: Fat is transported quickly.

A

False, since it’s mainly stored in muscle and not water soluble, there is a delayed transport of FFAs to the muscle

117
Q

What are the steps for fatty acid utlizization?

A
  1. Mobilization (Lipolysis) 2. circulation 3. uptake 4. activation 5. Translocation and mitochondrial uptake 6. Beta-oxidation 7. mitochondrial oxidation
118
Q

Describe the process of lipolysis.

A

lipases break down TG losing one Fatty acid at a time until there are 3 fatty acids

119
Q

What are some stimulators of lipolysis?

A

Epinephrine, norepinephrine, glucagon, TSH, Exercise

120
Q

What are some inhibiting factors of lipolysis?

A

Insulin, GH

121
Q

At 25% of VO2max, what does the fatty acid circulation look like?

A

slight increase at start and remains fairly constant

122
Q

At 65% of VO2max, what does the fatty acid circulation look like?

A

fairly steady increase is constant

123
Q

At 85% of VO2max, what does the fatty acid circulation look like?

A

it decreases followed by a steady state then increases drastically and gradually comes down as exercise ends

124
Q

Why is there such a steep slope for high intensity exercise in fatty acid circulation?

A

requirement of blood protein and blood so since blood is shunted away from adipose, there is not enough to release until the end of exercise

125
Q

Describe the process of the uptake of fatty acids.

A

LCFA in the circulation plus VLDL TG (broken down by LPL) enter the cell via FAT/CD36

126
Q

Describe the process of activation for fatty acid utilization.

A

LCFAs in the cell can either be re-esterfied and go to muscle, can bind to fatty acid binding protein and just store, or can be activated by the ACS (acetyl CoA synthase) for mitchondrial uptake

127
Q

What transporter uptakes LCFAs to mitochondria?

A

CPT1

128
Q

What happens during mitochondrial uptake?

A

LCFA + ACS = acyl CoA is taken up by CPT1 into the inner membrane where releases CoA and acyl binds with carnitine (acyl-carnitine). then translocase breaks down the acyl-carntine and the carnitine is recycled back and then CPT2 uptakes the acyl-CoA for Beta oxidation

129
Q

What are some stimulators of CPT1?

A

acyl-coA, increase [LCFA], exercise

130
Q

What are some inhibitors of CPT1?

A

Malonyl-CoA (intermediate in TG synthesis), acetyl CoA, decrease in pH, Free-coenzyme-A, lack of carntitine

131
Q

Describe the process of beta-oxidation.

A

Fatty acyl-CoA passes through and via a series of four Rxn’s removes two carbons to form acetyl-CoA and reducing equivalents are produced (NADH and FADH2) and the fatty acyl-CoA is now two carbon atoms shorter and this repeats until it is totally degraded

132
Q

How many rounds of Beta oxidation are required to break down the fatty acyl-CoA?

A

7

133
Q

What is the end result of beta oxidation?

A

8 acetyl CoA, 7 NADH, 7 FADH2

134
Q

How many ATPs does beta oxidation provide?

A

8 acetyl CoA = 96 ATP, 7 FADH2 = 10-11 ATP, and 7 NADH = 17-18 ATP

= 123-125 ATPs

135
Q

What can occur when large quantities of FA become available?

A

ketosis

136
Q

High levels of ketone bodies can lead to what?

A

ketoacidosis

137
Q

What is the “re-assembly” of TG?

A

re-esterification

138
Q

In muscle and adipose tissue, what is used for TG synthesis?

A

G3P from glycolysis

139
Q

What is the trend around muscle TG content following exercise?

A

decrease in the hours following, maybe due to replenishing of the glycogen stores?

140
Q

The breakdown of _ may provide additional energy to aid in muscle glycogen restoration.

A

IMTG

141
Q

True/False: Adipose tissue can act as an endocrine tissue.

A

true

142
Q

Adipose tissue secrete adipokines. What are those?

A

regulatory cytokines

143
Q

What are the important adipokines?

A

Leptin, MCP1, and adiponectin

144
Q

What does leptin do?

A

stimulates the hypothalamus that energy stores are too high and to decrease food intake and increase muscle-fat oxidation

145
Q

What stimulates leptin secretion?

A

increase adipose tissue mass

146
Q

What can occur to the leptin levels in obesity?

A

are chronically elevated and can become resistant

147
Q

What can reverse leptin resistance?

A

regular exercise and omega 3 PUFA rich diets

148
Q

What does MCP1 do?

A

increases monocyte infiltration into adipocytes which increase proinflammatory cytokines which can increase insulin resistance

149
Q

What does adiponectin do?

A

the opposite of MCP1 - increases insulin sensitivity from decreasing vascular inflammation

150
Q

What increases adiponectin serum levels?

A

weight loss

151
Q

What are proteins broken down into?

A

amino acids

152
Q

Muscle _ is dependent on the balance between protein synthesis and degradation.

A

Size

153
Q

More synthesis of protein leads to what effect on muscles?

A

growth

154
Q

More degradation of protein leads to what effect on muscles?

A

atrophy

155
Q

Name a few examples of things that increase protein synthesis.

A

eating, exercise

156
Q

Name a few examples of things that increase protein degradation.

A

unloading, starving

157
Q

True/False: there is a continuous exchange between free amino acids and protein pools.

A

true, they are constantly being synthesized and downgraded

158
Q

Where are the amino acid pools?

A

plasma, interstitium, muscle

159
Q

What does albumin do for proteins?

A

provides colloid osmotic pressure

160
Q

What effect does liver disease have on albumin levels?

A

can’t build up = decreases colloid osmotic pressure = edema

161
Q

What does globulin do?

A

helps with immunity

162
Q

What does fibrinogen do?

A

helps with blood clot formation

163
Q

What are the mechanisms of altering protein content/composition?

A
  1. change gene profile 2. change breakdown rate of mRNAs 3. selection of specific mRNAs for translation and protein synthesis 4. selection of specific mRNAs for preferential degradation
164
Q

Where do ionized amino acids circulate?

A

plasma (~35-65 mg/dL)

165
Q

By what mechanism is transport of amino acids into cells?

A

Carrier mediated = facilitated diffusion or primary active transport

166
Q

What effect does feeding have on muscle protein synthesis?

A

increases by 10-20% and decreases degradation by ~20%

167
Q

How much protein is lost during overnight fasting?

A

~20%

168
Q

What overall effect does protein have on exercise?

A

minimal energy disturbance = maintain net protein balance

169
Q

In conditions where fuel oxidation doe not match ATP turnover rates, what occurs to the protein balance?

A

energy disturbance is large = negative protein balance

170
Q

In a patient with McArdle’s disease, they lack the enzyme _ for glycogenolysis.

A

glycogen phosphorylase

171
Q

What affect does resistance exercise have on protein turnover?

A

Simultaneous increases that last for >24 hours after exercise (highest @ first 2-6 hours)

172
Q

One bout of resistance exercise can result in how much increases in MPS rates?

A

40-150%

173
Q

What after effects does endurance exercise have on protein synthesis?

A

increase in mitochondrial proteins, no change in myofibrillar proteins

174
Q

Describe the effects of aging on protein turnover.

A

aging = decreases physical activity = sarcopenia = decreased oxidative capacity (mitochondrial density) = decrease anabolic stimulus from resistance exercise and expression of mitochondrial enzymes from endurance exercise and decreases in protein diet EQUAL increase in MPS and decrease suppression of muscle protein degradation in response to meal ingestion