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Flashcards in Muscle Physiology Midterm 2 Deck (393):
1

Why is it important to study metabolism in a course on muscle?

To perform mechanical work (muscle contraction) during exercise, energy is required. Skeletal muscle is capable of enormous increases in force and velocity and consequently the rate of ATP utilization can change dramatically. Metabolic demand can increase more than 100 fold in a very short time

2

What is the problem with metabolic demand in muscles increasing over 100 fold in a very short time?

The concentration of ATP is low and can only sustain maximal muscle contraction for about 2-3 seconds. Approx 90-100 lbs. of ATP would be need to perform all metabolic reactions during one day of hard labour. Therefore, we need not only a lot of ATP daily but we need to produce ATP at various rates depending on work/exercise intensity. Muscle must be equipped with metabolic mechanisms to meet varaible energy requirements to maintain work

3

What is bioenergetics?

The study of how energy is generated in the cell; refers to the metabolic process of converting foodstuff (substrate) into ATP

4

Three energy systems in muscle?

High energy phosphate transfer (transfer of a phosphate group to ADP to regenerate ATP). Glycolysis (degradation of glucose or glycogen (glycogenolysis). Oxidative phosphorylation (complete combustion of fats or carbohydrates)

5

Anaerobic pathways?

Do NOT involve oxygen; HEPT and glycolysis

6

Aerobic pathways?

Requires oxygen; oxidative phosphorylation

7

Ammonium?

NH4+

8

Ammonia?

NH3+

9

How many high energy bonds does an ATP have?

2

10

How many high energy bonds does an ADP have?

1

11

How many high energy bonds does and AMP have?

NONE, but can be broken down into other things

12

If a reaction is closer to equilibrium, how much energy is produced?

Not very much

13

What happens to the the energy release as the reaction moves further from equilibrium?

More energy is released

14

Is there more ATP or PCr stored in muscle?

More Pcr (3-4x more)

15

ATPase reaction?

ATP + H2O ---> ADP + Pi + H+ + Energy

16

How many kcal/mol ATP?

7.3

17

Creatine kinase reaction?

ADP + PCr + H+ --> ATP + Cr

18

Adenylate kinase reaction?

ADP + ADP --> ATP + AMP

19

AMP deaminase reaction?

AMP --> IMP + NH3

20

Does PCr have a high or low capacity for producing ATP?

LOW CAPACITY because stores are limited in the muscle

21

Does an ATPase or creatine kinase have a higher power for producing ATP?

Creatine kinase activity is higher that ATPase activity in the cell...replenishes ATP rapidly as it is hydrolyzed. The reaction is near equilibrium, therefore, all you need is a very small decrease in [ATP] to start the reaction going to the right.

22

How does creatine kinase help buffer pH?

Uses an H+ in its reaction

23

Why is the creatine kinase reaction so rapid?

The reaction is near equilibrium, therefore, as you need is a very small decrease in [ATP] to start the reaction going to the right (making ATP and Cr)

24

How many isoforms of creatine kinase are there?

2...mitochondrial and cystolic

25

What does mitochondrial creatine kinase do?

Adds a phosphate from ATP to creatine, resulting in ADP and Creatine Phosphate. Creatine phosphate is shuttled into the cytosol.

26

What does cystolic creatine kinase do?

Removes phosphate from creatine phosphate and adds it to ADP to make ATP and Creatine. Creatine is shuttled back into mitochondria

27

Where can Creatine be obtained from?

Made in the liver or obtained from meat/supplementation

28

What does creatine supplementation do?

Increases both free CR and PCr stores

29

Creatine supplementation has shown increases in what types of activities?

Short duration (less than 30 seconds), high intensity exercise (mainly cycling) Little positive effects on running and swimming (water retention from kindey metabolizing it); these activities typically use glycolysis and oxidative phosphorylation because they are longer duration

30

What provides the fastest source of ATP to ATPases in muscle?

Stored ATP (no reaction involved. PCr is fast, but there is 1 reaction, so not as fast)

31

Why is the adenylate kinase reaction important during very intense exercise?

1. Increases the [ATP] (ATP hydrolysis is very rapid, so the [ADP] increases rapidly) 2. Helps keep [ADP] low to maintain high free energy for the hydrolysis of ATP and to minimize fatigue 3. Increase the [AMP] which is useful for activating other metabolic pathways (glycolysis and oxidative phosphorylation)

32

Why is it important to keep [ADP] low?

[ADP] influences the rate of ATP hydroylsis and the amount of energy that can be extracted from an ATP, in order to keep ATP hydrolysis moving quickly and efficiently, the [ADP] must be kept low

33

How does the increase of [ADP] cause fatigue?

Increased [ADP] slows the rate of ADP release from the myosin head, which causes a decrease in the rate of the power stroke, therefore decreasing force output

34

How does the increase in [AMP] from the adenylate kinase reaction stimulate other metabolic pathways?

An increase in [AMP] tells the cell that the [ATP] is decreasing and the only way the cell is making ATP is by using ADP. The [AMP] increase tells the cell it needs another way to make ATP, so it increases activation of glycolysis and oxidative phosphorylation

35

Why is the AMP demaminase reaction important during very intense exercise?

Helps to keep the [AMP] low, which will keep the adenylate kinase reaction moving to the right, therefore, ultimately prevents [ADP] buildup (maintains high [ATP]/[ADP])

36

What activates AMP deaminase?

Low pH ...very low activity at rest

37

Why is the reduction of the ammonia molecule to ammonium ion important in the AMP deaminase reaction?

Effectively removes H+ to help buffer pH, and the ammonium ion also known to stimulate glycolysis

38

How many reactions in anaerobic glycolysis?

11 reactions

39

Reaction of glycogen in anaerobic glycolysis?

Glycogen + 3 ADP + 3 Pi ---> 2 lactate + 2 H+ + 3 ATP

40

Reaction of glucose in anaerobic glycolysis?

Glucose + 2 ADP + 2 Pi ---> 2 Lactate + 2 H+ + ATP

41

What is the primary carbohydrate used in anaerobic glycolysis in skeletal muscle?

Glycogen

42

What can glycolysis use as a source of fuel?

Only carbs

43

2 sources of glucose in body?

Glucose found in blood and ECF, and glycogen stored in liver and muscle

44

What is glycogen?

Molecule made from many glucose molecules joined together to form a compact, highly branched, spherical structure

45

What enzyme makes glycogen?

Glycogen synthase

46

Where are most glyocogen granules stored in the muscle cell?

Near the mitochondria...can be used to make ATP in aerobic respiration

47

What can influence glycogen concentrations in the liver and muscle?

DIET!

48

What type of power does anaerobic glycolysis have in producing ATP?

Medium power...a large amount of ATP can be generated per unit time, because of the high activity of enzymes in the pathway

49

Why can't anaerobic glycolysis be used for more than 3-5 hours?

Capacity of the system is limited by the availability of substrates (i.e. muscle glycogen) and buildup of lactic acid (H+ causes acidosis)

50

What type of capacity does anaerobic glycolysis have for producing ATP?

Moderate capacity...lactic acidosis and/or glycogen depletion will ultimately limit work intensity (fatigue)

51

2 phases of anaerobic glycolysis?

Energy investment stage and energy generation phase

52

How many ATP are required in the inergy investment stage of glycolysis?

Up to 2 ATP

53

What does the energy generation phase produce in glycolysis?

ATP, NADH, and pyruvate or lactate

54

What enzyme is used to add a phosphate to glycogen?

Phosphorylase

55

What enzyme adds a phosphate from ATP to glucose to form Glucose-6-Phosphate?

Hexokinase

56

What enzyme adds a phosphate to fructose-6-phosphate to make fructose-1,3-bisphosphate?

Phosphofructokinase

57

How many ATP are invested in the energy investment stage of glycolysis for a glucose molecule?

2 (1 to make G-6-P via hexokinase and another to make F-1,6-BP via PFK)

58

How many ATP are invested in the energy investment stage of glycolysis for a glycogen molecule?

1 (to make F-1,6-BP via PFK)

59

How many isoforms of creatine kinase are there?

2...mitochondrial and cystolic

60

What does mitochondrial creatine kinase do?

Adds a phosphate from ATP to creatine, resulting in ADP and Creatine Phosphate. Creatine phosphate is shuttled into the cytosol.

61

What does cystolic creatine kinase do?

Removes phosphate from creatine phosphate and adds it to ADP to make ATP and Creatine. Creatine is shuttled back into mitochondria

62

Where can Creatine be obtained from?

Made in the liver or obtained from meat/supplementation

63

What does creatine supplementation do?

Increases both free CR and PCr stores

64

Creatine supplementation has shown increases in what types of activities?

Short duration (less than 30 seconds), high intensity exercise (mainly cycling) Little positive effects on running and swimming (water retention from kindey metabolizing it); these activities typically use glycolysis and oxidative phosphorylation because they are longer duration

65

Mechanisms of creatine supplementation?

Delay PCr depletion, increased ATP turnover (make ATP quicker because there is more creatine around), decreasing reliance on glycolysis (lactate formation), and decreases recovery time

66

What provides the fastest source of ATP to ATPases in muscle?

Stored ATP (no reaction involved. PCr is fast, but there is 1 reaction, so not as fast)

67

Why is the adenylate kinase reaction important during very intense exercise?

1. Increases the [ATP] (ATP hydrolysis is very rapid, so the [ADP] increases rapidly) 2. Helps keep [ADP] low to maintain high free energy for the hydrolysis of ATP and to minimize fatigue 3. Increase the [AMP] which is useful for activating other metabolic pathways (glycolysis and oxidative phosphorylation)

68

Why is it important to keep [ADP] low?

[ADP] influences the rate of ATP hydroylsis and the amount of energy that can be extracted from an ATP, in order to keep ATP hydrolysis moving quickly and efficiently, the [ADP] must be kept low

69

How does the increase of [ADP] cause fatigue?

Increased [ADP] slows the rate of ADP release from the myosin head, which causes a decrease in the rate of the power stroke, therefore decreasing force output

70

How does the increase in [AMP] from the adenylate kinase reaction stimulate other metabolic pathways?

An increase in [AMP] tells the cell that the [ATP] is decreasing and the only way the cell is making ATP is by using ADP. The [AMP] increase tells the cell it needs another way to make ATP, so it increases activation of glycolysis and oxidative phosphorylation

71

Why is the AMP demaminase reaction important during very intense exercise?

Helps to keep the [AMP] low, which will keep the adenylate kinase reaction moving to the right, therefore, ultimately prevents [ADP] buildup (maintains high [ATP]/[ADP])

72

What activates AMP deaminase?

Low pH ...very low activity at rest

73

Why is the reduction of the ammonia molecule to ammonium ion important in the AMP deaminase reaction?

Effectively removes H+ to help buffer pH, and the ammonium ion also known to stimulate glycolysis

74

How many reactions in anaerobic glycolysis?

11 reactions

75

Reaction of glycogen in anaerobic glycolysis?

Glycogen + 3 ADP + 3 Pi ---> 2 lactate + 2 H+ + 3 ATP

76

Reaction of glucose in anaerobic glycolysis?

Glucose + 2 ADP + 2 Pi ---> 2 Lactate + 2 H+ + ATP

77

What is the primary carbohydrate used in anaerobic glycolysis in skeletal muscle?

Glycogen

78

What can glycolysis use as a source of fuel?

Only carbs

79

2 sources of glucose in body?

Glucose found in blood and ECF, and glycogen stored in liver and muscle

80

What is glycogen?

Molecule made from many glucose molecules joined together to form a compact, highly branched, spherical structure

81

What enzyme makes glycogen?

Glycogen synthase

82

Where are most glyocogen granules stored in the muscle cell?

Near the mitochondria...can be used to make ATP in aerobic respiration

83

What can influence glycogen concentrations in the liver and muscle?

DIET!

84

What type of power does anaerobic glycolysis have in producing ATP?

Medium power...a large amount of ATP can be generated per unit time, because of the high activity of enzymes in the pathway

85

Why can't anaerobic glycolysis be used for more than 3-5 hours?

Capacity of the system is limited by the availability of substrates (i.e. muscle glycogen) and buildup of lactic acid (H+ causes acidosis)

86

What type of capacity does anaerobic glycolysis have for producing ATP?

Moderate capacity...lactic acidosis and/or glycogen depletion will ultimately limit work intensity (fatigue)

87

2 phases of anaerobic glycolysis?

Energy investment stage and energy generation phase

88

How many ATP are required in the inergy investment stage of glycolysis?

Up to 2 ATP

89

What does the energy generation phase produce in glycolysis?

ATP, NADH, and pyruvate or lactate

90

What enzyme is used to add a phosphate to glycogen?

Phosphorylase

91

What enzyme adds a phosphate from ATP to glucose to form Glucose-6-Phosphate?

Hexokinase

92

What enzyme adds a phosphate to fructose-6-phosphate to make fructose-1,3-bisphosphate?

Phosphofructokinase

93

How many ATP are invested in the energy investment stage of glycolysis for a glucose molecule?

2 (1 to make G-6-P via hexokinase and another to make F-1,6-BP via PFK)

94

How many ATP are invested in the energy investment stage of glycolysis for a glycogen molecule?

1 (to make F-1,6-BP via PFK)

95

Why is the creatine kinase reaction so rapid?

The reaction is near equilibrium, therefore, as you need is a very small decrease in [ATP] to start the reaction going to the right (making ATP and Cr)

96

How many isoforms of creatine kinase are there?

2...mitochondrial and cystolic

97

What does mitochondrial creatine kinase do?

Adds a phosphate from ATP to creatine, resulting in ADP and Creatine Phosphate. Creatine phosphate is shuttled into the cytosol.

98

What does cystolic creatine kinase do?

Removes phosphate from creatine phosphate and adds it to ADP to make ATP and Creatine. Creatine is shuttled back into mitochondria

99

Where can Creatine be obtained from?

Made in the liver or obtained from meat/supplementation

100

What does creatine supplementation do?

Increases both free CR and PCr stores

101

Creatine supplementation has shown increases in what types of activities?

Short duration (less than 30 seconds), high intensity exercise (mainly cycling) Little positive effects on running and swimming (water retention from kindey metabolizing it); these activities typically use glycolysis and oxidative phosphorylation because they are longer duration

102

Mechanisms of creatine supplementation?

Delay PCr depletion, increased ATP turnover (make ATP quicker because there is more creatine around), decreasing reliance on glycolysis (lactate formation), and decreases recovery time

103

What provides the fastest source of ATP to ATPases in muscle?

Stored ATP (no reaction involved. PCr is fast, but there is 1 reaction, so not as fast)

104

Why is the adenylate kinase reaction important during very intense exercise?

1. Increases the [ATP] (ATP hydrolysis is very rapid, so the [ADP] increases rapidly) 2. Helps keep [ADP] low to maintain high free energy for the hydrolysis of ATP and to minimize fatigue 3. Increase the [AMP] which is useful for activating other metabolic pathways (glycolysis and oxidative phosphorylation)

105

Why is it important to keep [ADP] low?

[ADP] influences the rate of ATP hydroylsis and the amount of energy that can be extracted from an ATP, in order to keep ATP hydrolysis moving quickly and efficiently, the [ADP] must be kept low

106

How does the increase of [ADP] cause fatigue?

Increased [ADP] slows the rate of ADP release from the myosin head, which causes a decrease in the rate of the power stroke, therefore decreasing force output

107

How does the increase in [AMP] from the adenylate kinase reaction stimulate other metabolic pathways?

An increase in [AMP] tells the cell that the [ATP] is decreasing and the only way the cell is making ATP is by using ADP. The [AMP] increase tells the cell it needs another way to make ATP, so it increases activation of glycolysis and oxidative phosphorylation

108

Why is the AMP demaminase reaction important during very intense exercise?

Helps to keep the [AMP] low, which will keep the adenylate kinase reaction moving to the right, therefore, ultimately prevents [ADP] buildup (maintains high [ATP]/[ADP])

109

What activates AMP deaminase?

Low pH ...very low activity at rest

110

Why is the reduction of the ammonia molecule to ammonium ion important in the AMP deaminase reaction?

Effectively removes H+ to help buffer pH, and the ammonium ion also known to stimulate glycolysis

111

How many reactions in anaerobic glycolysis?

11 reactions

112

Reaction of glycogen in anaerobic glycolysis?

Glycogen + 3 ADP + 3 Pi ---> 2 lactate + 2 H+ + 3 ATP

113

Reaction of glucose in anaerobic glycolysis?

Glucose + 2 ADP + 2 Pi ---> 2 Lactate + 2 H+ + ATP

114

What is the primary carbohydrate used in anaerobic glycolysis in skeletal muscle?

Glycogen

115

What can glycolysis use as a source of fuel?

Only carbs

116

2 sources of glucose in body?

Glucose found in blood and ECF, and glycogen stored in liver and muscle

117

What is glycogen?

Molecule made from many glucose molecules joined together to form a compact, highly branched, spherical structure

118

What enzyme makes glycogen?

Glycogen synthase

119

Where are most glyocogen granules stored in the muscle cell?

Near the mitochondria...can be used to make ATP in aerobic respiration

120

What can influence glycogen concentrations in the liver and muscle?

DIET!

121

What type of power does anaerobic glycolysis have in producing ATP?

Medium power...a large amount of ATP can be generated per unit time, because of the high activity of enzymes in the pathway

122

Why can't anaerobic glycolysis be used for more than 3-5 hours?

Capacity of the system is limited by the availability of substrates (i.e. muscle glycogen) and buildup of lactic acid (H+ causes acidosis)

123

What type of capacity does anaerobic glycolysis have for producing ATP?

Moderate capacity...lactic acidosis and/or glycogen depletion will ultimately limit work intensity (fatigue)

124

2 phases of anaerobic glycolysis?

Energy investment stage and energy generation phase

125

How many ATP are required in the inergy investment stage of glycolysis?

Up to 2 ATP

126

What does the energy generation phase produce in glycolysis?

ATP, NADH, and pyruvate or lactate

127

What enzyme is used to add a phosphate to glycogen?

Phosphorylase

128

What enzyme adds a phosphate from ATP to glucose to form Glucose-6-Phosphate?

Hexokinase

129

What enzyme adds a phosphate to fructose-6-phosphate to make fructose-1,3-bisphosphate?

Phosphofructokinase

130

How many ATP are invested in the energy investment stage of glycolysis for a glucose molecule?

2 (1 to make G-6-P via hexokinase and another to make F-1,6-BP via PFK)

131

How many ATP are invested in the energy investment stage of glycolysis for a glycogen molecule?

1 (to make F-1,6-BP via PFK)

132

Why is the creatine kinase reaction so rapid?

The reaction is near equilibrium, therefore, as you need is a very small decrease in [ATP] to start the reaction going to the right (making ATP and Cr)

133

How many isoforms of creatine kinase are there?

2...mitochondrial and cystolic

134

What does mitochondrial creatine kinase do?

Adds a phosphate from ATP to creatine, resulting in ADP and Creatine Phosphate. Creatine phosphate is shuttled into the cytosol.

135

What does cystolic creatine kinase do?

Removes phosphate from creatine phosphate and adds it to ADP to make ATP and Creatine. Creatine is shuttled back into mitochondria

136

Where can Creatine be obtained from?

Made in the liver or obtained from meat/supplementation

137

What does creatine supplementation do?

Increases both free CR and PCr stores

138

Creatine supplementation has shown increases in what types of activities?

Short duration (less than 30 seconds), high intensity exercise (mainly cycling) Little positive effects on running and swimming (water retention from kindey metabolizing it); these activities typically use glycolysis and oxidative phosphorylation because they are longer duration

139

Mechanisms of creatine supplementation?

Delay PCr depletion, increased ATP turnover (make ATP quicker because there is more creatine around), decreasing reliance on glycolysis (lactate formation), and decreases recovery time

140

What provides the fastest source of ATP to ATPases in muscle?

Stored ATP (no reaction involved. PCr is fast, but there is 1 reaction, so not as fast)

141

Why is the adenylate kinase reaction important during very intense exercise?

1. Increases the [ATP] (ATP hydrolysis is very rapid, so the [ADP] increases rapidly) 2. Helps keep [ADP] low to maintain high free energy for the hydrolysis of ATP and to minimize fatigue 3. Increase the [AMP] which is useful for activating other metabolic pathways (glycolysis and oxidative phosphorylation)

142

Why is it important to keep [ADP] low?

[ADP] influences the rate of ATP hydroylsis and the amount of energy that can be extracted from an ATP, in order to keep ATP hydrolysis moving quickly and efficiently, the [ADP] must be kept low

143

How does the increase of [ADP] cause fatigue?

Increased [ADP] slows the rate of ADP release from the myosin head, which causes a decrease in the rate of the power stroke, therefore decreasing force output

144

How does the increase in [AMP] from the adenylate kinase reaction stimulate other metabolic pathways?

An increase in [AMP] tells the cell that the [ATP] is decreasing and the only way the cell is making ATP is by using ADP. The [AMP] increase tells the cell it needs another way to make ATP, so it increases activation of glycolysis and oxidative phosphorylation

145

Why is the AMP demaminase reaction important during very intense exercise?

Helps to keep the [AMP] low, which will keep the adenylate kinase reaction moving to the right, therefore, ultimately prevents [ADP] buildup (maintains high [ATP]/[ADP])

146

What activates AMP deaminase?

Low pH ...very low activity at rest

147

Why is the reduction of the ammonia molecule to ammonium ion important in the AMP deaminase reaction?

Effectively removes H+ to help buffer pH, and the ammonium ion also known to stimulate glycolysis

148

How many reactions in anaerobic glycolysis?

11 reactions

149

Reaction of glycogen in anaerobic glycolysis?

Glycogen + 3 ADP + 3 Pi ---> 2 lactate + 2 H+ + 3 ATP

150

Reaction of glucose in anaerobic glycolysis?

Glucose + 2 ADP + 2 Pi ---> 2 Lactate + 2 H+ + ATP

151

What is the primary carbohydrate used in anaerobic glycolysis in skeletal muscle?

Glycogen

152

What can glycolysis use as a source of fuel?

Only carbs

153

2 sources of glucose in body?

Glucose found in blood and ECF, and glycogen stored in liver and muscle

154

What is glycogen?

Molecule made from many glucose molecules joined together to form a compact, highly branched, spherical structure

155

What enzyme makes glycogen?

Glycogen synthase

156

Where are most glyocogen granules stored in the muscle cell?

Near the mitochondria...can be used to make ATP in aerobic respiration

157

What can influence glycogen concentrations in the liver and muscle?

DIET!

158

What type of power does anaerobic glycolysis have in producing ATP?

Medium power...a large amount of ATP can be generated per unit time, because of the high activity of enzymes in the pathway

159

Why can't anaerobic glycolysis be used for more than 3-5 hours?

Capacity of the system is limited by the availability of substrates (i.e. muscle glycogen) and buildup of lactic acid (H+ causes acidosis)

160

What type of capacity does anaerobic glycolysis have for producing ATP?

Moderate capacity...lactic acidosis and/or glycogen depletion will ultimately limit work intensity (fatigue)

161

2 phases of anaerobic glycolysis?

Energy investment stage and energy generation phase

162

How many ATP are required in the inergy investment stage of glycolysis?

Up to 2 ATP

163

What does the energy generation phase produce in glycolysis?

ATP, NADH, and pyruvate or lactate

164

What enzyme is used to add a phosphate to glycogen?

Phosphorylase

165

What enzyme adds a phosphate from ATP to glucose to form Glucose-6-Phosphate?

Hexokinase

166

What enzyme adds a phosphate to fructose-6-phosphate to make fructose-1,3-bisphosphate?

Phosphofructokinase

167

How many ATP are invested in the energy investment stage of glycolysis for a glucose molecule?

2 (1 to make G-6-P via hexokinase and another to make F-1,6-BP via PFK)

168

How many ATP are invested in the energy investment stage of glycolysis for a glycogen molecule?

1 (to make F-1,6-BP via PFK)

169

The AMP Deaminase reaction is important because?

Stimulates glycolysis (NH4+ does), helps buffer pH (NH3 accepts H+), and indirectly helps maintain low ADP

170

The first reaction that utilizes ATP in glycolysis if blood glucose is used as a substrate is catalyzed by what enzyme?

Hexokinase

171

Why is the buildup of H+ a safety mechanism?

Tells the muscle to slow down/ stop contraction before mechanical damage occurs

172

How is ATP formed during glycolysis?

Substrate level phosphorylation

173

What causes the production of lactic acid?

When oxygen is not available in the mitochondria to accept H+ (and electrons) from Nadh produced in glycolysis, H+ and electrons from NADH are accepted by pyruvic acid to form lactic acidd

174

What enzyme is responsible for the conversion of pyruvic acid to lactic acid?

Lactate Dehydrogenase

175

What is the conversion of pyruvic acid to lactic acid important?

Allows anaerobic glycolysis to continue by maintaining a high NAD/NADH ratio (the redox potential). If the NADH/NAD ratio increases, GAPDH reaction slows/stops = no more glycolysis = no more ATP

176

How many ATP does a glucose molecule produce?

32 ATP

177

How many ATP does palmitic acid produce?

106 ATP

178

What is aerobic/oxidative metabolism?

The complete combustion of fatty acids (from fat cells or in muscle cells), carbs (blood glucose and liver/muscle glycogen), and to a limited extent, protein, in the presence of oxygen

179

What type of capacity for producing ATP does the aerobic pathway have?

Large capacity because of the continuous supply of ATP to large fat and glycogen stores

180

What type of power for producing ATP does the oxidative pathway have?

Low-moderate pathway because ATP regeneration is relatively low and is limited by oxygen supply (VO2 max)

181

What is oxidative phosphorylation?

The formation of ATP from ADP and Pi in association with electron transfer from fuel substrates to coenzymes to oxygen

182

Why are aerobic pathways slower at ATP resynthesis than anaerobic pathways?

Location of the substrate (liver glycogen has to be transported) and there are more steps/enzymes in oxidative phosphorylation versus HEPT and glycolysis

183

What is the Krebs cycle?

Completes the oxidation of substrates and produces NADH or FADH2 to enter the ETC

184

What is the electron transport chain?

Electrons removed from NADH and FADH2 are passed along a series of carriers to produce ATP...H+ from NADH and FADH2 are accepted by O2 to form water.

185

What are the three stages of oxidative metabolism?

1. Formation of Acetyl-CoA from CHO (pyruvate) or fats (fatty acids) 2. Oxidation of acetyl groups in Krebs cycle to form NADH and FADH2 3. Oxidation of NADH and FADH2 in ETC to form ATP from ADP and Pi

186

What enzyme is responsible for the conversion of pyruvate (3C) to acetyl CoA (2C)?

Pyruvate dehydrogenase...a NADH and a CO2 are produced in this reaction

187

In the beta-oxidation pathway, fatty acyl-CoA is split into?

2C acetyl groups that enter the Kreb's Cycle

188

When an acetyl group is cleaved in beta oxidation what is produced?

1 NADH and 1 FADH2 are produced

189

How many acetyl CoA, NADH, and FADH2 are produced from a 16 carbon fatty acid?

8 acetyl CoA, 7 NADH and 7 FADH2

190

How many ATP are used to uptake a fatty acid into the cell?

2 ATP

191

Where are fat droplets located in the muscle?

Located near mitochondria

192

What two Krebs cycle enzymes are measured in the muscle cell as a measure of oxidative potential?

Citrate synthase and succinate dehydrogenase

193

How many H+ are moved across the membrane for every NADH molecule?

10 H+

194

What ETC complexes pump hydrogen molecules?

1, 3, and 4

195

What drives the formation of ATP in the ETC chain?

Flow of H+ from the intermembrane space through ATP synthase to the matrix down their concentration gradient

196

How does ATP synthase make ATP?

H+ binding to the enzymes causes a confirmational shape change, which results in the formation of ATP from ADP and Pi

197

How many H+ are needed to make one ATP?

4 H+

198

How many ATP per NADH??

2.5 ATP

199

How many ATP per FADH2?

1.5 ATP

200

How many ATP from one glucose?

32 ATP

201

What is respiration efficiency?

Efficieny of converting energy from foodstuff into biologically usable energy (ie ATP)

202

Respiration efficiency of aerobic respiration?

34%, with the remaining 66% of the free energy being released as heat

203

How do UCP increase BMR?

They uncouple the H+ flow from the IMS to the matrix, so no ATP is made, only heat is produced, Body wants to keep high [H+], therefore, it burns more foodstuffs to make FADH2 and NADH to keep pumping e- for the ETC to continue to make ATP

204

Why are metabolic systems in muscle so tightly coordinated and controlled?

To maintain ATP homeostasis even when ATP utilization increases 200 fold

205

5 basic ways metabolic control occurs in muscle?

1. Mass action (increase substrate = increase product) 2. Allosteric control (inc. or dec. a pathway) 3, Enzymatic activation-deactivation by phosphorylation processes 4. Cellular compartmentalization 5. Substrate control

206

What is a rate limiting enzyme?

Enzymes that determine the rate of flux of a metabolic pathway and are therefore usually highly controlled. ANything that gets past a rate limiting enzyme will become product.

207

Name 5 sources that provide ATP for the muscle cell?

1. Creatine phosphate 2. Glucose 3. Stored ATP 4. Adenylate Kinase 5. Anaerobic glycolysis

208

Activators of phosphorylase?

Pi, AMP, and IMP...all are by-products of ATP utilization, their buildup tells cell that there may not be enough stored ATP or Pc to keep contraction going, so other pathway must start or become more activated.

209

Inhibitors of phosphorylase?

G-6-P and ATP

210

Why is G-6-P an inhibitor of phosphorylase?

Increase in its concentration tells the cell that it isn't being used to make ATP or glucose is being used to make G6P, so glycogen is not needed/

211

What activates phosphorylase?

Ca2+ and epinephrine through phosphorylation processes via PHOSPHORYLASE KINASE

212

What is phosphorylase "a"?

More active form or phosphorylase, phosphorylated form, physiologically active

213

What is phosphorylase "b"?

Unphosphorylated form of phosphorylase, main form at rest, inactive in the absence of AMP

214

At the onset of ecercise, what phosphorylase form is used?

At the onset of exercise, phos "b" --> phos "a" but then most of phos "a" converts back to phos "b" later in exercise, however, phos "b" mroe active during exercise than at rest due to allosteric activation by Pi, AMP, and IMP

215

What is the best example of a rate limiting metabolic enzyme?

PFK is probably the best example of a rate limiting metabolic enzyme such that flux through glcolytic reactions that take place downstream of PFK is determined simply by mass action

216

Activators of PFK?

Pi, ADP, AMP, IMP, increased pH

217

Inhibitors of PFK?

Citrate, ATP, decrease in pH

218

Why is citrate an allosteric inhibitor of PFK?

If its concentration is increased, it means it isn't being used OR it's being produced by some other pathwa (like aerobic) so no point in activating glycolysis. As soon as its concentration decreases, PFK is stimulated to make pyruvate, which cna make ACetyl CoA and then ATP

219

Why is decreased pH an inhibitor of PFK?

It can cause the buildup of lactic acid, so if pH is already low, we don't want to decrease it further by completing this reaction/

220

The control of what enzyme causes control of glycolysis?

PFK, not phosphorylase

221

What form of PDH is active?

Dephosphorylated

222

What form of PDH is inactive?

Phosphorylated

223

What controls the forms of PDH?

Phosphorylation-dephosphorylation processes

224

Activators of phosphatase in the control of PDH?

Mg2+ and Ca2+

225

Inhibitors of kinase in the control of PDH?

Pyruvate, increased mitochondria NAD+/NADH, decreased ATP/ADP and decreased Acetyl CoA/CoA

226

What activates PDH?

Activators of phosphatase and inhibitors of kinase

227

How does ATP synthase make ATP?

H+ binding to the enzymes causes a confirmational shape change, which results in the formation of ATP from ADP and Pi

228

How many H+ are needed to make one ATP?

4 H+

229

How many ATP per NADH??

2.5 ATP

230

How many ATP per FADH2?

1.5 ATP

231

How many ATP from one glucose?

32 ATP

232

What is respiration efficiency?

Efficieny of converting energy from foodstuff into biologically usable energy (ie ATP)

233

Respiration efficiency of aerobic respiration?

34%, with the remaining 66% of the free energy being released as heat

234

How do UCP increase BMR?

They uncouple the H+ flow from the IMS to the matrix, so no ATP is made, only heat is produced, Body wants to keep high [H+], therefore, it burns more foodstuffs to make FADH2 and NADH to keep pumping e- for the ETC to continue to make ATP

235

Why are metabolic systems in muscle so tightly coordinated and controlled?

To maintain ATP homeostasis even when ATP utilization increases 200 fold

236

5 basic ways metabolic control occurs in muscle?

1. Mass action (increase substrate = increase product) 2. Allosteric control (inc. or dec. a pathway) 3, Enzymatic activation-deactivation by phosphorylation processes 4. Cellular compartmentalization 5. Substrate control

237

What is a rate limiting enzyme?

Enzymes that determine the rate of flux of a metabolic pathway and are therefore usually highly controlled. ANything that gets past a rate limiting enzyme will become product.

238

Name 5 sources that provide ATP for the muscle cell?

1. Creatine phosphate 2. Glucose 3. Stored ATP 4. Adenylate Kinase 5. Anaerobic glycolysis

239

Activators of phosphorylase?

Pi, AMP, and IMP...all are by-products of ATP utilization, their buildup tells cell that there may not be enough stored ATP or Pc to keep contraction going, so other pathway must start or become more activated.

240

Inhibitors of phosphorylase?

G-6-P and ATP

241

Why is G-6-P an inhibitor of phosphorylase?

Increase in its concentration tells the cell that it isn't being used to make ATP or glucose is being used to make G6P, so glycogen is not needed/

242

What activates phosphorylase?

Ca2+ and epinephrine through phosphorylation processes via PHOSPHORYLASE KINASE

243

What is phosphorylase "a"?

More active form or phosphorylase, phosphorylated form, physiologically active

244

What is phosphorylase "b"?

Unphosphorylated form of phosphorylase, main form at rest, inactive in the absence of AMP

245

At the onset of ecercise, what phosphorylase form is used?

At the onset of exercise, phos "b" --> phos "a" but then most of phos "a" converts back to phos "b" later in exercise, however, phos "b" mroe active during exercise than at rest due to allosteric activation by Pi, AMP, and IMP

246

What is the best example of a rate limiting metabolic enzyme?

PFK is probably the best example of a rate limiting metabolic enzyme such that flux through glcolytic reactions that take place downstream of PFK is determined simply by mass action

247

Activators of PFK?

Pi, ADP, AMP, IMP, increased pH

248

Inhibitors of PFK?

Citrate, ATP, decrease in pH

249

Why is citrate an allosteric inhibitor of PFK?

If its concentration is increased, it means it isn't being used OR it's being produced by some other pathwa (like aerobic) so no point in activating glycolysis. As soon as its concentration decreases, PFK is stimulated to make pyruvate, which cna make ACetyl CoA and then ATP

250

Why is decreased pH an inhibitor of PFK?

It can cause the buildup of lactic acid, so if pH is already low, we don't want to decrease it further by completing this reaction/

251

The control of what enzyme causes control of glycolysis?

PFK, not phosphorylase

252

What form of PDH is active?

Dephosphorylated

253

What form of PDH is inactive?

Phosphorylated

254

What controls the forms of PDH?

Phosphorylation-dephosphorylation processes

255

Activators of phosphatase in the control of PDH?

Mg2+ and Ca2+

256

Inhibitors of kinase in the control of PDH?

Pyruvate, increased mitochondria NAD+/NADH, decreased ATP/ADP and decreased Acetyl CoA/CoA

257

What activates PDH?

Activators of phosphatase and inhibitors of kinase

258

What are activators of the PDH kinase...inactivate PDH?

Increased ATP/ADP and increased acetyl CoA/CoA

259

Rate limiting enzyme of ATP-PC system?

Creatine Kinase

260

Rate limiting enzyme of Krebs Cycle?

Isocitrate dehydrogenase

261

Stimulators of isocitrate dehydrogenase?

ADP, Mito Ca2+, NAD

262

Inhibitors of Isocitrate dehydrogenase?

ATP and NADH

263

Rate limiting enzyme of ETC?

Cytochrome C oxidase

264

Stimulators of Cytochrome C Oxidase?

ADP and Pi

265

Inhibitors of cytochrome c oxidase?

ATP

266

What causes activation of isocitrate dehydrogenase and other dehydrogenases in Krebs Cycle?

Mitochondrial Ca2+ binding directly to enzyme...not through phosphorylation processes

267

The complete combustion of a glucosyl unit from glycogen would produce?

33 ATP

268

Enzyme responsible for accepting an e_ from cytochrome c is?

Cytochrome C Oxidase (it is oxidizing cytochrome c)

269

What does cellular comparmentalization do?

Has to with getting ATP to the sites where it is needed (i.e. ATPases) as quickly as possible (i.e. locating the sites of ATP production near the sites of ATP utilization)

270

3 examples of compartmentalization in muscle?

1. Sarcolemmal mitochondira...supplies Na/K+ ATPase with ATP 2. SR-Glycogenolytic Complex 3. Cr Shuttle

271

What is the purpose of the SE-Glycogenolytic complex?

Glycogen and glycolytic enzymes are attached to SR, so they supply SERCA with ATP, also helps with Ca2+ activation of phosphorylase

272

How does the Cr Shuttle help with energy in the muscle cell?

ATP very slow to diffuse through cytoplasm, so Cr is a much faster way to get energy through muscle fibre

273

Glucose transporter in muscle?

GLUT4

274

Fatty acid transporter in muscle?

FAT and CD 36

275

Lactate transporters in muscle?

MCT 1 (in) and MCT 4 (out)

276

What are the 3 ways substrate transport is regulated in muscle?

1. Amount of available protein (gene regulation) 2. Protein localization (translocation) 3. Activity of transporter (allosteric)

277

Why is it important to control substrate transport in muscle cells?

We want to have control over how much and what kind of substrate gets into cell during different activities

278

What causes translocation of GLUT4 to sarcolemma?

Insulin and Exercise

279

What is maximal exercise?

WOrk rate that would require energy production equivalent to VO2 max (short term intense)

280

Submaximal high intensity exercise?

Work rate is greater than lactate threshold but less than 100% VO2 max (prolonged)

281

What is supramaximal exercise?

Work rate that would require energy production greater than 100% VO2 max (short-term very intense)

282

Submaximal steady state exercise?

Work rate is less than lactate threshold where 100% of the energy is supplied by aerobic metabolism

283

Progressive (incremental) exercise?

Exercise that begins at a low work rate (intensity) and involves step (or ramp) increases in work rate until exhaustion (i.e. VO2 max test)

284

When does oxygen consumption reach a steady state?

1-4 minutes into exercise

285

What is the oxygen deficit?

Lag in oxygen uptake at the beginning of exercise. Suggests that anaerobic pathways contribute to total ATP production

286

After steady state is reached, how is ATP requirement met?

Aerobically

287

Before state state is reached, how is ATP produced?

Anaerobically because there is not sufficient oxygen supply to make ATP aerobically

288

Which of the following is/are true regarding PDH?

1. inactive when phosphorylated 2. Activation of PDH kinase reduced PDH activity 3. Can be indirectly activated by Ca2+ 4. Inactive when ATP/ADP ratio is high

289

A mitochondrial enzyme activated/stimulated by Ca2+?

Isocitrate dehydrogenase...NOT phosphorylase because it is NOT a mitochondrial enzyme, although it is activated by Ca2+

290

What was "serial mobilization?"

Margaria in the 1960s thought that PCr provided immediate and only substrate for ATP synthesis in the first 10 seconds of exercise, and when PCr was depleted, glycolysis activated to provide a continued ATP supply

291

Why is the "serial mobilization" idea not true?

Glycolysis is also immediately activated at the onset of exercise and blood flow increases and enzymes involved in oxidative phosphorylation are activated...All pathways are activated at the onset of exercise, but they may not all be fully activated.

292

Equation for the total anaerobic ATP provision during intense exercise?

Change in PCr + (1.5 x change in Lactate) + (2 x change in ATP)

293

Approximate contributions of anaerobic vs aerobic sources to total ATP production during high-intensity exercising lasting approx. 3 minutes?

80%/20% in initial 30 seconds. 45%/55% from 60-90 seconds. 30%/70% from 120 to 180 seconds.

294

As exercise intensity increases, how does ATP provision/power change?

Greatly increases, too

295

Why does IMP increase as a function of decrease in ATP during high-intensity exercise?

During high-intensity exercise, the adenylate kinase reaction is also activated, which means the AMP deaminase reaction will also be activated in order to keep the [ADP] low and the adenylate kinase reaction moving. Therefore, as ATP decreases due to utilization, IMP increases.

296

For the total ATP provision due to the anaerobic system during high-intensity exercise, why is it 1.5 times lactate?

Because for every glucosyl unit that comes from glycogen (preferred substrate in muscle), 3 ATP are produced for every 2 lactate. Therefore, there is 1.5 lactates for every 1 ATP.

297

In the equation for total anaerobic ATP provision during high-intensity exercise, why is the change in ATP multiplied by 2?

For every 1 ATP that is split by an ATPase, another one is regenerated due to the adenylate kinase reaction that is activated during high-intensity exercise.

298

Oxygen deficit is...

1. The anaerobic portion of the total ATP used at the onset of exercise 2. Refers to the lag in oxygen at the onset of exercise 3. Is equivalent to the O2 needed to supply ATP aerobically

299

What is excess post exercise oxygen consumption (EPOC)?

The elevated VO2 that occurs for several minutes immediately following exercise

300

What is the "fast" portion of EPOC consist of?

20%...resynthesis of stored PCr and replacing the muscle and blood oxygen stores

301

What does the "slow" portion of EPOC consist of?

80%...elevated body temperature and cathecholamines, conversion of lactic acid to glucose in the liver (gluconeogenesis), and elevated HR and ventilation (diaphragm) above resting values

302

Once steady state is reached, how is ATP produced?

AEROBICALLY

303

Why does elevated body temperature and catecholamines increase oxygen consumption?

The increase in temperature causes increased activation of enzymes and epipnephrine stimulates phosphorylase to breakdown glycogen, so oxygen is needed to take this glycogen and make ATP aerobically.

304

Why does the conversion of lactic acid to glucose contribute to the slow portion of EPOC?

Oxygen is needed to turn it back into glucose

305

EPOC tends to be equal to the area of?

Oxygen deficit

306

What is VO2 max?

The point at which no further increase in oxygen consumption occurs, even with increasing work rate

307

Physiological factors influencing VO2 max?

Ability of cardiorespiratory system to deliver oxygen to muscles, and the ability of muscles to take up the oxygen and produce ATP aerobically

308

Why do byproducts dramatically increase at higher work rates?

Because of increased ATP utilization

309

What is the lactate threshold?

Work rate/point where there is a dramatic increase in blood lactate levels

310

Where does OBLA (onset of blood lactate accumulation) occur?

4 mmol lactate/L

311

What is the ventilatory breakpoint?

Point at which ventilation dramatically increases.

312

What causes the ventilatory breakpoint?

Increased lactate at the muscle would lead to excess H+ and could decrease muscle and blood pH. Sodium bicar, a weak base, is used as a pH buffer, which forms sodium lactate and CARBONIC ACID. Carbonic acid readily dissociates into CO2 and water. Increased blood CO2 causes increased ventilation.

313

How does low muscle oxygen contribute to the lactate threshold?

A decrease availability of )2 will slow down electron transport and lead to NADH accumulation in the mitochondrial matrix and cytosol, which will cause pyruvate to accept an H+ to regenerate NAD and allow glycolysis to continue. This leads to the formation of lactate, which leads to the lactate threshold.

314

How does accelerated glycolysis lead to the lactate threshold?

Increased levels of ADP can stimulate PFK and glycolysis, which leads to lactate formation. Epinephrine levels will increase with exercise which will stimulate phosphorylase and glycolysis.=, leading to lactate formation.

315

How does the recruitment of fast twitch fibres lead to lactate threshold?

Fast twitch fibres are activated at high intensities of exercise. Type IIx don't have as many mitochondria, but are doing the same amount of absolute work as the aerobic Type I fibres, so they need to make the same amount of ATP. But they cannot produce it all aerobically. Therefore, it is make anarobically, which leads to accumulation of lactate.

316

What causes the reduced rate of lactate removal that contributes to the lacate threshold?

As exercise intensity increases, bloodflow to the liver is diverged from the liver to the skeletal muscles. Less blood to liver = less lactate removal = more buildup in blood

317

Sites of lactate removal during exercise?

The liver (Cori Cycle), the heart, resting slow twitch, and active slow twitch fibres

318

5 different types of LDH isoforms?

M4, M3H1, M2H2, M1H3, H4

319

Type of LDH isoform in Type II fibres?

M4

320

Type of LDH isoform in Type I fibres and heart?

H4

321

What does the M form of LDH isoform do?

Converts pyruvate ----> lactate

322

What does the H form of LDH isoform do?

Convert lactate -----> pyruvate

323

Red muscle would have what LDH isoform?

M4

324

Why does light exercise increase lactate removal versus just sitting down for rest?

The H4 LDH isoform is found in Type I fibres, which are most active during low intensity exercise (35% VO2), therefore, exercising will increase lactate removal

325

Explain 2 reasons why the recruitment of more FT fibres would contribute to lactate threshold?

1. Type II fibres are activated at higher intensities and primarily use glycolysis for ATP production, so more lactate production. 2. Type II fibres have M4 LDH isoform, which converts pyruvate to lactate, rather than lactate utilization

326

Why is there a plateau in the concentrations of metabolites during prolonged exercise around 30 minutes?

Steady state is reached, so ATP is being produced aerobically. However, is intensity changes, there will be an increase in metabolites until steady state is reached again, if it can be reached.

327

How is fuel utilization estimated during exercise?

The Respiratory Exchange Ration (RER)

328

What is RER?

Ratio of VCO2 to VO2

329

RER for 100% fat utilization?

0.7

330

RER fro 50% CHO and 50% fat utilization?

0.85

331

RER fro 100% CHO utilization?

1.0

332

If steady state is not reached, why do VCO2 and VO2 NOT reflect O2 consumption and CO2 production at the cellular level?

At high intensities, when steady state is not achieved, CO2 is produced by hte buffering system. This "extra" CO2 will throw off RER, so values will be greater than 1.

333

During low intensity exercise (<30% VO2 max) what is the primary fuel source?

Fats

334

During high-intensity exercise (>70% VO2 max) what is the primary fuel source?

CHO

335

What is the crossover concept?

Describes the shift from fat to CHO metabolism as exercise intensity increases

336

What is the crossover concept due to?

1. Recruitment of fast muscle fibres (cannot utilize fat very well because so few mitochondria) 2. Increasing blood levels of epinephrine (stimulates glycolysis through activating phosphorylase)

337

During prolonged exercise why is there a shift from CHO metabolism toward fat matabolism?

Increased rate of lipolysis (breakdown of TAGs into glycerol and FFAs)

338

What stimulates increased lipolysis during prolonged exercise?

Rising blood levels of E, NE, and glucagon

339

What inhibits lipolysis?

Insulin and blood lactic acid

340

How does insulin lower lipolysis?

Insulin --> GLUT 4 translocation to sarcolemma --> inc. glucose uptake --> more glucose in muscle --> glucose used in glycolysis, so lipolysis is not necessary anymore

341

How does lactic acid decrease lipolysis in the muscle?

Causes stimulation of pathway that converts FFA into TAGs, not breaking TAGs into glycerol and FFAs

342

Sources of CHO and fat during prolonged exercise (60-75% VO2 max)?

Muscle glyocogen and muscle TAGs are used at first, then plasma FFA and blood glucose as exercise progressese (up to 4 hrs.) due to depletion of intramuscular energy stores.

343

Metabolic fatigue is caused by?

1. Reduced energy supply (ATP and PCr) 2. Build-up of metabolic by-products (i.e. ADP, Pi, H+)

344

3 metabolites that affect the cross bridge cycle?

Reduced pH, Increased Pi, Increased ADP

345

What type of exercise results in greater and more rapid glycogen depletion?

High-intensity

346

What type of exercise is associated with depleted muscle glycogen stores?

Prolonged sub-maximal exercise to exhaustion (<70% VO2 max)

347

Where does H+ come from in the muscle?

Breakdown of ATP and anaerobic glycolysis

348

What effect does decreased pH have on free energy release?

A decrease in pH brings the [reactants] and [products] of ATP utilization closer together, so LESS free energy is released per ATP molecule. This means more energy/ATP is needed to do the same amount of work, which leads to fatigue quicker.

349

What effect does decreased pH have on Fmax and Vmax?

Decreased both in fast twitch and slow twitch muscle fibres

350

What effect does Pi have on Fmax and Vmax?

Decreases both in slow, but only decreases Fmax in fast twich fibres (no change in Vmax).

351

What effects does increased Pi have in the muscle?

Increased Pi reduces the rate of Pi release from myosin and therefore reduces strong binding and force goes down.

352

What effect does increased ADP have in the muscle?

Increased ADP reduces the ADP release from myosin and therefore more corss-bridges are locked in strong binding and force goes up BUT sliding of filaments is slowed.

353

Reduced pH leads to?

Lower Vmax and lower maximal isometric force (Po) (FT>ST)

354

Increased Pi leads to?

Reduces Po in FT and ST fibres (and Vmax only in ST fibers)

355

Increased ADP leads to?

Reduced Vmax and Increased Po

356

Why does an increase in Pi on reduced Vmax in ST fibres?

FT fibres hydrolyze ATP and release Pi so rapidly, that an increase in Pi doesn't really affect Vmax

357

Adaptations in aerobic/endurnace training depend on?

1. Genetics 2. Initial training status (greater gains in someone who starts program out of shae=pe)

358

What is the general adaptatio to aerobic/endurnace training?

Improved metabolic control ("tight" as opposed to "loose" metabolic control)

359

What is tight metabolic control?

Over a braod range of metabolic and work rates, the concentrations of PCr, Pi, ATP, ADP, AMP, and IMP show very minimal changes despite large increases in flux through actomyosin ATPases and mitochondrial ATP synthesis (phosphrylation potential remains high)

360

What is loose metabolic control?

Over a braod range of metabolic and work rates, the concentrations of PCr, Pi, ATP, and ADP show large changes when large increases in flux occurs through actomyosin ATPases and mitochondrial ATP synthesis (phosphorylation potential shows large reductions)

361

Metabolic response to exercise following training compared with sedentary?

1. Decreased glycolysis 2. Decreased CHO utilization 3. Decrease in net glycogen 4. Decrease in PCr hydrolysis 5. Decrease in ATP degradation products (i.e. ADP, Pi, AMP, IMP) 6. Increase in fat oxidation

362

Why is there an increase in glycogen storage in muscle following training?

Increased levels of glycogen synthase enzyme as a result of the training/stimulus to muscle

363

What are the 2 reasons for less glyocgen depletion following training?

1. Increased transport and utilizatoin of fat as fuel 2. Decreased translocation of GLUT 4 to sarcolemma at submaximal intensities (drop in glucose in muscle - increase in fat oxidation)

364

Why are blood lactate levels reduced at a give intensity of exercise and and lactate threshold increased following training?

There is less lactate produced due to increased fat oxidation, and there is also an increased rate of lactate removal due to change in LDH isoform to H4 and more capillaries

365

How does the decrease in ATP degradation products (ADP, Pi, AMP, IMP) account for a lower glycolytic rate?

These metabolites can allosterically activate or inihibt enzymes that control glycolysis. So, when their concentrations are decreased, there is less activation of glycolysis, so less lactate production, so less fatigue.

366

Why do the concentrations of succinate dehydrogenase and citrate synthase increase due to prolonged endurance training?

Increased number and size of mitochondria

367

2 factors that influence training adaptations?

1. Genetics 2. Initial training status

368

Due to aerobic training, is there a complete lack of glycogen utilization as a fuel source?

NO

369

What does a change in mitochondrial content mean?

There is either an increase in size or number of mitochondria, which increases the concentrations of aerobic enzymes = less lactate production

370

Why do Type IIx fibres show a greater increase in citrate synthase activity in response to higher intensity training versus slow twitch who show no difference in CS activity in response to different training intensities?

Type IIx gain more michtochondrial content in response to high intensity training because they are only recruited at higher intensities. Therefore, at low intensities, they are not recruited, so no stress = no adaptations

371

Know why more mitochondria following training leads to tighter metabolic control...

Less emphasis on glycolysis because more mitchondria = more fat oxidation. Less glycolysis = less lactate. More mitochondria = use pyruvate faster. More mitchondria = shuttle ADP and Pi into mitochondria quicker, so their concentrations in cytosol drop, so less stimulation of glycolysis and fatigue caused by their altering of the powerstroke and Pi's interaction with calcium to form calcium percipitate. More mitochondria = takes up pyruvate and NADH quicker and uses them to make ATP aerobically

372

How does the increased mitchondrial content in response to training increase the activation of aerobic energy at the onset of exercise?

More mitochondria = more sensitive to changes in [ADP, Pi, AMP, IMP], so increases activation of mitochondrial enzymes faster = aerobic metabolism occurs sooner = less lactate

373

How does oxidation of plasma fatty acids decrease PFK activity/

The oxidation causes an increase in citrate, which is an allosteric inhibitor of PFK

374

Ways in which glycolysis is regulated in response to tighter metabolic control?

1. Lack of glycoylsis causes a buildup of glucose in cell, which decreases its transport into the cell. 2. Decreased glycolysis+increased intracellular glucose = increase in G6P = decrease in phosphorylase activity 3. Increased G6P = decreased hexokinase activity 4. Increased acetyl Coa/CoA ratio, increased NADH/NAD+ ratio = decreased PDH 5. increased citrate from beta oxidation = decreased activity of PFK

375

What is calcineurin, and how does it change fibre type/mitochondrial content?

Calcineurin is a Ca2+ regulated phosphatase that dephosphorylates nuclear factor of activated T-cells transcription factors. A second target of calcineurin is the transcriptional co-activator, peroxisome-proliferator-activated receptor gamma co-activator 1 (PGC-1). Activation of calcineurin in skeletal myocytes selectively up-regulates slow-fibre-specific gene promoters and PGC-1 expression. PGC-1 activates mitochondrial biogenesis.

376

Adaptations to endurance training besides increased mitochondrial content, glyocgen synthase, etc.

1. increased muscle capillaries and myoglobin 2. Increased muscle TAG stores (because you are using fat more) and increaesd fat oxidation enzymes 3. Increase in MCT-slow and LDH H4 isoform 4. Increased VO2 max

377

In Heritage family study, how much of the increase in VO2 max was influenced by genetics?

%

378

How much of increase in VO2 max is a result of maternal genetics (mtDNA)?

30%

379

Why does mtDNA influence VO2 so much?

Mitochondrial DNA that codes for proteins in ETC comes from maternal DNA

380

What can explin the metabolic adaptations to short term training that occur before mitochondrial potential and increases in VO2 max?

Increased blood flow and VO2 kinetics at the onset of exercise during the non-steady state. Improvements may be due to increased vasodilation of arterioles.

381

What are the 2 main factors that determine the ability for the muscle to adapt to strength/resistance training?

1. Overload 2. Specificity

382

What is overload?

Muscle will increase its function and size when it is forced to contract at forces near their maximal output (loaded beyond point which normally loaded). Once significant improvements are made load applied to muscle must be progressively increased for adaptation to continue

383

What is specificity?

Muscle will adapt specifically to the exercise stress placed on it.

384

What is muscular strength?

Peak force developed during a maximum voluntary effort (depends on muscle length and velocity of contraction)

385

Muscular power

The explosive aspect of strength defined as the rate at which mechanical work is performed

386

Muscular endurance

ability to sustain repeated muscle actions (repetitions) or to sustain fixed static muscle actions for an extended period of time (max number of repetitions at a given % of 1 RM)

387

Intensity, reps, and rest for power training

.85% 1 RM, 1-2 reps, 2-5 min

388

Intensity, reps, and rest for strength

80-85% 1 RM, <6 reps, 2-5 min

389

Intensity, reps, and rest for endurance

30-70% 1 RM, > 12, 0.5 min

390

Intensity, reps, and rest for hypertrophy

70-85% 1 RM, 6-12, 1 min

391

If training increases Vmax then peak power...

increases and occurs at higher velocity

392

If training increases MVC then peak power...

increases and occurs at a lower velocity

393

Strength training increases muscle strength/power by...

1. Neural adaptation 2. Increased muscle size (more actin and myosin)