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SPH-K 409 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

2 Primary Groups of Fiber Type Named By The Speed Action due to..

A

Different Myosin Atpase

Different level of Sacroplasmic Reticulum Development

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2
Q

What does faster myosin removal mean?

A

Corresponds to Fast Twitch Muscles

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3
Q

How does Sacroplasmic Recticulum relate to fiber type?

A

Fast twitch have better developed sacroplasmic reticulum. Calcium can be released in a wider area.

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4
Q

What is stored in the Sarcoplasmic Reticulum?

A

Stores Calcium and releases it.

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5
Q

Slow Twitch Muscle name?

A

Type I or

Slow Oxidated

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6
Q

Fast Twitch A Name?

A

Type IIA or

Fast Oxidated Glycolytic

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7
Q

Fast Twitch B Name?

A

Type IIX or

Fast Glycolytic

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8
Q

How is a fiber type determined?

A

Muscle Biopsy

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9
Q

What is a Muscle Biopsy?

A

Small (10-100g) piece of muscle removed. Frozen, sliced, and examined under a microscope.

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10
Q

Type I Contractile Speed?

A

110 ms

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11
Q

Type II Contractile Speed?

A

50 ms

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12
Q

Motor Unit Force for Muscle Fibers from smallest to largest?

A

Type I < Type IIa < Type IIx

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13
Q

Motor Neuron Size from Smallest to Largest?

A

Type I < Type IIa < Type IIx

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14
Q

Nerve Conduction Velocity from Smallest to Largest?

A

Type I < Type IIa < Type IIx

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15
Q

Type of Myosin ATPase for Type I?

A

Slowest

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16
Q

Type of Myosin ATPase for Type II?

A

Fast

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17
Q

SR Development for Type I?

A

Least Developed

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18
Q

SR Development for Type II?

A

Highly Developed?

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19
Q

Speed of Relaxation from Slowest to Fastest?

A

Type I < Type IIa < Type IIx

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20
Q

Oxidative Capacity from Slowest to Fastest?

A

Type IIx < Type IIa < Type I

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21
Q

Myoglobin Content from Slowest to Fastest?

A

Type IIx < Type IIa < Type I

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22
Q

Color of Type I?

A

Red

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23
Q

Color of Type IIa?

A

Red to Pink

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24
Q

Color of Type IIx?

A

White

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25
Q

Mitochondrial Density from Lowest to Highest?

A

Type IIx < Type IIa < Type I

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26
Q

Capillarization (Area of Contact with Capillaries) from Lowest to Highest?

A

Type IIx < Type IIa < Type I

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27
Q

Glycogen Stores from Lowest to Highest?

A

Type I < Type IIa < Type IIx

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28
Q

Glycolytic Capacity from Lowest to Highest?

A

Type I < Type IIa < Type IIx

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29
Q

Fatigue Resistance from Lowest to Highest?

A

Type IIx < Type IIa< Type I

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30
Q

Typical Type I Fiber Make Up?

A

50%

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31
Q

Typical Type IIa Fiber Make Up?

A

25%

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32
Q

Typical Type IIx Fiber Make Up?

A

25%

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33
Q

Fiber Type Determinants: Genetic Factors

A

Determine which a-motor neurons innervate fibers and Fibers differentiate based on a-motor neuron.

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34
Q

Fiber Type Determinants: Training Factors

A

Can induce small changes in fiber type

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35
Q

Fiber Type Determinants: Aging

A

Muscles lose type II motor units. They tend to slow down with an increased risk of falling.

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36
Q

Pre-Training of Type II Fibers?

A

25% Type IIa and 25% Type IIx

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37
Q

Post-Training of Type II Fibers?

A

35% Type IIa and 15% Type IIx

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38
Q

How many Type II fibers can you change with training?

A

10% change from IIx to IIa

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39
Q

What is the nickname given to Type IIx fibers?

A

“Reservoir” Fibers

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40
Q

What percentage of Type I fibers can be converted to Type II?

A

Only 1-3%. Only Type IIx can be converted to Type I

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41
Q

What fiber type dominates Endurance Athletes?

A

Type I

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42
Q

What fiber type dominates Sprinters?

A

Type II

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43
Q

Other predictors of success for fiber types?

A

Cardiovascular Function
Motivation
Training Habits
Muscle Size

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44
Q

Graded Muscle Response

A

Controlling force output for a muscle organ to achieve the task at hand

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45
Q

3 Primary Mechanisms to Control Force Output?

A

Rate Coding within Individual Motor Units
Motor Unit Recruitment
Size Principle

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46
Q

Rate Coding Within Individual Motor Units

A

Send nerve signals at slow rate. Causes a twitch. We must send APs @ a fast rate. Send them until we’re at a tetanus reaction. This causes Calcium to be released with more Myosin interaction.

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47
Q

Motor Unit Recruitment

A

Use more motor units. Keep recruiting until we get to peak force.

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48
Q

Size Prinziple

A

As we recruit, we get different motor units.

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49
Q

Size Principle - Which is the fastest/strongest?

A

Type IIx is the fastest and strongest.

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50
Q

Size Principle - What is recruited first?

A

Type I first (slow)

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51
Q

Size Principle - Why do we use Type IIx?

A

For Sprinting, Lifting. This is activated last so we don’t fatigue. Take’s a lot of power to turn on.

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52
Q

Where is the Central Pathway Generator Found?

A

Found in the Spinal Cord. Control of voluntary movements.

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53
Q

What do the Muscles and Skeleton do?

A

Muscle spindles are sensory receptors that let us know how to move.

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54
Q

Coactivation of Antagonistic Muscles

A

Normal part of movement in humans; helps control movement/

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55
Q

What does Antagonist muscle contraction improve?

A

Control allowing for smooth motion.

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56
Q

What happens of too much antagonist muscle contraction occurs?

A

WIll decrease net torque in the intended direction of movement. (Reciprocal Inhibition)

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57
Q

What is Reciprocal Inhibition?

A

Need to keep antagonist contraction under control to allow appropriate net torque in direction of intended movement.

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58
Q

Do muscle units need to be contracted in size order or all at one time?

A

Neither

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59
Q

Asynchronous Motor Unit Recruitment

A

Allows for relatively constant force output while allowing fibers time to rest to prolong the activity. We tend to fire different motor units @ different times. We alternate between them.

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60
Q

What type of adaptations occur first in Strength Training?

A

Neural Adapatations

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61
Q

How many Neural Adapatations occur in Strength Training?

A

Five

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62
Q

What types of Neural Adaptations occur in Strength Training?

A
  1. Increased number of motor units recruited -> Decreased central governor
  2. Increase Reciprocal Inhibition
  3. Increased Synchrony of MU’s
  4. Increased Firing Rates
  5. Decreased Autogenetic Inhibition -> GTO Sensitivity Decreased
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63
Q

Neural Adaptions - Increased # Motor Units Recruited

A

Body only allows access to 80% of motor units. Can increase to 88% in extreme situations.

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64
Q

Neural Adaptions - Increased Reciprocal Inhibition

A

Teaching other muscles to resist firing

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65
Q

Neural Adaptions - Increased Synchrony of MU’s

A

Learning how to fire at the same time

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66
Q

Neural Adaptions - Increased Firing Rates

A

If they increase firing rate, they are able to then generate more foce

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67
Q

Neural Adaptions - Decreased Autogenetic Inhibition -> GTO sensitivity decreased

A

If the body not developed to be stronger, golgi tendon organ realizes they won’t rip tendon in training and allows then to use more force.

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68
Q

When do Neural Changes occur??

A

2-3 months later, you’ll see significant increase. Can’t get bigger yet because of neurological changes

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69
Q

What are the two possible mechanisms for growth of muscle tissue?

A

Hypertrophy

Hyperplasia

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70
Q

Hypertrophy

A

The most common, done at the end of puberty

They take the number of cells we have and simply make them bigger.

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71
Q

HYperplasia

A

*Usualy doesn’t happen past puberty.

Number of cells divide and bind to similar cells.

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72
Q

Types of Muscle Hypertrophy?

A

Acute/Transient Hypertrophy

Chronic Hypertrophy

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73
Q

Acute/Transient Hypertrophy

A

“Pump” (To get bigger muscles)

Fluid accumulation in muscle organ

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74
Q

Chronic Hypertrophy

A

*Actual adaptation of increasing muscle cells.
Occurs after months of training
Increase in protein synthesis that is reversible.

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75
Q

Simple definition of Catabolism?

A

Energy-yielding metabolism

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76
Q

Simple definition of Anabolism?

A

Biosynthetic Metabolism

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77
Q

What three things can Catabolism produce?

A

Heat
Utilizable Energy
Metabolic Products

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78
Q

What does Utilizable Energy lead to?

A

ATP

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79
Q

In Anabolism, what is ATP used for

A

External Nutrients
Intracellular Precursor Pool
Biosynthetic Intermediates
Biopolymers

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80
Q

What physical changes occur with Muscle Cell Hypertrophy?

A

More Myofibrils
More Actin, Myosin Filaments
More Sacroplasm (Change it. Cells bigger so we make more)
More CT (Connect to tendon, which helps muscle growth)

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81
Q

What are the control mechanisms of muscle growth that excite protein synthesis? (1-3)

A 
Activity (Can get big very easily. Resistance Training)
Growth Factors (Hormone Deficiancy)
Amino Acids (Need to build new proteins)
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82
Q

What are the control mechanisms of muscle growth that prohibit protein synthesis? (4-6)

A

SIRT1 / AMPK
High Fat Diet
Alcohol (Inhibits Muscle Growth when broken down)
Oxidation (A lot of diseases lead to inhibition)

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83
Q

What does Endurance Activities do in relation to Muscle Growth?

A

Running doesn’t hurt this. Some people can go for runs and get msucle. It just takes a while. Extreme running inhibits muscle growth.

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84
Q

What is mTOR?

A

Causes a chemical response, leading to protein synthesis.

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85
Q

What does 1-5 reps focus on?

A

Increase neuromuscular efficiency

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86
Q

What does 6-8 reps focus on?

A

Myofibilar Hypertrophy

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87
Q

What does 9-15 reps focus on?

A

Sacroplasmic Hypertrophy

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88
Q

Hypertrophy Training

A

Typically >65% of 1RM
Focuses on ~90 b/w sets
Eccentric Loading (What causes damage to muscles)
Failure? (We need to fatigue all muscles)

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89
Q

What does Resistance Training do to protein synthesis?

A

Increases it

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90
Q

How many grams of protein needed after resistance exercise for muscle growth?

A

20-25 grams/

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91
Q

How many grams of protein needed for increasing muscle masss?

A

1.6-1.7 grams protein / kg body weight / day

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92
Q

Whats the recommendation for protein synthesis?

A

Small doses (20g) every 2-3 hours

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93
Q

Causes of DOMS?

A 
Structural Damage
Chemical Mediators (Inflammatory makers)
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94
Q

How can you cope with DOMS?

A

Limit eccentric contractions when starting training
Start low intensity and progress (muscles are new)
Ice/Rolling Out/Massage (try for yourself)

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95
Q

DOMS - Anti-Inflammatories

A

May reduce swelling therefore DOMS
May interfere with recovery/adaptation

This is a sign of repair occurring in the muscles

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96
Q

What contains larger glycogen storese?

A

Type II

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97
Q

What has slower myosin ATPase?

A

Type I

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98
Q

What contains larger amount of myoglobin?

A

Type I

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99
Q

What contains a smaller fiber diameter?

A

Type I

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100
Q

What has a lower oxidative energy production capacity?

A

Type II

101
Q

What is the most fatigue resistant?

A

Type I

102
Q

What is the maximum percentage of total skeletal muscles fibers that can be converted from Type IIx fibers to type IIa with training?

A

10

103
Q

An increase in the number of excitatory signals sent per second in a motor unit leading to greater force output

A

Rate Coding

104
Q

Activating multiple motor units to produce greater forces

A

Motor Unit Recruitment

105
Q

Activating motor units in s sequential order from slow to fast twitch fibers as greater force is required

A

Size Principle

106
Q

(T/F) The average human fibers total type distribution is 50% Type IIa and 50% Type IIx

A

False

107
Q

____ fibers are recruited first due to the ___ size of the cell body of the alpha motor neuron in the motor unit

A

Type I, Smaller

108
Q

An inhibitory graded potential can make cells more negative due to

A

Potassium leaving the cell, chloride entering the cell

109
Q

Strength gains observed in the first month of training can be attributed to all of the following EXCEPT:

Increase in the total number of motor units recruited
Decrease in Reciprocal Inhibition
Increase motor unit synchrony
Decrease in Autogenic Inhibition

A

Decrease in Reciprocal Inhibition

110
Q

(T/F) Motor units are fired asynchronously during prolonged low intensity activities in order to limit fatigue of muscle fibers

A

True

111
Q

How long does Phosphocreatine last for?

A

10-15 seconds

112
Q

How long does Anaerobic Glycolysis last for?

A

1-2 minutes

113
Q

How long does Aerobic Metabolism of Fats last for?

A

Hours

114
Q

How long does Aerobic Metabolism of Carbohydrates last for?

A

~ 90 minutes

115
Q

Which of the following is a rate limiting enzyme as well as the only enzyme needed to complete ATP production in its energy pathway?

A

Creatine Kinase

116
Q

What is the net number of ATP produced by the enzymes of anaerobic glycolysis when metabolizing 1 glucose molecule?

A

2

117
Q

Where do humans house the vast majority of carbohydrate stores?

A

Muscle

118
Q

Where in the cell are Kreb’s cycle enzymes located?

A

Mitochronidra

119
Q

The difference in contraction velocity between Type I and Type II fibers is attributed, in part, to which of the follow __

A

Different ATPase

120
Q

(T/F) Type I fibers have a more developed sarcoplasmic reticulum which allows calcium to spread through sacromere faster, in turn making this fiber type faster than other fiber types

A

False

121
Q

The Margaria - Kalamen Test involves which motion?

A

Stair running

122
Q

Which of the three tests takes the longest to compete?

Winggate Anaerbic Test
Vertical Jump
Margaria - Kalamen

A

Wingate Anaerobic Test

123
Q

(T/F) The power output achieved during a Wingate test represents a participants aerobic power

A

False

124
Q

What is the mode of exercise used for the Forestry Exercise Test?

A

Stepping

125
Q

In the Forestry and Astrand Tests, what is the common physiological variable that is directly measured?

A

HR

126
Q

(T/f) The Astrand Cycling Test is a shorter more intense test than the Wingate Cycling Test

A

False

127
Q

Where are Carbohydrates primarily stored?

A

Muscle Glycogen

128
Q

Where are Fats primarily stored?

A

Subcutaneous and Visceral

129
Q

What are carbohydrates converted to?

A

Glucose

130
Q

Energy of Carbohydrates?

A

4.1 kcal/g

131
Q

Whats the main purpose of Carbohydrates?

A

Primary ATP substrate for muscles, brain

132
Q

Where is extra glucose stored?

A

Stored as Glycogen in liver, muscles

133
Q

Glycogen store limits?

A

2,500 kcal. Must rely on dietary carbohydrates to replenish

134
Q

Fats main thing?

A

Efficient Substrate, Efficient Storage

135
Q

Energy of Fats?

A

9.4 kcal/g

136
Q

What are Fats used for?

A

Energy substrate for prolonged, less intense exercise.

137
Q

ATP - Fats

A

High net ATP yeild but slow ATP production

138
Q

Fats - Broken down into

A

Must be broken down into free fatty acids (FFAs) and Glycerol

139
Q

Fats- What’s used to make ATP?

A

FFAs only used to make ATP

140
Q

Protein basic description?

A

Energy substrate during starvation

141
Q

Protein Energy Conversion?

A

4.1 kcal/g. Must be converted into another form to be used in energy production.

142
Q

What can Protein be converted into?

A

Glcose (When needed)

FFAs (Lipogenesis) (For energy storage and celllar energy substrate)

143
Q

What is a Rate Limiting Enzymes?

A

Control the rate of enzymatic energy pathways

144
Q

What can Rate Limiting Enzymes do?

A

Can create bottleneck at an early step
Activey influenced by negative feedback
Slows overall reaction, prevents runaway reaction

145
Q

How much ATP is stored?

A

Only for a few seconds of energy

146
Q

Three ATP Synthesis Pathways?

A 
ATP-PCr System (Anaerobic Metabolism)
Glycolytic System (Anaerobic Metabolism)
Oxidative System (Aerobic Metabolism)
147
Q

ATP-PCr System name and description?

A

Phospho-Creatine System

Anaerobic, Substrate Level Metabolism

148
Q

ATP-PCr ATP Yield?

A

1 ATP : 1 PCr

149
Q

ATP-PCr Duration?

A

10-15 seconds

150
Q

What is ATP-PCr used for?

A

To quickly restore ATP production

151
Q

Where does ATP-PCr occur?

A

In the cytoplasm

152
Q

PCr Rate Limiting Enzyme?

A

Creatine Kinase controls rate of ATP production; a negative feedback system

153
Q

What does Creatine Kinase do?

A

Decrease ATP (Increase ADP) –> Increase CK Activity

Increase ATP –> Decrease CK Activity

154
Q

How is ATP-PCr formed?

A

Phosphate stolen from Creatine and Attaches to ADP

155
Q

PCr Byproducts?

A

Creatine and ATP

156
Q

How much weight put on in first couple weeks because of Pcr?

A

6-8 lbs, mainly water weight

157
Q

What happens when exercising with PCr?

A

More creaine means PCr will be raised higher, allowing the duration to last longer while slowly depleting ATP as well.

158
Q

What type of reaction is the Glycolytic System?

A

Anaerobic?

159
Q

Glycolytic System ATP yield

A

2-3 mol ATP / 1 mol Substrate

160
Q

Glycolytic System Duration

A

15s - 2 min (1 min - 2 min in healthy individuals)

161
Q

Glycolytic System Breakdown?

A

Breakdown of Glucose (2 ATP) or Glycogen (3 ATP) via Glycolsys

162
Q

How many enzymes involves in Glycolytic System?

A

10-12 Enzymes

163
Q

Glycolysis Rate Limiting Enzyme?

A

Phosphofructokinase (PFK)

164
Q

What does Phosphofructokinase do?

A

Decrease ATP (Increase ADP) –> Increase PFK Activity

Increase ATP –> Decrease PFK Activity

Regulated by products of Krebs Cycle

165
Q

By products of Glycolytic System?

A

2-3 ATP
2 Pyruvate (Aerobic Continues ON)
2 Lactate + H+ (anaerobic)

166
Q

What are the fates of Lactate?

A

Taken into Mitochondria

Release from cells to be used by other cells

Release from cell and taken up by liver sent through gluconeogensis

167
Q

Pros of Glycolysis?

A

Allows muscles to contract when O2 is limited

Permits shorter-term, higher-intensity exercise than oxidative metabolism can sustain

168
Q

Cons of Glycolysis?

A

Low ATP yield, inefficicent use of substrate

Lack of O2 converts pyruvic acid to lactic acid

H+ impairs glycolysis, muscle contraction

169
Q

Why do we produce Lactate?

A

Produced to allow NAD to be recycled, allowing glycolysis to continue.

170
Q

Aerobic Energy Production begins with ATP production from….

A

Fats

171
Q

What kinda of reaction is Oxidative Metabolism?

A

Aerobic

172
Q

Oxidative Metabolism - ATB Yield

A

Per Glucose: 32-33 ATP

Per FFA: 100+ ATP

173
Q

Oxidative Metabolism Duration

A

Steady supply for hours

174
Q

How complex is Oxidative Metabolism?

A

Most complex of three bio-energetic systems

175
Q

Where does Oxidative Metabolism occur?

A

Occurs in the Mitochondria, not cytoplasm

176
Q

Krebs Cycle First Step?

A

1 Molecule Glucose = 2 Acetyl - CoA

1 Molecule Glucose -> 2 Complete Krebs Cycles

177
Q

Kreb Cycle Produces

A

2 Acetyl-CoA -> 2 GTP -> 2 ATP

NADH, FADH, H+

178
Q

Kreb Cycle; What of too many H+ in cell?

A

Too Acidic

179
Q

Kreb Cycle; Where is H+ moved to?

A

Electron TRansport Chain

180
Q

Kreb Cycle: H+ and Electrons carried to and how?

A

ETC via NADH, FADH molecules

181
Q

What happens as H+ and electrons travel down the chain?

A

H+ combines with O2 (Neutralized, forms H20)

Electrons + O2 Help Form ATP

182
Q

ETC: ATP per NADH?

A

2.5

183
Q

ETC: ATP per FADH?

A

1.5

184
Q

Total ATP Yield from Aerobic Breakdown of Carbohydrates?

A

1 Glucose = 32 ATP

1 Glycogen = 33 ATP

185
Q

Rate Limiting Enzyme for all Oxidative Cycles?

A

Isocitrate Dehhydrogenease

Similar to PFK for Glycolysis. Inhibited by ATP, Activated by ADP. Regulates Krebs and ETC

186
Q

FInal byproducts of aerobic CHO Metabolism?

A

ATP, H20, CO2

Other byproducts is recycled and used in next Kreb cycle turn.

187
Q

Fat Metabolism Basic Information

A

Features Triglycerides: Major Fat Energy Source

188
Q

Fat Metabolism: What are Triglycerides broken into?

A

1 Glycerol and 3 FFAs

Lipolysis carried out by lipases

189
Q

Yield for Fat Metabolism?

A

Yields ~3 to 4 times more ATP than Glucose.

190
Q

Is Fat Metabolism slower than Glucose Oxidation?

A

Yes

191
Q

How is Fatty Acid Transported into the Mitochondria?

A

By using membrane transporter to enter the muscle cell where it is activated. Combines with carnitine to enter the mitochondria.

192
Q

What is Beta Oxidation?

A

Process of converting FFAs to Acetyl-CoA before entering Krebs Cycle

193
Q

Cost of Beta Oxidation to start?

A

2 ATP

194
Q

Beta Oxidation: How much does 16-carbon FFA yield?

A

8 acetyl-CoA

195
Q

Beta Oxidation: How much does 1 glucose yield?

A

2 acetyl-CoA

196
Q

Beta Oxidation: What does Fat Oxidation requires?

A

Requires more O2 but yields far more ATP later.

197
Q

Total ATP yield from Oxidation of 16 carbon fatty acid?

A

116 ATP

198
Q

Beta Oxidation Rate Limit?

A

Limited by FFA Availability in musclce and Kreb’s Speed

199
Q

All three Energy Systems interact for all activities but…

A

not one system contributes 100% but one system often dominates for a given task.

200
Q

Byproducts of one system can…….

A

affect another systems function. Citrate produced in the Krebs cycle can inhibit PFK and slow glycolysis sparing muscle glycogen.

201
Q

Order of Maximal Rate of ATP Generation?

A

Fat Oxidation < CHO Oxidation < Glycolysis < PCr

202
Q

Order of Maximal Available Energy?

A

PCr < Glycolysis < CHO Oxidation < Fat Oxidation

203
Q

Oxygen Consumption Abbrevition?

A

VO2 - Volume of Oxygen Consumed

204
Q

Rate of Oxygen Consumed by the body

A

Typically reported as an amount per minute.

205
Q

Absolute Oxygen Consumption

A

Oxygen consumed per min (L/min)

206
Q

Relative Oxygen Consumption

A

Oxygen consumed per minute relative to body mass (ml/kg/min)

207
Q

VO2 Max

A

(Plateau) Max rate of oxygen consumption

Point at which O2 consumption doesn’t increase with further increase in intensity

208
Q

VO2 Peak

A

(No Plateau)

Highest measurement of VO2 with no observable plateau. They could drop off after they reach the peak.

209
Q

How much Relative VO2 Max consumed depends on Ab. VO2 and Body Mass. How do you know if you have a good amount burned?

A

The individual who burns a higher amount per ml/kg/min.

210
Q

VO2 Max Norms for Average Fit

A

Male - 45 ml/kg/min

Female - 40 ml/kg/min

211
Q

VO2 Max Norms for Elite

A

Male - >70 ml/kg/min

Female - >60 ml/kg/min

212
Q

VO2 Max for Couch Potato

A

= 30 ml/kg/min

213
Q

VO2 Max for End Stage COPD

A

~15 ml/kg/min

214
Q

Order from highest to lowest VO2

Running
Cycling
Cross Country Skiing

A

Cross Country Skiing
Running
Cycling

215
Q

What is the Lactate Threshold (LT)?

A

Point/Intensity at which blood lactate accumulation increases markedly.

Lactate production rate > Lactate Clearance Rate.

216
Q

Lactate Threshold Interaction between

A

Aerobic and Anaerobic Systems. Formally called the anaerobic threshold.

Measure of anaerobic threshold.

217
Q

Lactate Threshold usually expressed as ..

A

percentage of VO2 Max

218
Q

Lactate Threshold for Training and Untrained

A

Untrained - 55-65% of VO2 Max

Trained - 80-90% of VO2 Max

219
Q

How much can VO2max increase in untrained?

A

15-20%

220
Q

Training Effects on Vo2 MAx and LT affected by

A

Genetics (Amount of Type I)
Weight at Start of Training
Initial Fitness

221
Q

Causes of increase for VO2max and LT

A 
Increase Oxidative Enzymes
Increase Mitochondrial Content and Density
Increase Capillary Density
Increase Myoglobin Content
Conversion of Type IIx to Type IIa
222
Q

Lactate threshold can increase to

A

90% of VO2 Max

223
Q

Causes of increases for Lactate?

A

Increase Oxidative Capacity (Increase oxidative enzymes and increase mitochondrial content and density)

Increase number of transporter around body

224
Q

PhosphoCreatine Alternative Name

A

Creatine Phosphate

225
Q

Glycolysis Alternative Name

A

Anaerobic Glycolysis

226
Q

Oxidative Alternative Name

A

Aerobic Metabolism

227
Q

PhosphoCreatine Substrate/Fuel Entering Pathway

A

Phosphocreatine

228
Q

Glycolysis Substrate / Fuel Entering Pathway

A

Glucose

Glycogen

229
Q

Oxidative Substrate / Fuel Entering Pathway from Glycolysis

A

Pyruvate/Lactate

Acetyl CoA, NADH

230
Q

Oxidative Substrate / Fuel Entering Pathway from Beta Oxidation

A

Acetyl CoA

NADH & FADH

231
Q

PhosphoCreatine Relative Speed of ATP Production

A

Fastest

232
Q

Glycolysis Relative Speed of ATP Production

A

~ 2 Times slower the PCr

233
Q

Oxidative Relative Speed of ATP Production

A

4-7 Times Slower than PCr

234
Q

Phosphocreatine By-Products

A

ATP

Creatine

235
Q

Glycolysis By-Products

A

ATP

Pyruvate & NADH/Lactate + H+

236
Q

OxidativeBy-Products

A

ATP
H20
CO2
Recycled Intermediate

237
Q

Phosphocreatine Location of Pathway Within Cell

A

Cytosol

238
Q

Glycolysis Location of Pathway Within Cell

A

Cytosol

239
Q

Oxidative Location of Pathway Within Cell

A

Mitochondria

240
Q

PhosphoCreatine Time Limit

A

~10-15 seconds

241
Q

Glycolysis Time Limit

A

~1-2 minutes

242
Q

Oxidative Time Limit

A

Hours

243
Q

PhosphoCreatine Control Of Rate

A

Increase Rate means Decrease ATP

And Vice Versa

244
Q

Glycolysis Control of Rate

A

Increase Rate means Decrease ATP

And Vice Versa

245
Q

Oxidative Control of Rate

A

Increase Rate means Decrease ATP

And Vice Versa

246
Q

PhosphoCreatine Rate Limiting Enzyme

A

Creatine Kinase

247
Q

Glycolysis Rate Limiting Enzyme

A

Phosphofructokinase

248
Q

OXidative Rate Limiting Enzyme

A

Isocitrate Dehydrogenase

SPH-K 409 (4 decks)

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