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Applied physiology and pharmacology > Exercise physiology > Flashcards

Exercise physiology Flashcards

1
Q

The precise value of RQ is determined by the balance of substrates being metabolised. Which of the following substances gives the lowest RQ?

A

Fat

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2
Q

By how many fold can whole-body O2 consumption at maximal exercise intensity be greater than the resting value in a normal sedentary 20 year old student?

A

12/13 fold

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3
Q

What is VO2?

A

O2 consumption

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4
Q

What is basal VO2?

A

250ml/min

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5
Q

On a normal mixed diet, each ml of O2 is associated with how many joules of heat or work energy?

A

20J/ml

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6
Q

How to calculate power?

A

(VO2ml x energyJ/ml)/time sec = power watt (J/sec)

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7
Q

What is VO2 max for a bed rested, trained and Olympic athlete individual?

A

2.5L/min, 3.9L/min and up to 5.5L/min

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8
Q

How to calculate work stepping onto a box?

A

Mass of human x g x height of box

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9
Q

Power stepping onto a box?

A

Mass of human x g x height x step per min / time (secs)

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10
Q

What is average efficiency in exercise, why is it so low?

A

0.2

Much of energy expended as heat

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11
Q

How many ATP does glucose yield with oxidative phosphorylation?

A

36-39

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12
Q

How many ATP does glucose yield anaerobically?

A

2-3

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13
Q

How many ATP do fatty acids yield per CH2-CH2 unit?

A

16

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14
Q

Arterial PaO2

A

100mmHg, 13.3kpa

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15
Q

Venous PvO2

A

40mmHg, 5.3kpa

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16
Q

Why must VO2 increase in exercise?

A

To satisfy the demands of active muscle

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17
Q

How is VO2 increased?

A

Increase pulmonary blood flow (cardiac output increased), increase in O2 added to blood

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18
Q

What is Q at rest?

A

5L/min

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19
Q

What happens to Q in exercise?

A

Increases 4 fold from 5L/min up to 20L/min

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20
Q

What is muscle flow at rest?

A

0.85L/min

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21
Q

What happens to muscle flow in max exercise?

A

Rises 20x to 17L/min

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22
Q

Why does skin blood flow not fall?

A

For heat loss

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23
Q

Why does O2 uptake per min increase

A

Not because there is an increase in arterial O2 - but, the mixed venous O2 entering the lungs is reduced (more extracted by respiring muscle)

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24
Q

What is O2 uptake per min and what happens to it in exercise?

A

Ca-Cv- increases about three fold

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25
Q

What happens to Cv in exercise?

A

Cv falls from roughly 145mLO2/L at rest to around 40mLO2/L in exercise

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26
Q

What happens to Ca in exercise?

A

Ca remains at around 195mLO2

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27
Q

How does CO increase with to O2 consumption?

A

Almost linear proportion

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28
Q

How is CO increased?

A

Mainly by HR and a minor increase in SV

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29
Q

What brings about the initial raised HR?

A

Initial tachycardia brought about by withdrawal of the vagal inhibition of the pacemaker.

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30
Q

What later adds to the tachycardia?

A

Later sympathetic drive to the pacemaker adds to the tachycardia.

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31
Q

How is SV raised?

A

Partly through increased filling pressure, which increases the ventricular end diastolic volume and partly through increased ejection fraction (reduces end systolic volume).

CVP increases during exercise due to the skeletal muscle pump and splanchnic vasoconstriction, more important in sudden maximal effort exercise.

Ejection fraction increase as cardiac sympathetic activity increases

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32
Q

How can we deal with increasing the cardiac output (not experience counteracting with baroreceptor)?

A

Baroreceptor reflex is reset at a higher operating pressure

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33
Q

How is baroreflex reset?

A

To reset baroreflex need to get vagus off the system

Premotor and supplementary motor areas send signals to insula cortex which sends GABAergic projection to nucleus ambiguus - turns off higher centre vagal control.

Baroreceptors still fire to show high bp but brain not integrating this information.

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34
Q

What happens with the reset baroreflex when you stop exercise?

A

As soon as you stop exercise heart rate drops instantly, as removed inhibition on baroreflex and nucleus ambiguus respond to hypertension by facilitating bradycardia and drop in cardiac output and bp.

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35
Q

Why can adaptation of baroreflex be dangerous when you stop exercise?

A

Vagus rebounds aggressively so that cardiac output drops so lose cerebral perfusion pressure and people may faint.

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36
Q

How much does blood flow in active skeletal muscle increase during exercise?

A

40 fold

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37
Q

How does blood flow rise in muscle?

A

Primarily by the dilation of the local resistance vessels in the active muscle. Fall in vascular resistance enhances O2 and glucose delivery and permits CO to increase optimally.

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38
Q

What triggers the vessel dilation in muscle?

A

Metabolic vasodilation - by local metabolic factors

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39
Q

K+ effect on muscle

A

Important in skeletal muscle vasculature. K+ leaves the cell to repolarise, increasing extracellular [K+], this becomes greater than the capacity for the Na-KATPase.

Due to non-Nernstian activity at low extracellular K+, a small increase, leads to increased permeability for K+, Vm approaches Ek, vascular myocytes then hyperpolarize, leading to vasodilation.

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40
Q

H+ effect on muscles

A

A decrease in pH arises from metabolic acid like lactic acid or respiratory acid due to high pCO2.

Acidosis hyperpolarises vascular myocytes KATP channels respond to pH, this closes the VGCC, vasodilation occurs. Acidity also reduces MLCK activity.

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41
Q

Where is adenosine an important vasodilator?

A

The myocardium

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42
Q

Adenosine affect on the heart

A

Adenosine binds to A2a receptors which are Gs protein coupled, this leads to an increase in cAMP concentration which activates PKA which phosphorylates MLCK so it doesn’t phosphorylate MLC and smooth muscle relaxes.

In hypoxia, adenosine release is triggered

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43
Q

How is adenosine formed in muscle?

A

It is formed in active myocardium and skeletal muscles by the dephosphorylation of AMP, produced with low levels of ATP (metabolic insufficiency).

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44
Q

How does dynamic exercise affect blood pressure?

A

Muscle alternately shortens and lengthens under a low load.

Rise in MAP quite moderate due to rise in CO is offset by the fall in TPR (increase of 20mmHg up to 120mmHg).

Systolic increases more than diastolic.

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45
Q

How does static exercise affect blood pressure?

A

Sustained muscle contraction

Much bigger rise in MAP due to rise in TPR.

Isometric contraction compresses the intramuscular blood vessels attenuating the fall in vascular resistance

Activates the muscle pressor reflex

46
Q

Why does Hyperkalemia occur in exercise?

A

Potassium rises due to efflux from depolarized muscle cells: K+ high

47
Q

Why does catecholamine rise during exercise?

A

Adrenaline released from adrenal medulla: High sympathetic drive

48
Q

What are the potential harmful affects of hyperkalemia?

A

Inward rectifier K+ channels are overactive (higher gradient) which leads to rapid repolarizations.

Smaller calcium transient - negatively inotropic.

Lack of calcium for CICR - acidemia also likely - H+ binds to TrpC before calcium can - negative inotropic.

This can lead to the heart going into cardiac arrest

49
Q

What are the potential harmful affects of raised catecholamines?

A

Pro-arrhythmogenic

50
Q

How does hyperkalemia and high catecholamine negate the others effect?

A

Noradrenaline increases inward calcium current negates the negative ionotropic effect that the K+ can have on the heart

Conversely, high potassium shortens the AP by activating IK1 for fast repolarisation, prevents the sympathetic arrhythmic effects of a longer repolarisation.

51
Q

Why does hypokalaemia occur post exercise

A

Aldosterone acts on the kidney to promote retention of sodium and excretion of potassium.

During exercise, aldosterone production is increased, promoting excretion of potassium.

Maintenance of blood volume by moderate fluid intake is likely to minimise excessive engagement of the renin-angiotensin-aldosterone system.

52
Q

What happens to respiration in exercise?

A

In mild/moderate exercise – pulmonary ventilation increases proportionately with oxygen consumption but as exercise becomes more strenuous, ventilation (VE) becomes disproportionately large

53
Q

When does hyperventilation occur?

A

Hyperventilation occurs beyond anaerobic threshold – due to lactic acid production and fatigue.

54
Q

How large can VE rise to in exercise?

A

During exercise VE can reach 100L/min (20x greater than at rest)

55
Q

What are the three stages of ventilation and what controls them?

A

Phase 1: rapid increase occurs slightly before exercise begins due to central command

Phase 2: ventilation increase in proportion to exercise intensity – under chemical/neurogenic control

Phase 3: steady state of submaximal effort – ventilation maintained

56
Q

What are the two factors that lead to CV/respiratory responses?

A

Humoral (peripheral chemoreceptor response to hypoxia, pH hypercapnia etc)

Neural (signals from muscle afferents and higher brain centres.)

57
Q

Give some evidence that phase I of the respiratory curve is neurogenic? What is a criticism? And some alternate evidence?

A

Asmussen 1963: Used a pneumatic cuff to occlude venous return from exercising legs of individuals and observed that exercise hyperpnoea not attenuated - increase in ventilation not caused by release of humoral factors from muscles.

CRITICISM doesn’t negate possibility of other humoral factors mediating response

Kao 1963: Produced electrically induced contractions in hind limbs of a dog, hind limbs of second dog were simultaneously perfused with blood from first – increase in ventilation seen in first dog (neural dog) not second dog (humoral dog) - neurogenic mechanism responsible for exercise hyperpnoea not humoral agents.

58
Q

What is thought to be responsible for the initial tachycardia brought about by withdrawal of the vagal inhibition of the pacemaker and for the initial hyperpnoea?

A

Central command

59
Q

What mechanism brings about initial tachycardia?

A

Withdrawal of vagus

60
Q

What is the optimisation theory, what brain areas are involved?

A

Decision is first determiner of heart rate/ventilatory response.

Parts of cerebral cortex e.g. insula, anterior cingulate and subcortical regions (e.g. STN, PAG) both initiate voluntary movement and command CV/respiratory centres of medulla.

61
Q

Describe organisation of neuronal controlling regions?

A

SMA and PMA feed into the dorsal lateral pre frontal cortex, which then feeds to PAG / muscle contraction

62
Q

Evidence of the role of STN in central command?

A

Eldridge 1985: decorticated cats STN was stimulated, causing them to locomote. Measured relative changes in HR and BP in cats.

Then cats were injected with tubocurarine, STN was stimulated again and despite no efferent/afferent (PNS inhibited thus no muscle movement or feedback) cats mimicked CV profile of a locomoting cat.

Therefore compelling evidence for central command

63
Q

Role of the PAG

A

PAG is a central CV integrating site

Paterson 2007: monitored local field potentials occurring before and during light exercise, in the PAG region, increase in strength of recorded potentials in PAG region increased from 43% to 87% during exercise.

Lateral PAG activation shown to activate sympathetic outflow
Ventral PAG activation shown to inhibit sympathetic outflow

64
Q

How does volitional control of breathing contribute?

A

Respiratory centres also receives inputs from PMA/SMA so is under volitional control

Learned combination of effort sense and ventilatory rate at certain intensities - ventilatory motor programmes in dorsolateral prefrontal cortex, connected to PMA/SMA - working memory

65
Q

What is the central reflex?

A

Signals from muscles take part in a feedback control of heart rate, blood pressure and breathing. Through the sensing of K+ and H+ in the muscle

66
Q

When is the central reflex most important?

A

In static exercise - high compression leads to trapping of metabolites.

67
Q

Muscle pressor reflex

A

Occurs in skeletal muscle, driven by the activation of C fibre nerve endings activated by muscle contraction (not muscle spindle mechanism).

Mechanoreceptors: stimulated by local pressure and muscle contraction, served mainly by small myelinated axons (III)

Metaboreceptors: chemosensitive endings of unmyelinated group IV axons. These are activated my stimuli including raised K+ levels.

C fibres then enter the brain and synapse onto the NTS, they also synapse onto the PAG (center for sympathetic outflow)

Increase sympathetic outflow

68
Q

Evidence of metaboreceptor action in the MPR

A

When cut the dorsal route, no response from CNS to ventral route showed it’s a feedback mechanism

Smirk et al 1937: participant performed a forearm exercise, cuff inflated around the arm just prior to end of exercise. This trapped local chemical stimulants

The metaboreceptor CNS response was maintained for longer after exercise was finished with the cuff, only subsided when cuff released.

69
Q

What is the role of humoral changes in respiratory regulation?

A

PERIPHERAL chemoreceptors mediate fine tuned regulation:

Although average arterial blood gases hardly change in exercise, greater fluctuations - stimulation of glomus cell (close ATP gated TASK K+ channels - depol - Ca2+ entry, neurotransmitter release) discharge pattern of carotid sinus reflect this – shows similar fluctuations during respiratory cycle.

70
Q

What happens to PaCO2 in exercise

A

Stays constant

71
Q

What happens to PvCO2 in exercise

A

Rises

72
Q

What happens to PaO2 in exercise

A

Remains constant

73
Q

What happens to PvO2 in exercise

A

Falls (more extracted)

74
Q

The change in ventilation during exercise is thought mainly to be due to

A

Neurogenic mechanisms NOT CHEMORECEPTION

75
Q

Metabolic rate in Watts can be estimated from the oxygen consumption if we know

A

that the energy yield of body fuel is about 20 kJoules per litre of oxygen

(O2 consumption/ time) x 20j/ml

76
Q

What is minute ventilation and units?

A

Minute ventilation (VE) is the total volume of gas entering (or leaving) the lung per minute.

It is equal to the tidal volume (TV) multiplied by the respiratory rate (f). Minute ventilation = VE = TV x f At rest, a normal person moves ~450 ml/breath x 10 breath/min = 4500 ml/min.

77
Q

What is normal tidal volume?

A

500ml

78
Q

What is functional residual capacity?

A

the volume in the lungs at the end-expiratory position (ERV+RV)

79
Q

What is vital capacity?

A

the volume of air breathed out after the deepest inhalation. (IRV+ERV+TV)

80
Q

What is IRV?

A

Inspiratory reserve volume: the maximal volume that can be inhaled from the end-inspiratory (normal) level ~3.1L

81
Q

What is ERV?

A

Expiratory reserve volume: the maximal volume of air that can be exhaled from the end-expiratory (normal) position ~1.51L

82
Q

What is residual volume?

A

Residual volume: the volume of air remaining in the lungs after a maximal exhalation ~1.2L

83
Q

Name one mechanism that may stimulate the increase in ventilation that occurs during
muscular exercise.

A

Feedforward control by central command (Increases ventilation before changes in pO2/pCO2 are detected)

Peripheral chemoreceptors stimulate medullary respiratory centre

84
Q

What change would be expected to occur in the arterial partial pressure of oxygen in
response to moderate exercise (increase, decrease or little change)?

A

Little change

85
Q

What change would be expected to occur in the mixed venous partial pressure of carbon
dioxide in response to moderate exercise (increase, decrease or little change)?

A

Rise

86
Q

What change would be expected to occur in the plasma concentration of potassium in
response to moderate exercise (increase, decrease or little change)?

A

Increase

87
Q

How to calculate MAP?

A

MAP = PDias+ 1/3(PSys - PDias)

88
Q

On the Guyton curve where is exercise shown as?

A

Sympathetic stimulation curve (above), higher CVP line due to venoconstriction

89
Q

A short period of sustained exercise such as running for two minutes would lead acutely to

A

Increased cardiac output/Increased BP/Lowered pH due to lactic acid build up

90
Q

What might account for the breath-by-breath gas exchange ratio (R) being greater
than 1.0?

A

If R is near 1.0, then the body is using mostly carbohydrates for energy production.

If R is above 1.0, then carbon dioxide is being produced by other means, usually from the buffering of lactic acid. This indicates that the person is working very hard, or that they are hyperventilating

91
Q

What is the RER?

A

Respiratory exchange ratio

92
Q

What is the difference between the RQ and RER?

A

Respiratory Exchange Ratio (RER) directly measures Vol CO2 released/Vol O2 absorbed at the mouth and does not require invasive procedures. Respiratory quotient, on the other hand, measures directly at the tissue, requiring an arterial and venous catheter while monitoring blood pressure for optimal results

93
Q

Why may the RER be less than 1?

A

Fat is main fuel source

94
Q

Name two factors which tend to make the volume of gas expired greater than that
inspired.

A

Exercise and metabolic acidosis?

95
Q

Name one factor which tends to make the volume of gas expired smaller than that
inspired.

A

Altitude?

96
Q 
If the normal value for CO2 production is 200 mL/min, what is the normal 
respiratory quotient (RQ)?
A

(RQ = CO2 eliminated (200) / O2 consumed (250) ) = 0.80

97
Q

The energy content of butter is similar to that of pure lipid and is approximately

A

37kJ/g

98
Q

The energy content of toasted bread is similar to that of pure carbohydrate, which is

A

16kJ/g

99
Q

Metabolic rate in Watts (Joules per second) can be estimated from the oxygen consumption if we know

A

Energy per litre of O2

100
Q

What is the RQ when the respiratory substrate is fat?

A

0.7

101
Q

What is VCO2, what is a normal value?

A

Carbon Dioxide Output (VCO2): refers to the amount of carbon dioxide exhaled from the body per unit time. It is expressed in ml/min. A normal value at rest is around 200 ml/min. This value increases with progressive exercise.

102
Q

Why may ventilation increase more rapidly past a certain point (measured by VCO2)?

A

Passes anaerobic threshold

103
Q

What happens to PaCO2 past anaerobic threshold?

A

CO2 decreases as you are now ventilating disproportionately to metabolic needs

104
Q

What happens to PaO2 past anaerobic threshold?

A

PO2 rises (not being able to utilize O2 efficiently hence anaerobic metabolism).

105
Q

What happens to K+ past anaerobic threshold?

A

Rises

106
Q

How much does metabolic rate increase during exercise?

A

12-13 fold

107
Q

What effect does doubling the metabolic rate have on PaCO2?

A

Roughly stays the same

108
Q

What effect does doubling the metabolic rate have on PvCO2?

A

Doubles

109
Q

During muscular exercise, renal glomerular filtration would be expected to

A

Decrease

110
Q

During vigorous muscular exercise, ventilation would be expected to increase partly as a result of

A

Increased plasma H+ concentration

Applied physiology and pharmacology (18 decks)

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