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SPH-K 409 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

With most energy not able to be seen, how can we detect it?

A

Heat is our means of detection

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2
Q

Substrate Metabolism Efficiency for ATP and Heat

A

40% of Substrate Energy –> ATP 60% of Substrate Energy -> Heat

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3
Q

What is Direct Room Calorimetry?

A

Measuring all mechanics related to energy production such as Heat and Gases

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4
Q

What is Indirect Calorimetry?

A

Estimates total body energy expenditure based on O2 used, and CO2 produced.

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5
Q

What does Indirect Calorimetry measure?

A

Measures respiratory gas concentrations

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6
Q

Indirect Calorimetry only accurate for?

A

Oxidative Metabolism. Only good for up to VO2max and below!

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7
Q

What is VO2?

A

Volume of O2 consumed per minute. OR Rate of O2 Consumption

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8
Q

VO2: O2 usage during metabolism depends on

A

type of fuel being oxidized.

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9
Q

VO2: What happens if more carbon atoms are in molecule?

A

More O2 is needed.

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10
Q

VO2: Equation

A

Glucose (C6H12O6) < Palmitic Acid (C16H32O2)

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11
Q

What is VCO2?

A

Volume of CO2 produced per minute. OR Rate of CO2 production

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12
Q

What does RER stand for??

A

Respiratory Exchange Ratio

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13
Q

What is the Respiratory Exchange Ratio?

A

Ratio between rates of CO2 production and O2 use.

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14
Q

Formula for RER?

A

VCO2 / VO2

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15
Q

RER for 1 Molecule Glucose?

A

1.0

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16
Q

What is primarily consumed with a RER of 1.0?

A

Carbohydrates

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17
Q

RER for 1 Molecule Palmitic Acid?

A

0.70

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18
Q

What is primarily consumed with a RER of 0.7?

A

Fats

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19
Q

Formula for 1 Glucose Molecule?

A

6 O2 + C6H12O6 –> 6 CO2 + 6 H2O + 32 ATP

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20
Q

RER for Glucose?

A

6 CO2 / 6 O2 = 1.0

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21
Q

Formula for 1 Molecule Palmitic Acid?

A

23 O2 + C16H32O2 -> 16 CO2 + 16 H2O + 106 ATP

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22
Q

RER for Palmitic Acid?

A

16 CO2 / 23 O2 = 0.7

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23
Q

Assumptions for Gas Measurement of O2?

A

Storage of O2 is constant

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24
Q

Assumptions for Gas Measurement of CO2?

A

CO2 breathed off is equal to CO2 production at cells

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25
Q

Assumptions for Gas Measurements of CO2 Produced Via

A

Energy Pathways H+ being added to bicarbonate system

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26
Q

VO2 can lead to ..

A

Max or Peak Submax

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27
Q

Measures related to Training Prescription, Performance, and Fatigue

A

VO2 Lactate Threshold Critical Power / Speed

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28
Q

Slow Component of O2 Uptake Kinetics

A

At high power outputs, VO2 continues to increase. More Type II (less efficient) fiber recruitment.

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29
Q

What is the Critical Power / Speed?

A

Threshold between sustainable intensities and unsustainable intensities. Calculated asymptote of the power / speed curve.

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30
Q

What can Critical Power be used for?

A

To determine sustained race pace for a given distance or time. Other calculations can tell you how much energy you spend above CP. (Can go at 98-99% of CP for duration of race.)

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31
Q

What happens if you train?

A

Use O2 better, normal internal changes, and in 8 weeks, you can add 50 W to CP

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32
Q

Definition of Fatigue for Inability?

A

Inability to maintain required power output to continue muscular work at given intensity

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33
Q

Definition of Fatigue for Decrements?

A

Decrements in muscular performance with continued effort, accompanied by sensations of tiredness.

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34
Q

Is Fatigue reversible?

A

Yes, at rest.

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35
Q

Fatigue causes?

A

Complex Phenomenon Major Causes Phosphocreatine

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36
Q

Fatigue - Complex Phenomenon

A

Type, Intensity of Exercise Muscle Fiber Type Training Status, Diet

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37
Q

Fatigue - Major Causes (1-2)

A

Accumulation of metabolic by-products Failure of muscle contractile mechanism

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38
Q

Fatigue - Major Causes (3-4)

A

Inadequate energy delivery/metabolism Altered neural control of muscle contraction (Ionic valances can go whack after intense exercises)

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39
Q

Definition of Exhaustion?

A

Action or state of using something up or something being used up.

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40
Q

Fatigue - Phophocreatine

A

PCr depletion coincides with fatigue. PCr used for short term, high-intensity effort. PCr depletes more quickly than total ATP

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41
Q

What helps eliminate PCr Depletion?

A

Pacing helps eliminate PCr depletion

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42
Q

Fatigue - Phophocreatine by products?

A

The by products are Phosphate and Hydrogen, and they will be fatigued quicker.

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43
Q

Increased resistance in the arterial system would decrease cardiac output. Which of the following mechanisms related to cardiac output deals with the resistance of the arterial system?

A

increase in afterload

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44
Q

Following aerobic training, How would a person’s heart rate change at a given workload versus what their heart rate was before training at that same workload?

A

Lower heart rate

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45
Q

Which of the following contribute to the observed increase in stroke volume with aerobic training? (choose all that contribute)

A

increase in ventricular wall thickness increased ventricular internal diameter increase in blood volume

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46
Q

Which of the following is a normal value for stroke volume?

A

70 mL

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47
Q

Choose the factors from the list below that are an important part of the Frank-Starling mechanism (preload) and lead to increased stroke volume. (choose all that apply)

A

stretching the sarcomeres to a more optimal length connective tissue adding to tension

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48
Q

Of the factors included in the blood flow (Hagen Poiseuille) equation, which can be quickly changed to help control blood flow around the body? (choose all that apply)

A

Blood pressure created by the heart Blood vessel diameter/radius

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49
Q

In the average person, cardiac output increases throughout a ramped exercise bout (continued increase in workload). True or False, The continued increase in cardiac output seen between 75 and 100% of VO2max is due to increases in heart rate with no further increase stroke volume.

A

True

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50
Q

Which of following adaptations are related to the ability of the skeletal muscle to increase extraction of oxygen from the blood stream? (choose all that apply)

A

Increase myoglobin content Increase capillary density Increased mitochondrial content

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51
Q

RER represents

A

VCO2/VO2

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52
Q

RER would have a value near ____ when relying heavily on carbohydrate for energy production

A

1.0

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53
Q

True or False, RER values can be observed above 1.0; this high value is due to acidic by-products of energy production.

A

True

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54
Q

Cardiac and Type I muscle fibers have many things in common, which of the following is seen in cardiac fibers but not Type I fibers?

A

Utilized calcium from intra- and extracellular spaces

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55
Q

In the image of a Pacemaker and Action potential above, what ion is responsible for the depolarization in the portion labeled “0”?

A

Calcium

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56
Q

Phase 0?

A

Sodium

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57
Q

Phase 1

A

Potassium

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58
Q

Phase 2

A

Calcium

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59
Q

Phase 3

A

Potassium

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60
Q

True or False, cardiac output is defined as the volume of blood pumped out of the heart in one cardiac cycle.

A

False

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61
Q

Increased resistance in the arterial system would decrease cardiac output. Which of the following mechanisms related to cardiac output deals with the resistance of the arterial system?

A

increase in afterload

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62
Q

Metabolic Byproducts - How is phosphate Accumulated?

A

un-bonded phosphates build up in the cells during short intense activity.

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63
Q

Metabolic Byproducts - what does phosphate accumulation interefere with?

A

Interferes with power stroke. Accumulation in cytosol slows Pi release from myosin heads.

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64
Q

Metabolic Byproducts - Hydrogen Accumulation consists of what?

A

Lactic Acid Accumulation, which occurs during brief, high-intensity exercises.

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65
Q

Metabolic Byproducts - What happens if Hydrogen isn’t cleared immediately?

A

Converted into Lactate and H+

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66
Q

Metabolic Byproducts - Hydrogen accumulation causes?

A

Decrease of musce pH (acidosis).

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67
Q

Metabolic Byproducts - Hydrogen Accumulations - Buffers

A

Bufers help muscle pH but its not emough. Buffers minimize drop in pH (7.1 to 6.5). Cells can survive but don’t function well.

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68
Q

Metabolic Byproducts - Hydrogen Accumulation - pH < 6.9…

A

inhibits glycolytic enzymes, ATP synthesis. Glycolytic enzymes slowing them down and not producing ATP as quickly.

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69
Q

Free hydrogen around the filaments…

A

H+ competes with CA2+ for the binding sits of troponin. Leads to blocking of actin binding sites. Inhibits release fo ADP from myosin head and slowing shortening velocity. Can’t produce as much force!

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70
Q

What happens in Heat accumulation?

A

High muscle temperature may impair muscle function. Increases rate of carbohydrate utilization and hastens glyogen depletion.

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71
Q

Glycogen Levels in Fatigue?

A

Glycogen reservs limited and deplete quickly. Depletion corelated with fatigue.

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72
Q

Fatigue - Glycogen levels related to..

A

total glycogen depletion

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73
Q

Fatigue - Glycogen levels unrealted to

A

rate of glycogen depletion. Glycogen depletion –> blood glucose.

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74
Q

Fatigue - Glycogen Levels - Depletion and Blood Glucose

A
  • muscle glycogen insufficient for prolonged exercise.
  • Muscle will use more blood glucose causing in an increase in liver flycogenolysis and leading to hypoglycemia.
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75
Q

Muscle Glyogen Depletion and Hypoglycemia =

A

Fatigue

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76
Q

Fatigue - Glycogen Levels - Certain Rate of Muscle Glycogenolysis required to maintain

A

Oxidative pathways (fat burns in CHO flame)

*** No glycogen = Inhibited substrate oxidation.

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77
Q

Fatigue - Glycogen Levels - With Oxygen Depletion…

A

FFA Metabolism increases. Fat burns at slow rate. Won’t move as quickly. We want carbohydrate supplemation.

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78
Q

Fatigue - Glycogen Levels - To Limit Carbohydrate Related Fatigue …

A

One must ingest CHO. If glycogen depleted, you will be fatigued. You want to take carbohydrates throughout a race.

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79
Q

Movement of heart during contraction?

A

When the heart contracts, it twists up too. Blood thus moved from the bottom and has to exit at the top

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80
Q

Fiber type in the cardiac muscle?

A

Only one fiber type (similar to type I)

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81
Q

Cardiac Myocyte descriptions

A
  • Higher capillary density
  • T tubules are wide but less
  • SR is simpler than skeletal
    • Numerous large mitochondria (25-35% of cell volume
      *
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82
Q

Cardiac Myocyte Calcium location?

A

From the inside and outside of the cells

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83
Q

Cardiac Myocyte control type?

A

Completely involuntary

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84
Q

Cardiac muscle fibers connected by?

A

Intercalated Discs

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85
Q

Cardiac Myocytes - What are desmosomes and Gap Junctions?

A

Desmosomes: Hold cells together

Gap Junctions: Rapidly conduct action potentials

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86
Q

Cardiac Myocyte - SA Node

A

Primary pacemaker. 100 bpm with no input

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87
Q

Cardiac Myocyte - AV Node

A

Secondary Pacemaker

Connection to Ventricles - 100 milisecond dealy to make sure we ejected enough blood

50 bpm with no input from atrium to ventricles

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88
Q

What is an Electrocariogram (ECG or EKG)

A

A composite of all the action p otentials generated by nodal an contractile cells at a given time.

Electrodes placed on the skin which monitor electrical changes around many areas of the heart.

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89
Q

ECG - P wave

A

Artial Depolarization

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90
Q

ECG - QRS Complex

A

Corresponds with a ventricular depolarization

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91
Q

ECG - T Wave

A

Repolarization of the ventricles

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92
Q

Cardiac Cycle - Coordinated Control of

A

Parasympathetic and Sympathetic systems

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93
Q

Cardiac Cycle - Innervation Areas

A

PArasympathetic - Innvervate SA Node

Sympathetic - Innervate SA Node and Ventricular Muscle

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94
Q

SA Node HR

A

100 bpm

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95
Q

Normal Sinus Rhythm HR

A

60 - 100 bpm

~75 bpm

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96
Q

Elite Athlete HR

A

~ 40 bpm

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97
Q

Bradycardia HR

A

< 60 bpm

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98
Q

Tachycardia HR

A

> 100 bpm

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99
Q

HR from lying down to running?

A

Continues to increase as the intensity increases.

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100
Q

SV from Lying down to Running?

A

Stroke volume high when lying down then decreases and increases once jogging and running occurs.

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101
Q

CO from lying down to running?

A

CO lowest at lying down and increases as intensity increases.

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102
Q

What is Cardiac Drift?

A

An increase in HR seen during prolonged constant pace exercise.

103
Q

Endurance exercise, MAP….

104
Q

Endurance Exercise - Systolic BP..

A

increases proportional to exercise intensity

105
Q

Endurance Exercise - Diastolic BP

A

slight decrase or slight decrease (at max exercise)

106
Q

Resistance Exercise - MAP

A

Periodic large increases in MAP

107
Q

How high can mmHg get in REsistance Exercise?

A

Up to 480/350 mmHg

108
Q

Resistance exercise more common when using

A

Valsalva Maneuver

109
Q

Isometric Exercise Information

A

Large increases in pressure. Huge spikes in SBP and DBP. Probably holding breath, 3 second squats. Squats can be near 800 SBP meaning heart generated this much pressure. When you contract, you squeeze and cut off blood vessels.

110
Q

Cardiac Cycle

A

All events associated with blood flow through the heart during one complete heartbeat.

111
Q

4 Steps in Cardiac Cycle?

A

Ventricular Filling

Isovolumic Contraction

Ejection

Isovolumic Relaxation

112
Q

SV Definition

A

Volume of blood ejected in one beat

113
Q

SV - During systole..

A

most (not all) blood ejected.

114
Q

Formula for SV?

A

EDV - ESV = SV

115
Q

Types values for SV?

A

100 mL - 30 mL = 70 mL

116
Q

Ejection Fraction DEfinition

A

Percent of EDV pumped

117
Q

Ejection FRaction Formula

A

SV / EDV = EF

118
Q

Typical values for Ejection Fraction

A

70 mL / 100 mL = 0.7 = 70%

119
Q

Cardiac Output Definition

A

Total volume of blood pumped per minute

120
Q

Formula for CO

A

Q = HR x SV

121
Q

Normal RHR and Standing SV

A

RHR - 70 Beats / Min

Standing SV - 70 mL / Beat

122
Q

Typical CO?

A

70 beats / min * 70 mL / beat = 4900 mL/min = 4.9 L / min

123
Q

Typical Resting CO?

A

4.2 to 5.6 L /min

124
Q

Preload Definition

A

Degree of stretch of cardiac muscle cells before they contract ( Also known as Frank-Starling Law)

125
Q

Cardiac muscle exhibits what type of relationship?

A

A length-tension relationship. At rest, cardiac muscles sarcomeres are shorter than optimal length

126
Q

What does increased venous return do?

A

Distends (Stretches) the ventricles and increases contraction force. Through contractile and connective tissue mechanism.

127
Q

Preload - Slow Heartbeats allows..

A

more filling time. While exercising, increase in venous return. Increase in filling time/more blood returning.

128
Q

Contractility Definition

A

Contractile strength at a given muscle length, independent of muscle stretch and EDV ( Less EDV = more blood left).

129
Q

Contractility - Positive Inotropic Agents …

A

increase contractility. Utilize Norepinephrine / Epinephrine. Increased Ca 2+ influx due to sympathetic simulation

130
Q

Contracility - Negative Inotropic Agents …

A

decrease contractility

131
Q

Afterload Definition

A

Resistance that must be overcome for ventricles to eject blood.

132
Q

Afterload - What is needed to overcome resistance?

133
Q

Afterload - Greater vessel resistance forces…

A

the heart to increasepressure to eject the same volume of blood.

134
Q

Afterload - Hypertension caused by

A

increased afterload due to increased resistance.

135
Q

Resting HR for Healthy Normal

136
Q

HR Resting for Elite Endurance Athlete

137
Q

Max HR During Exercise Equation

138
Q

What is the human max that a HR could get up to?

A

Around 240 bpm

139
Q

SV Resting for Normal Healthy Individual

A

60-80 mL / beat

140
Q

SV Resting for Elite Endurance Athlete

A

100-125 mL / beat

141
Q

SV during Maximal Exercise for Normal Healthy Individual

A

120-130 mL / beat

142
Q

SV during Maximum Exercise for Elite Endurance Athlete

A

175-200 mL / beat

143
Q

Q at Rest for Normal Healthy Individual

144
Q

Q at Rest for Elite Endurance Athlete

145
Q

Q during Max Exercise for Normal Human

A

20-25 L / Min

146
Q

Q during Max Exercise for Elite Endurance Athelte

A

30-35 L / Min

147
Q

If venous return decreases, waht happens to EDV?

A

Decreases. Fills heart less, so less blood to get rid of.

148
Q

If venous return descreases, what happens to SV?

A

Decreases. Fills heart less, so less blood to get rid of.

149
Q

If afterload increases, what happens to ESV?

A

Increases. More blood left in the heart.

150
Q

If afterload increases, what happens to SV?

A

It decreases. More blood left in the heart.

151
Q

If preload increases, what happens to EDV?

A

Increases. More blood filled in the heart, more to get rid of.

152
Q

If preload increases, what happens to SV?

A

Increases. More blodo fileld in heart, more to get rid of

153
Q

If contractility increases, what happens to ESV?

A

Decreases. More blood getting ejected.

154
Q

If contractility increases, what happens to SV?

A

Increases. More blood is getting injected.

155
Q

What does the Hagen Poiseuille equation show?

A

That blood travels from high to low (Heart to the rest of the body)

156
Q

Pressure definition.

A

Pressure is the driving force for blood flow. Gradient that moves a fluid from an area of high pressure to an area of lower pressure.

157
Q

Where is the greatest fgriction encountered in the body?

A

The arterioles. There is a big drop is pressure whcih means a big drop in energy.

158
Q

Left Side is called waht?

A

Systemic Circuit

159
Q

Right side is called what?

A

Pulmonary Circuit

160
Q

Left Ventricular Pressure ?

A

Diastole - 7 mmHg

Systole - ~120 mmHg

161
Q

Brachial Arterial Pressure ?

A

Systole - 110 - 120 mmHg

Diastole - 70-80 mmHg

162
Q

Right Ventricular Pressure ?

A

Diastole - 3-4 mmHg

Systole - 25mmHg

163
Q

Pulmonary arterial Pressure ?

A

Systole - 25 mmHg

Diastole - 8mmHg

164
Q

Pulmonary Arterial Pressure - Diastole

165
Q

Why are systolic pressures lower for the right side?

A

Arteriers are like veins and system is shorter with it traveling from the heart to the lungs

166
Q

Viscosity definition

A

Property of fluid that resists the force tending to cause fluid flow.

167
Q

Viscosity Information

A

Internal friction of fluid

3-4 times greater than water. (Blood is thicker than water, ~3-4 times more viscious)

168
Q

What are the two major controls of blood flow in vessels?

A
  • Systemic Controls
    • Sympathetic and Hormonal
  • Local Controls
    • Chemical in Local Area and Mechanical
169
Q

Extrinsic Neural Control of Blood Flow

A

Redistribution of flow at system and organ levels. Sympathetic nervous system innervates smooth muscle in arteries and arterioles.

170
Q

Extrinsic Neural Control of Blood Flow - Baseline sympathetic activity –>

A

Vasomotor Tone (Vasoconstrict)

171
Q

Extrinsic Neural Control of Blood Flow - Increase in sympathetic activity –>

A

Increase in vasoconstriction.

172
Q

Extrinsic Neural Control of Blood Flow - Decrease in sympathetic activity –>

A

Decrease in vasoconstriction (Passive increase in vasodilation)

173
Q

Extrinsic Hormone Control of Blood Flow - EPinephrine

A
  • Constrict aroudn most organs (alpha receptors)
    • Dilation around skeletal muscles (Beta Receptors - A smooth muscle)
174
Q

Intrinsic Control of Blood Flow

A

Local chemical and physical changes in the active tissue afffect vessel diameter

175
Q

Intrinsic Control of Blood FLow - Metabolic Regulation

A

Controls during exercise

Buildup of local metabolic by products cause:

  • Decrease O2
    • Increase CO2, K+ , H+ , Lactic Acid
176
Q

Intrinsic Control of Blood FLow - Endothelium-Mediated Vasodilation

A

Controls during exercise

Increases in chear force activates endotheial cells to release NO and causes vasodilation

177
Q

Intrinsic Control of Blood FLow - Myogenic Mechanisms

A

Maintains constant blodo flow with ever changing pressures. Local pressure changes can cause VC and VD.

Increase Pressure - Increase VC.

Decrease Pressure - Increase VD

178
Q

At rest, veins contain…

A

2/3 of blood volume

179
Q

Veins have a ..

A

high capactiy to hold blood volume due to elastic, baloonlike vessel walls. Serve as blood reservoir

181
Q

Venous reservoir can be..

A

liberated, send back to heart and into arteries. Skeletal muscle and respiratory pumps with venoconstriction. Muscle and skin use most cardiac output during exercise

182
Q

CO Response

A

Increases linearly with workload.

183
Q

CO and VO2Max relation

A

Continues to icnreases until a Qmax is reached

184
Q

HR and VO2 Max relationship

A

Continues to increase until a HRmax met

185
Q

SV and VO2 MAx relationship

A

There is a plateau. Can’t fill heart with more blood. Pericardium stops you from stretching the heart futher.

186
Q

Fick equation

A
  • determines VO2
  • delivery
  • extraction
187
Q

Increase in maximal CO

A

due primarily to changes in SV . Hrmax doesn’t change.

188
Q

Increase in heart mass means

A

increase in LV volume

189
Q

Cardiac Mypertrophy has what affect on SV?

190
Q

Increase in LV results in what for EDV and SV?

A

Increase for both

191
Q

Aerobic Training results in what happening to the hearT?

A

Eccentric Hypertrophy. Thinner walls

192
Q

REsistance Training results in what king of hypertrophy?

A

COncentric Hypertrophy. The walls become extremely thick.

193
Q

Blood Flow Changes - Improved control of arterial system results in

A

Increase of blood flow to active muscle

Decrease of blood flow to inactive muscle

194
Q

Blood Flow Changes - Increase Capillarization leads to

A

Increase in Capillary:Fiber Ratio

Increase in Total Cross-Sectional Area for Capillary Exchange

195
Q

Blood Volume Changes – TV …

A

Increases rapidly

196
Q

Blood Volume Changes — Increase Plasma Volume because of

A

Increase of plasma proteins , increase water, and NA+ retention in first two weeks of training

197
Q

Blood Volume Changs - RBC Volume?

A

Increass, though hamatocrid may decrease

198
Q

Blood Voume Changes : Plasma Viscosity?

A

Decrease, can still c arry more O2 though.

199
Q

SV after training?

200
Q

PLasma Volume with TRaining? and leads to?

A

Incerase plasma volume –> Increase EDV –> Increases preload

201
Q

AFter Training – HR

A

Resting and submaximal Hr decrease with training –> increases filling time and increased EDV

202
Q

Increase LV after training leads to

A

Increased force of contraction

203
Q

Resting HR after training?

A

~75 vs ~ 40 bpm

204
Q

Submax HR after training?

A

HR is lower for a given worklaod because of higher SV and more efficient muscles

205
Q

HRR after training?

A

Fastery recovery with training. Indrect index of cardiorespiratory fitness and overtraining.

206
Q

What does HRR tell us?

A

Tell us abut if we are likely to die soon from disease. Should drop within 14 bpm. IF it doesn’tm you are more likely to die in the next five years.

207
Q

After Exercise, Resting BP changes?

A

REsting BP may not significanlty change in ,most

208
Q

Blood pressure changes after submax exercise?

A

Decrease in BP at given submaximal workout

209
Q

Blood pressure changes after max exercise?

A

Increases in systolic BP. Decrease in diastolic BP at maximal intensity.

210
Q

Skeletal Muscle Changes, Fiber Type

A

Type IIX perform more like Type IIa

211
Q

Skeletal Muscle Changes - Capilalry Supply

A

Increase number of capillaries supplying each fiber. May be key factor in increase ov VO2 max

212
Q

Skeletal Muscle Changes - Myoglobin

A

Increase myoglobin content by 75 -80%. (Gets oxygen to mitochondria better).

Supports increase in oxidative capacity in muscle

213
Q

Skeletal Muscle Changes - Mitochondrial Function

A

Increase in size and number. MAgnitude of change depends on training volume

214
Q

Skeletal Muscles Changes - Oxidative Enzymes

A

Increase 2-3 Times

Increased Activity with Training

COntinues to increase even after VO2max plateaus

Enhanced glycogen sparing

215
Q

Resting VO2 after training?

A

Remains unchanged

216
Q

Submax VO2 after traiing?

A

Unchanged or decreased slightly with training

217
Q

Max VO2 after training?

A

Best indiciator of cardiorespiratory fitness.

Increases substantilaly with training 15-20%

Increase due to increase of CO and capilalry density

218
Q

Long Term Improvement - VO2

A

Highest possible VO2max achieved after 12 - 18 months

219
Q

Long-Term Improvement - Performance

A

Continues to icnrease after VO2max plateaus because lactate threshold continues to increase with training .

220
Q

Individual responses dictated by…

A

Training status and pretraining VO2max. And
Heredity.

221
Q

Lactate Threshold Changes After Exercise - VO2Max

A

Increase to higher percentage of VO2max

222
Q

Lactate Threshold Changes After Exercise - Lactate Production

A

Decease lactate production leads to increase in lactate clearance. Allows higher intensity without lactate accumulation

223
Q

Lactate Threshold Changes After Exercise - RER (Formula)

A

VCO2 / VO2 ; Improved mitochrondia pathways show you burn more fats whcih means you’re more efficient.

224
Q

Lactate Threshold Changes After Exercise - RER Exercise

A

Decrease at both absolute and relative submax intensities. increased dependence of fat , decreased dependent on glucose.

225
Q

Boyles Law

A

At constant temp. Pressure varies inversely with volume.

226
Q

Tidal Volume at Rest?

A

500 mL. We have reserves above or below this

227
Q

Pulmonary Function Testing

A

Diagnosis and evaluation of the disease.

Testing volumes and capacities in athletes. Asseed by spirometry.

228
Q

What is FEV1?

A

The amount of expired air after one second. This should be above 80%.

229
Q

FEV1 for Normal Subject?

A

Around 80%

230
Q

FEV1 for Obstructive Subject?

A

Around 40%

231
Q

FEV1 for Restrictive?

A

Around 90%, but they can take in much much less air.

232
Q

What is VE?

A

Minute Ventilation

Volume of air moved per minute. 5 L / min.

233
Q

What is VT?

A

Tidal Volume. Volume of air moved per breath

234
Q

What is FB?

A

Frequency of breathes. Aka Respiratory Rate. At Rest, around 12 bpm

235
Q

What is Pulmonary Diffusion?

A

Gas exchange between aveoli and capillaries. Capillaries surrounded by alveoli

236
Q

Function of Pulmonary Diffusion?

A

REplenishes blood oxygen summply

Removed CO2 from blood helping to control pH

237
Q

Pulmonary Diffusion - Lung Blood Flow

A

At rest, lungs recieve 5 l / min.

RV CO = LV CO

Pulmonary = systemic Blood Flow

Low Pressure Circulation

Resistance much lwoer due to thinner vessel wall.

238
Q

Lung MAP?

239
Q

Aortic MAP?

240
Q

REspiratory Membrane Also called?

A

Alveolar Capillary Membrane

241
Q

Whats in the Respiratory Membrane?

A

Alveolar Wall

Capillary Wall

Respective Basement Membranes

242
Q

Respiratory Membrane is also a surface where

A

Gases are exchanged. Very thin wall with alrge surface area. Maximized gas exchange.

243
Q

Daltons Law of Partial PRessure

A

Total pressure exerted by a mixture of gases is the sum of the pressures exerted by each gas. The partial pressure of each gas is directly propertional to its percentage in the mixture.

244
Q

Henrys Law

A

When a mixture of gases is in contact with a liquid, each gas will dissolve in the liquid in proprtion to its partial pressure and solubility coefficient.

245
Q

Henry’s Law - Amount of gas that will dissolve in a liquid also depends upon..

A

its solubility

246
Q

CO2 solubity vs O2 and N2

A

CO2 is 20 times more soluble in water than O2. N2 barely dissolves in water.

247
Q

Cute saying for Henrys Law?

A

Henry passing gas in the bathroom..

Know that this is about gas and water.

248
Q

Ficks Equation for Diffusion components

A

A = Surface Area

T = Thickness of Membrane

D = Diffusion Constant

(P1-P2) = Pressure Gradient

249
Q

Partial Pressure Around Body At Rest

A

In Alveoli , PO2 @ 105, while PCO2 @ 40. Low CO2 . Large gradient for O2 because it doesn’t mix with water and cannot move easily thorugh membrane and fluids.

Larger gradeint for O2 than CO2

250
Q

Ventilation Perfucsion Coupling (At Rest)

A
  • O2 Diffusion capacity limited due to incomplete lung perfusion.
    • Only bottom 1/3 of lung perfusesd with blood. 2/3 upper lung -> poor gas exchange.
251
Q

Ventilation - Perfusion Coupling (DUring Exercise)

A

During exercise, O2 diffusion capacity increase due to even more lung perfusion. System blood pressure increases and opens top 2/3. Gas exchange over all lungs now.

252
Q

Zone 1 - Lung

A

Perfusion is Absent.

253
Q

Zone 2 - Lung

A

Perfusion is sporadic. During exercise, zone 2 is activated.

254
Q

Zone 3 - Lungs

A

Lowest Zone. Perfusion is constant. Tends to get a lot of gas exchange.

SPH-K 409 (4 decks)

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