Muscle Physiology Midterm 2 Flashcards
(393 cards)
1
Q
Why is it important to study metabolism in a course on muscle?
A
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
Q
What is the problem with metabolic demand in muscles increasing over 100 fold in a very short time?
A
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
Q
What is bioenergetics?
A
The study of how energy is generated in the cell; refers to the metabolic process of converting foodstuff (substrate) into ATP
4
Q
Three energy systems in muscle?
A
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
Q
Anaerobic pathways?
A
Do NOT involve oxygen; HEPT and glycolysis
6
Q
Aerobic pathways?
A
Requires oxygen; oxidative phosphorylation
7
Q
Ammonium?
A
NH4+
8
Q
Ammonia?
A
NH3+
9
Q
How many high energy bonds does an ATP have?
A
2
10
Q
How many high energy bonds does an ADP have?
A
1
11
Q
How many high energy bonds does and AMP have?
A
NONE, but can be broken down into other things
12
Q
If a reaction is closer to equilibrium, how much energy is produced?
A
Not very much
13
Q
What happens to the the energy release as the reaction moves further from equilibrium?
A
More energy is released
14
Q
Is there more ATP or PCr stored in muscle?
A
More Pcr (3-4x more)
15
Q
ATPase reaction?
A
ATP + H2O —> ADP + Pi + H+ + Energy
16
Q
How many kcal/mol ATP?
A
7.3
17
Q
Creatine kinase reaction?
A
ADP + PCr + H+ –> ATP + Cr
18
Q
Adenylate kinase reaction?
A
ADP + ADP –> ATP + AMP
19
Q
AMP deaminase reaction?
A
AMP –> IMP + NH3
20
Q
Does PCr have a high or low capacity for producing ATP?
A
LOW CAPACITY because stores are limited in the muscle
21
Q
Does an ATPase or creatine kinase have a higher power for producing ATP?
A
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
Q
How does creatine kinase help buffer pH?
A
Uses an H+ in its reaction
23
Q
Why is the creatine kinase reaction so rapid?
A
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
Q
How many isoforms of creatine kinase are there?
A
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)
