Exam 2 Flashcards

1
Q

What percent of total body weight do skeletal muscles make up

A

40-50%

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2
Q

What is the origin of the muscle

A

The end of the muscle attached to bone that does not move

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3
Q

What is the insertion of the muscle

A

The end of the muscle fixed to a bone that moves during muscular contraction

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4
Q

What is unique about muscle cell organelles

A

One muscle cells can have mulitiple nuclei

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5
Q

Where are subsarcolemmal (SS) mitochondria loacted

A

Directly beneath the sarcolemma (cell membrane)

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6
Q

What do subsarcolemmal (SS) mitochondria do

A

Provide cellular energy needed to mainatain active transport of ions across the sarcolemma (e.g. power the Na/K pump)

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7
Q

Where are intermyofibrillar (IMF) mitochondria located

A

Near the myofribillar/contractile proteins

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8
Q

What do intermyofibrillar (IMF) mitochondria do

A

Provide energy for muscle contraction

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9
Q

What do satellite cells in muscle tissues do

A

Aid in muscle growh and repair by increasing the number of nuclei

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10
Q

Why is retraining easier than training

A

Because satellite cells take longer to degrade than sarcomeres and they increase the number of nuclei, making it easier to recover

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11
Q

What are 3 functions of skeletal muscle

A

Force production for locomotion and breathing, force production for postural support, and heat production during cold stress

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12
Q

How do muscles act as endocrine glands

A

They secrete myokines, IL-6, and promote an anti-inflammatory environment resulting from regular exercise

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13
Q

What do myokines do

A

Stimulate glucose uptake and fatty acid oxidation, promote blood vessel growth in muscle, and promote liver glucose production and triglyceride breakdown

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14
Q

Is IL-6 pro or anti-inflammatory

A

It can be both but during exercise it is anti-inflammatory

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15
Q

What are some anti-inflammatory benefits of regular exercise

A

Reduction in chronic inflammation and reduced risk of heart disease, type 2 diabetes, and certain cancers

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16
Q

Are concentric or eccentric movements associated with muscle fiber injury, soreness, and subsequently growth

A

Eccentric

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17
Q

What is the motor end plate

A

The pocket formed around motor neurons by folded sarcolemma

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18
Q

What is the Z line also known as

A

The Z disk

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19
Q

What is the M line

A

In the middle of both sides of thick filaments

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20
Q

What is the I band (light zone)

A

The spacing between myosin (Z line in the middle)

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21
Q

What is the A band (dark zone)

A

The length of myosin

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22
Q

What is the H zone (middle of A band)

A

Space between thin filaments that gets reduced during contraction

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23
Q

Which structures of the sarcomere experience decreased width during contraction

A

H-zone and I-band

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24
Q

What are muscle cramps

A

Spasmodic, involuntary muscle contractions often associated with prolonged, high intensity exercise

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25
Q

What is the electrolyte depletion and dehydration theory

A

That water and sodium loss from sweating causes muscle cramps (more likely in a hot environment)

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26
Q

Why is the electrolyte depletion and dehydration theory not well supported

A

Because there is no differences between cramping in severely dehydrated vs. hydrated individuals or in those with electrolyte imbalances. Also cramping is localized while electrolyte loss and dehydration are not

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27
Q

What is the altered neuromuscular control theory

A

That abnormal spinal reflex results in increased excitatory activation of muscle spindles and reduced inhibition of the Golgi tendon organ, leading to muscle cramp

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28
Q

What do muscle spindles do

A

Detect stretch in muscle and cause contraction to resist stretch

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29
Q

What do Golgi tendon organs do

A

Detect tension in tendons and inhibit alpha motor neurons so that muscles can relax to relieve tension

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30
Q

How can muscle cramping be relieved

A

Via passive stretching which will activate the Golgi tendon organ or ginger and capsaicin

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31
Q

How do ginger and capsaicin help with muscle cramping

A

They activate TRP channels that inhibit the signal to the spinal cord so that overactive motor neurons can be inhibited

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32
Q

What is the primary pathway for ATP synthesis in each muscle fiber type

A

Type I: Aerobic
Type IIa: Combination
Type IIx: Anaerobic

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33
Q

What is the myoglobin content/number of in each muscle fiber type

A

Type I: High
Type IIa: Intermediate
Type IIx: Low

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34
Q

What are glycogen stores like in each muscle fiber type

A

Type I: Low
Type IIa: Intermediate
Type IIx: High

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35
Q

What is the speed of contraction in each muscle fiber type

A

Type I: Slow
Type IIa: Fast
Type IIx: Fastest

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36
Q

What is the maximal force production and power output in each muscle fiber type

A

Type I: Moderate
Type IIa: High
Type IIx: Highest

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37
Q

What is the rate of fatigue of each muscle fiber type

A

Type I: Slow
Type IIa: Intermediate
Type IIx: Fast

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38
Q

What is the type of motor unit innervating each muscle type

A

Type I: Slow (S)
Type IIa: Fast Fatigue Resistant (FR)
Type IIx: Fast Fatigable (FF)

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39
Q

What is the recruitment order of each muscle type

A

Type I first, then IIa, then IIx

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40
Q

What type of activities are type I fibers best suited for

A

Endurance

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41
Q

What type of activities are type IIa and IIx fibers best suited for

A

Power-type

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42
Q

Which muscle type can generate the most power

A

Type IIb but it isn’t really expressed in humans despite mRNA expression during intense exercise

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43
Q

What are the characteristics of type I fibers

A

They are slow twitch and slow-oxidative

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44
Q

What are the characteristics of type IIa fibers

A

They are intermediate and fast-oxidative fibers

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45
Q

What are the characteristics of type Iix fibers

A

They are fast-twitch, fast-glycolytic fibers

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46
Q

How do muscle fiber types generate different speeds

A

Based on what isoform of ATPase they have and how quickly they can release Ca++ from the SR

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47
Q

Why do larger muscle fibers produce more force than smaller muscle fibers

A

Because they contain more actin and myosin

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48
Q

How does force production vary between men and women

A

Men are significantly stronger than women in terms of absolute and relative force production despite no apparent sex or age differences in fiber distribution perhaps because men have significantly skeletal muscle mass

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49
Q

What is the equation for power generated by a muscle fiber

A

Force * Shortening velocity

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50
Q

How does muscle fiber efficiency (lower amount of ATP to generate force) vary between muscel fiber types

A

Type I: Low
Type IIa: Moderate
Type IIx: High

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51
Q

What percent of variation in VO2max can be explained by percentage of type I fibers between individuals

A

40%

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52
Q

What are the smallest and largest motor neurons

A

Type S is smallest and type FF is largest

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53
Q

What is the size principle

A

Progressive recruitment of motor units starts with smallest units and then progresses to larger and larger motor neurons

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54
Q

What are the 4 phases of a muscle twitch

A

Stimulus, latent period, contraction, and relaxation

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55
Q

Why is force production in muscles additive with increased stimulus frequency

A

Because not all of the Ca++ is sequestered back to the SR, increasing it’s availability once more is released

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56
Q

What is DOMS

A

Delayed onset muscle soreness

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57
Q

What causes DOMS

A

Microscopic tears in muscle fibers or connective tissue (more likely during eccentric exercise)

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58
Q

What are the 7 steps in DOMS

A

1) Strenous exercise causes structural damage to muscle fibers
2) Membrane damage
3) Ca++ leaks out of SR
4) Immune-induced apoptosis compounds initial damage by activating proteases
5) Inflammatory response happening throughout
6) Edema and pain
7) Satellite cells repair damages

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59
Q

What are consequences of DOMS

A

E-C coupling failure, contractile protein loss (due to immune system), and physical disruption

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60
Q

Why can creatine kinase (CK) and myoglobin levels spike ~ 4 days after exercise

A

Due to rupture of muscles where they once resided

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61
Q

Why do subsequent bouts of exercise not cause the same response as DOMS

A

Because of adaptation in nervous system, connective tissue, and cells themselves

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62
Q

What are 3 purposes of the cardiorespiratory system

A

To transport O2 and nutrients to tissues, remove CO2 wastes from tissues, and regulate body temperature

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63
Q

How does blood flow change during exercise

A

Cardiac output increases and blood flow is redirected from inactive organs to active muscle (thermoregulation)

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64
Q

Where is the Tricuspid valve

A

It is separating the right atrium from the right ventricle

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65
Q

Where is the mitral valve

A

It is separating the left atrium from the left ventricle

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66
Q

Where is the pulmonary semilunar valve

A

It separates the right ventricle from the pulmonary artery

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67
Q

Where is the aortic semilunar valve

A

It is separating the left ventricle from the aorta

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68
Q

Which side of the heart pumps oxygenated blood

A

The left side

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69
Q

What is hematocrit

A

The percentage of blood composed of packed RBCs

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70
Q

What is average hematocrit of college-aged individuals

A

42% for males and 38% for females

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71
Q

What effect would a change in hematocrit have

A

It would change blood viscosity and flow

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72
Q

What is the equation for blood flow

A

Blood flow = Change in pressure / Resistance (viscosity, length, and r^4)

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73
Q

What is pressure proportional too in hemodynamics

A

The difference between MAP and right atrial pressure

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74
Q

What are the characteristics of diastole

A

Pressure in the ventricles is low while pressure in the atria is high, causing mitral and tricuspid valves to open and fill the ventricles with blood

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75
Q

What are the characteristics of systole

A

Pressure in the ventricles rises until it forces aortic and pulmonary (semilunar) valves open to eject blood into pulmonary and systemic circulation

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76
Q

How does the ratio of diastole compare to systole at rest vs. during exercise

A

At rest, diastole is longer than systole (2/3 : 1/3) but at exercise both is shorter and they are about equal

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77
Q

What is end diastolic volume (EDV) also known as

78
Q

What is after load

A

Average aortic BP/MAP that the ventricles must pump against to eject blood

79
Q

What nerve does the parasympathetic nervous system use to innervate the heart

A

The vagus nerve

80
Q

What nerves does the sympathetic nervous system use to innervate the heart

A

The sympathetic cardiac nerve and cardiac accelerator nerves

81
Q

How does the PSNS slow down HR

A

By releasing ACh onto muscarinic cholinergic (mAch) receptors to block calcium from coming into autorhythmic cells and effectively inhibiting the SA and AV nodes

82
Q

How does the SNS speed up HR

A

It releases catecholamines that stimulate b1-ADR on autorhythmic cells which use cAMP pathway to open Funny channels and T-type calcium channels to excite SA and AV nodes

83
Q

What causes the increase in HR during exercise

A

Initially it is due to parasympathetic withdrawal (1st 40% intensity), then due to increased SNS outflow

84
Q

How can a change in body temperature influence HR during exercise

A

Vasodilation to periphery to cool down the body can decrease BP that body tries to overcome by increasing HR

85
Q

What is heart rate variability (HRV)

A

The variation in time between heart beats (measured at R-R time interval) with wide variation indicating “healthy” balance between SNS and PNS

86
Q

Why does low HRV indicate an imabalance in autonomic regulation

A

It means there is more influence from the SNS because the SNS controls HR

87
Q

What diseases are known to decrease HRV

A

Depression, hypertension, heart disease (including myocardial infarction), and physical inactivity

88
Q

What is the Frank-Starling mechanism

A

Greater EDV results in a more forceful contraction (because more blood comes around to the heart and stretches ventricles) which is dependent on venous return

89
Q

What 3 things increase venous return

A

Venoconstriction via SNS, skeletal muscle pump, and respiratory muscle pump

90
Q

How does the skeletal muscle pump work

A

Veins have one way valves that prevent backflow so rhythmic muscle contractions increases pressure in the section to push blood up and towards the heart

91
Q

How does the respiratory pump work

A

Changes in thoracic pressure pull blood towards the heart

92
Q

What two factors affect the filling time of the ventricles

A

Heart rate and body position (takes longer when standing than laying down)

93
Q

Howa are afterload and end-systolic volume (ESV) related

A

They are directly related (decreasing afterload decreases ESV which increases SV)

94
Q

How is stroke volume regulated

A

EDV, afterload, and strength of ventricular contractility (inotropy)

95
Q

How are inotropy and ESV related

A

They are inversely related (increases in contractility decrease ESV because you’re squeezing everything out)

96
Q

How much greater is oxygen demand in the muscles during exercises compared to rest

97
Q

What two ways can O2 delivery be increased

A

Increased Q or redistribution of blood flow

98
Q

Do changes in VO2max result from increased HR or SV

A

Initially (40-60%), changes result from boht HR and SV, but above that results from increased HR

99
Q

What is the calculation for max HR

A

208 - 0.7*age

100
Q

What happens to SV in untrained subjects as a result of exercise

A

Due to high HR, fill time decreases, leading to decreased EDV and thus decreased SV

101
Q

What percent of Q goes to muscle during rest vs exercise

A

At rest, 15-20%, then increases so 80-85% during maximal exercise

102
Q

How is muscle blood flow primarily mediated during exercise

A

By local factors (autoregulation) like metabolites (e.g. NO, prostaglandins, ATP, adenosine, and endothelium-derived hyperpolarization factors) which promote vasodilation to increase flow to working muscles

103
Q

What is the Fick Eqation

A

VO2 = Q x a-vO2 difference

104
Q

How does arteriovenous difference change during exercise

A

It increases due to higher O2 uptake in tissues (used for oxidative ATP production)

105
Q

What impact do emotions have on the circulatory response to exercise

A

In emotionally charged environement, BP and HR increase due to SNS activity which can increase pre-exercise HR and BP but doens’t impact peak HR or BP during exercise

106
Q

What is the circulatory response at the onset of exercise

A

Rapid increase in HR, SV, and Q until a plateau is reached in submaximal (below lactate threshold) exercise

107
Q

What is the circulatory response to graded exercise

A

HR and Q increase linearly with increasing work rate until they plateau at 100% VO2 max, and MAP increases linearly (sBP increases while dBP remains pretty constant)

108
Q

What is the circulatory response to arm vs leg exercise

A

At same VO2, arm work results in higehr BP (due to vasoconstriction of large inactive muscle mass), and HR (SNS stimulation)

109
Q

What 3 things does the recovery of HR and BP between bouts of intermittent exercise depend on

A

Fitness level, temp and humidity, and duration and intensity

110
Q

What is the circulatory response to prolonged exercise

A

Q is stable, gradual decrease in SV (due to dehydration and reduced plasma V), and gradual increase in HR especially in heat (because of cardiovascular drift)

111
Q

What is the circulatory response to recovery

A

Decrease in HR, SV, and Q towards resting depending on duration and intensity of exercise and training of the subject

112
Q

What is pulmonary respiration

A

Exchange of O2 and CO2 in the lungs resulting from ventilation (breathing)

113
Q

What is circulatory respiration

A

O2 utilization and CO2 production by the tissues

114
Q

What are the 2 purposes of the respiratory system during exercise

A

Gas exchange between the environment and the body and regulation of acid-base balance

115
Q

How does ventilation (movement of air) occur

A

Via bulk flow (movement of molecules due to pressure difference)

116
Q

What is the pressure difference during inspiration

A

Negative Presssure (Intrapulmonary pressure < Atmospheric pressure due to diaphragm pushing downward and lifting ribs outward)

117
Q

What is the pressure difference during expiration

A

Positive pressure (Intrapulmonary pressure > Atmospheric pressure due to diaphragm relaxing and pulling ribs down)

118
Q

What is pulmonary ventilation/minute ventilation (Ve)

A

The amount of air moved in or out of the lungs per min (L/min)

119
Q

What is tidal volume (Vt)

A

The amount of air moved per breath (L/breath)

120
Q

What is the equation for minute ventilation

A

Ve = Vt * f

121
Q

What is the anatomical dead space during pulmonary ventilation

A

The space from the bottom of the trachea to the top of the nasopharynx where no gas exchange is occuring (why hyperventilation is inefficient)

122
Q

What is the average pulmonary ventilation at rest vs during max exercise

A

Rest = 7.5 L/min
Max exercise = 120-175 L/min

123
Q

What is average breathing frequency at rest vs during max exercise

A

Rest = 15 breaths/min
Max exercise = 40-50 breaths/min

124
Q

What is average tidal volume at rest vs during max exercise

A

Rest = 0.5 L/breath
Max exercise = 3-3.5 L/breath

125
Q

What changes in breathing pattern occur during exercise

A

In the beginning there are changes in both frequency and tidal volume, but in more extreme changes (e.g between 70% - 100% intensity), almost all changes result from frequency

126
Q

How is ventilation at rest controlled

A

Via somatic motor neurons in the spinal cord and the respiratory control center in the medulla oblongata

127
Q

What are the 2 inputs to the respiratory control center

A

Neural input from motor cortex and skeletal muscle mechanoreceptors (muscle spindles, Golgi tendon organs, and joint pressure receptors), and humoral chemoreceptors

128
Q

Where are central chemoreceptors located

A

In the medulla

129
Q

What do central chemoreceptors detect

A

Changes in PCO2 and H+ concentration in CSF

130
Q

Where are peripheral chemoreceptors located

A

Aortic and carotid bodies

131
Q

What do peripheral chemoreceptors detect

A

Changes in PO2, PCO2, H+, and K+ in the blood

132
Q

Does the respiratory control center respond to changes in PCO2 or PO2 first

A

Usually PCO2 (why holding one’s breath makes them need to breathe), but changes to PO2 if at elevation

133
Q

What primarily controls ventilation during submaximal exercise

A

Neural input

134
Q

What primarily controls ventilation during maximal exercise

A

Humoral input

135
Q

How does blood flow to the lung during upright resting conditions

A

Most blood flows to the base of the lung due to gravity

136
Q

How does blood flow to the lung during upright exercise

A

Blood flow increases to the top (apex) of the lung

137
Q

What is PO2 and PCO2 in the alveoli/arteries

A

PO2 = 104 mmHg
PCO2 = 40 mmHg

138
Q

What is PO2 and PCO2 in the tissues/veins

A

PO2 = 40 mmHg
PCO2 = 46 mmHg

139
Q

What kind of blood flows through the pulmonary artery

A

Mixed venous blood

140
Q

What kind of blood flows through the pulmonary vein

A

Oxygenated blood

141
Q

What does the ventilaition/perfusion ratio (V/Q) indicate

A

Matching blood flow to ventilation (ideal is 1 or more if blood flow is high)

142
Q

What causes exercise-induced asthma (bronchoconstriction)

A

Contraction of smooth muscles around the airways (brochospasms) and mucus in the airways during or after exercise causing labored breathing (dyspnea) and wheezing

143
Q

If V/Q is < 1, what local control occurs

A

Pulmonary arterioles constrict to reduce perfusion to match reduced ventilation

144
Q

If V/Q is > 1, what local control occurs

A

Pulmonary arterioles dilate to increase perfusion to match increased ventilation

145
Q

How is V/Q impacted by exercise

A

Low/moderate intensity improves V/Q while high intensity results in slight V/Q inequality

146
Q

What is pulmonary capillary transit time

A

Essentially there needs to be enough time for O2 binding sites to be saturated, so if blood flow increases too much, there will not be enough time to saturate these sites

147
Q

How does O2 travel in the blood

A

99% travels bound to Hb, the other 1% is just dissolved in plasma

148
Q

What 3 factors influence the amount of O2 that can be transported per unit volume of blood

A

[Hb], arterial oxygen saturation, and amount of O2 dissolved in plasma (minor contribution)

149
Q

What is the PO2 in the mitochondria of muscles

150
Q

Why does decreased pH favor O2 offloading to tissues

A

Because H+ ions bind hemoglobin, reducing it’s O2 transport capacity

151
Q

Why does increased temp favor O2 offloading to tissues

A

Because increased temp affects protein folding and weakens the bond between O2 and hemoglobin

152
Q

Is 2-3 DPG a major cause of rightward shift during exercise

A

No, it is only really a main factor during altitude exposure

153
Q

Why do RBCs undergo glycolysis and make so much 2-3 DPG

A

Because they have no mitochondria to undergo aerobic ATP production

154
Q

What is resting temp and pH in the body

A

37°C and pH of 7.4

155
Q

How is the a-v O2 difference affected by exercise

A

It increases because the muscles are using more O2, decreasing the venous O2

156
Q

What do myoglobin do when the muscle is at rest

A

They act almost as an O2 reserve because they are close to saturated

157
Q

How do myoglobin influence O2 debt (EPOC)

A

After exercising stops, myglobin O2 must be replenished and this O2 consumption above resting values contributes to EPOC

158
Q

How is CO2 transported in the blood

A

10% dissolved in plasma, 20% bound to hemoglobin (forms carbaminohemoglobin), and 70% as bicarb (HCO3-)

159
Q

How does CO2 primarily get from tissues into the blood

A

It is transported into RBCs where it combines with water to form carbonic acid that then dissociates further into bicarbonate and H+ (H+ combines with the hemoglobin), and the bicarb is transported into the plasma using the chloride shift

160
Q

How is CO2 primarily transported from the blood into the lung

A

Bicarb enters RBCs using chloride shift, then combines with H+ to form carbonic acid, then dissociates into CO2 and H20 where CO2 simply diffuses out into the alveoli

161
Q

Why does ventilation increase during exercise

A

Muscles undergo lots of aerobic ATP production, producing CO2 and H+, the lungs remove H+ by increasing ventilation to remove CO2 and force the bicarb reaction left

162
Q

What are the characteristics of ventilation and partial pressures of gases at the onset of submaximal, steady state exercise

A

PO2 and PCO2 are relatively unchanged while ventilation initially increases rapidly but then rises slowly until steady state

163
Q

What are the characteristics of ventilation and partial pressures of gases during prolonged exercise in a hot environment

A

There is little change in PCO2 and ventilation tends to drift upward because increased blood temp affects respiratory control center (breathing frequency increases but tidal volume doesn’t change which is why gas exchange of CO2 doesn’t change)

164
Q

Is the pulmonary system seen as a limitation during submaximal exercise in untrained subjects

165
Q

Does arterial PO2 change during graded exercise in untrained individuals

A

No, it remains within 10-12 mmHg of it’s resting value

166
Q

Is the pulmonary system seen as a limitation during maximal exercise in highly trained elite endurance athletes

A

It can be limiting because of mechanical limitations, respiratory muscle fatigue during prolonged (>120 min) high intensity (90-100%) exercise, causing 40-50% to experience exercise-induced arterial hypoxemia (EIAH)

167
Q

What causes exercise-induced arterial hypoxemia (EIAH)

A

Decreased pulmonary capillary transit time and right shift in O2-Hb dissociation curve due to decreased pH that lungs can’t overcome reduces arterial PO2 in highly trained elite endurance athletes during maximal exercise

168
Q

What 3 factors does H+ production depend on

A

Exercise intensity, amount of muscle mass involved, and duration of exercise

169
Q

What are sources of H+ ions in skeletal muscle

A

ATP breakdown, aerobic metabolism which creats carbonic acid, and anaerobic metabolism which creates lactate

170
Q

How is CO2 produced in skeletal muscles

A

It is the end of oxidative phosphorylation (made in Krebs Cycle)

171
Q

What are 2 main ways increased [H+] can impair performance

A

It inhibits enzymes in aerobic and anaerobic ATP production (specifically PFK in glycolysis), and it can impair muscle contraction by competing wiht Ca++ for binding sites on troponin

172
Q

How do buffers maintain acid-base balance

A

They release H+ when pH is high and accept H+ when pH is low

173
Q

What is the first line of defence against muscle pH shift during exercise

A

Cellular buffer systems

174
Q

What is the second line of defence against muscle pH shift during exercise

A

Blood buffer systems

175
Q

What are the 5 cellular buffer systems

A

Bicarbonate, phosphates, protiens, carnosine (60%), and transport of H+ out of the muscle

176
Q

What are the 3 blood buffer systems

A

Bicarbonate, phosphates, and proteins

177
Q

What is NHE

A

A sodium/hydrogen exchanger that brings sodium into skeletal muscle with it’s gradient and pushes H+ out

178
Q

What is MCT

A

Monocarboxylate transporter that pushes lactate and H+ out of skeletal muscle

179
Q

Which muscle fibers have higher buffering capacity

A

Fast (type 2)

180
Q

How does high intensity exercise training improve muscle buffering capacity

A

By increasing carnosine and H+ ion transporters (HNE and MCT) in trained muscle fibers

181
Q

What 6 things cause Tvent

A

Increasing blood PCO2 and H+ as well as increases in blood K+, rising body temp, elevated blood catecholamines, and possible neural influences

182
Q

How do we know lactate threshold is separate from ventilatory threshold

A

McArdle’s pts still experience Tvent

183
Q

How does graded exercise affect Arterial PO2 in untrained subjects

A

It doens’t really, PO2a is mainted within 10-12 mmHg of resting value

184
Q

How does graded exercise affect Arterial PCO2 in untrained subjects

A

It slightly decreases with maximal exercise

185
Q

How does graded exercise affect Arterial pH in untrained subjects

A

It decreases with maximal exercise because bicarb gets saturated and ventilation can’t fully compensate for H+ accumulation

186
Q

How does graded exercise affect ventilation in untrained subjects

A

There is a linear increase up to 50-75% VO2 max and then an exponsntial rise (hyperventilation during recovery intervals attenuates performance decrements)

187
Q

Why might ingesting buffer help with performance in untrained subjects during graded exercise

A

It can help attenuate drop in arterial pH because while straight bicarb might cause alkalosis, beta-alanine (carnosine precursor) improves the cellular buffer system rather than blood buffering system

188
Q

How do kidneys regualte acid-base balance during rest

A

When pH decreases, bicarb excretion is reduced and when pH increases, bicarb excretion is increased

189
Q

How is lactate removed after exercise

A

70% of lactic acid (H+ acceptor) is oxidized to pyruvate and used as a substrate by heart and skeletal muscle, 20% is converted to glucose (Cori cycle), and 10% is converted to amino acids

190
Q

Why is lactic acid removed more rapidly with light exercise in recovery (30-40% VO2max)

A

Because there is increased blood flow to the liver, etc. without producing too much more lactate

191
Q

How can lactic acid be removed quicker following exercise without continuing light exercise

A

Compression wear improves recovery my mimicking skeletal muscle pump