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Exercise & Environment > Integrated cardiovascular and respiratory reflexes > Flashcards

Integrated cardiovascular and respiratory reflexes Flashcards

1
Q

what does the only energy system that can fuel prolonged muscular exercise require

A

oxygen

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2
Q

what is the challenge of exercise

A

controlling the CR system so that mitochondrial oxygen consumption and CO2 production can continue, homeostasis is maintained

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3
Q

what causes the challenge of exercise

A

at onset of exercise there is:
- rapid increase in oxygen consumption
- rapid increase in carbon dioxide production
the body ability to tolerate rapid changes in local PCO2 and PO2 is limited
- CR system must respond rapidly for contraction to continue and PCO2, PO2 homeostasis be maintained

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4
Q

VO2

A

rate of oxygen uptake by lungs

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5
Q

VCO2

A

rate of carbon dioxide output by lungs

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6
Q

VE

A

minute ventialtion

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7
Q

PaO2

A

partial pressure of arterial oxygen

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8
Q

PAO2

A

partial pressure of alveolar oxygen

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9
Q

PVO2

A

partial pressure of mixed venous oxygen

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10
Q

PVCO2

A

partial pressure of mixed venous carbon dioxide

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11
Q

VO2 at BMR compared to excersie

A

rest: 250ml/min
exercise: 3000ml/min

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12
Q

VE at BMR compared to exercise

A

rest: 5l/min
exercise: >150l/min

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13
Q

where do gas partial pressures change the most in exercise

A

skeletal muscle capillaries.

small changes in venous blood too

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14
Q 
Partial pressures at BMR
OXYGEN
arterial blood
skeletal muscle
venous blood 
CARBON D
arterial blood
skeletal muscle
venous blood
A 
Partial pressures at BMR
OXYGEN
arterial blood- 100mmHg
skeletal muscle 40mmHg
venous blood 40mmHg
CARBON D
arterial blood 40mmHg
skeletal muscle 46mmHg
venous blood 46mmHg
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15
Q 
Partial pressures during exercise
OXYGEN
arterial blood
skeletal muscle
venous blood 
CARBON D
arterial blood
skeletal muscle
venous blood
A 
Partial pressures during exercise
OXYGEN
arterial blood- 100mmHg
skeletal muscle 0mmHg
venous blood 0mmHg
CARBON D
arterial blood 30mmHg
skeletal muscle 90mmHg
venous blood 90mmHg
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16
Q

mmHg : kpA

A

7.5mmHg : 1 kPa

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17
Q

where does venous blood go

A

heart

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18
Q

where does arterial blood go

A

all tissues

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19
Q

what causes the drop in arterial PCO2 in exercise?

A

drops from 40 at rest to 30, despite raised PCO2 in skeletal muscle.
This is because acidosis causes more CO2 to be exhaled during exercise

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20
Q

how is oxygen carried in blood

A
  • physically dissolved in plasma solution

- chemically bound to Hb

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21
Q

how much oxygen is dissolved in plasma

A

3ml/L of blood

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22
Q

which oxygen in blood accounts for PO2

A

only oxygen dissolved in plasma exerts partial pressure

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23
Q

what does PO2 play a role in

A
  • regulation of breathing

- loading of Hb in lungs and release of O2 at tissues

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24
Q

how much oxygen is bound to Hb

A

197ml / L of blood

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25
Q

how does oxygen bind to Hb

A

Hb has 4 Fe2+ sites per Hb molecule, each bind to one O2 molecule

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26
Q

total oxygen in blood

A

200ml per litre of blod
3ml dissolved in plasma
197ml bound to Hb

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27
Q

CO2 carriage in blood

A
  • physically dissolved in plasma
  • bound to terminal amine groups of proteins in plasma and RBC
  • as bicarbonate ions
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28
Q

what role does PCO2 play

A

chemical basis for control of breathing

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29
Q

which carbon dioxide in blood accounts for PCO2

A

only CO2 dissolved in plasma

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30
Q

what does CO2 bind to on RBC

A

alpha and beta chains in Hb

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31
Q

Role of bicarbonate ions in tissues

A

CO2 + H2O -> H2CO3 -> HCO3- + H+

H+ is buffered by RBC to maintain pH

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32
Q

Role of bicarbonate ions in lungs

A

H+ + HCO3- -> H2CO3 -> H2O + CO2

as CO2 leaves the blood, equilibrium is reversed

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33
Q

what is carbonic anhydrase and were is it found

A

reversibly catabolises conversion of CO2 and H2O to carbonic acid

found in RBC

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34
Q

where is majority of CO2 transported in blood

A

70% in RBC

30% in plasma

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35
Q

how is ventilation controlled

A

different negative feedback loops, based on sensors in the body

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36
Q

important sensors in body for controlling ventilation

A

Central and peripheral chemoreceptors

  • detect changes in PO2, PCO2 and pH
  • send signals back to respiratory control centres in brain stem
  • reflex adjust ventilation to maintain blood gas homeostasis
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37
Q

where are respiratory control neurones

A

pons, medulla and other regions

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38
Q

what are effectors in ventilation control

A 
respiratory muscles
inspiration:
- diaphragm
- external intercostals
expiration
- internal intercostals
-abdominal muscles
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39
Q

what are the sensors in ventilation control

A

central and peripheral chemoreceptors are the main ones. Others:

  • lung and airway receptors
  • joint and muscle receptors
  • arterial baroreceptors
  • pain and temperature
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40
Q

where are central chemoreceptors

A

just below viral surface of medusa, bathed in brain extracellular fluid

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41
Q

what stimulates central chemoreceptors

A

changes in pH when CO2 diffuses out of capilaries

  • H+ cannot cross BBB but CO2 can
  • CO2 reacts to form carbonic acid once passed BBB
  • rapidly dissociates to form bicarbonate and H+ which are detected by chemoreceptors
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42
Q

what happens when central chemoreptors detect change in H+

A

signal to medullary respiratory neurones which controls adjustment of ventilation

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43
Q

how much of the ventilatory response are chemoreceptors responsible for

A

70%

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44
Q

where are peripheral chemoreceptors

A

in carotid bodies - not carotid sinus

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45
Q

what is the primary site for detecting arterlia hypoxia

A

peripheral chemoreceptors

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46
Q

what do peripheral chemoreceptors detect

A
  • arterial hypoxia (low PaO2)

- sensitive to PC and pH, K+ and other substances like adrenaline

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47
Q

phases of ventilation response to constant load exercise

A

I) immediate increase at onset
II) exponential rise
III) steady state

  • steady state will not be achieved above anaerobic threshold
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48
Q

when is steady state ventilation not achieved

A

in heavy exercise, above anaerobic threshold

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49
Q

what does ventilation increase proportionately to

A

metabolic rate

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50
Q

what can ventilation increase to

A

beyond 150L/minute

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51
Q

what does the relationship between ventilation and metabolic rate tell us

A

ventilation increases proportionally to metabolic rate, and can increase beyond 150L/min
THEREFORE
control mechanism that drives increase in breathing must be responsible for:
- immediacy of response
- large magnitude of exercise
- tight matching of response to metabolic rate

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52
Q

arterial gas tensions during sub maximal exercise

A

remain constant, despite increases in metabolic rate

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53
Q

metabolic rate in terms of ventilation

A

VO2 and VCO2

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54
Q

are arterial gas tensions maintained beyond the anaerobic threshold

A

no; pH and PaCO2 decrease because of acidoses and hyperventilation

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55
Q

how does PaCO2, PaO2 and pH remain constant in sub maximal exercise

A

breathing increase is

  • immediate at onset of exercise
  • has magnitude proportional to change in metabolic rate
  • O2 delivery to muscles in CV system is proportionate to workload and VO2
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56
Q

what controls the breathing response to exercise?

A

poorly understood:

  • no error signal for chemoreceptors bc PaCO2, PaO2 and pH remain constant
  • there are changes in the venous blood, but that isn’t where chemoreceptors are located

?????

57
Q

speculations of how breathing response to exercise is controlled

A
  • mixed venous chemoreceptors, would be perfectly located to detect changes in metabolic rate, but none have been found
  • neural feedback from skeletal muscle afferent nerves
  • neural feedforward signals from motor regions in the brain; central command
  • humeral stimuli from blood-born factors; circulating K+, adrenaline, , which could increase chemoreceptor sensitivity to minute changes o PaO2 and PaCO2
58
Q

multiple mechanisms responsible for breathing response to exercise

A

neural-humoral theory
argued that only a mixture of mechanisms could explain the characteristics of breathing response:
- neural mechanism responsible for immediacy of response in phase I
- humoral mechanism responsible for fine tuning of response to tightly match ventilation with metabolic rate

59
Q

neural-humoral theory

A

breathing response to exercise

60
Q

evidence for neural mechanisms of breathing response

A

feedforward central command, and neural feedback mechanisms of skeletal afferent nerves are known to be important in CV control
- evidence suggests the control CR too

61
Q

evidence for humoral mechanisms

A

not PaO2, PaCO2 or pH cus they don’t change in sub max exercise

  • increase in sensitivity of chemoreceptors, giving a bigger response to same stimuli - conflicting data and only small effect size
  • plasma K+ and adrenaline increase in exercise and experiments suggest they case increased ventilation, but very small effect size
62
Q

conclusions of breathing response to exercise

A
  • ventilation is closely matched to work load and respiratory control mechanisms exist that maintain arterial blood gas homeostasis
  • unsure how this is coordinated but like likely central command feed forward and muscle afferent feedback play a role
  • likely that no single proposed mechanism accounts for the response
  • element of redundancy
63
Q

VO2 measured at mouth during exercise

A

rises linearly with work rate during an incremental exercise task
- because oxygen consumption of working muscles increases

64
Q

how is increased VO2 in active muscles achieved

A
  • central mechanisms which increase CO
  • peripheral mechanisms which redistribute blood to exercising muscles
  • all occur along side respiratory response
65
Q

CV responses during dynamic whole body exercise

A 
- HR and stroke volume increase 
= increase CO
- increase vasodilation of active muscles
-some vasoconstriction of inactive muscles
= decreased TPR
- increased CO 
- decreased TPR
= increased MABP
66
Q

what happens to systolic BP during exercise

A

increases as stroke volume increases

67
Q

what happens to MABP during exercise

A

increases as CO increases and TPR decreases

68
Q

what happens to diastolic BP

A

remains constant because of balances vasodilation and vasoconstriction of active and inactive muscles (redirection of blood flow)

69
Q

CV response to dynamic incremental exercise

A
  • linear increase in HR with work loud
  • increase in stroke volume, then plateaus
  • close to linear increase in CO
  • Decrease in TPR due to muscle vasodilation
  • increase in SV tends to increase SBP
  • TPR tends to keep DBP constant, but may decrease
  • MABP increases moderately because = CO x TPR
70
Q

why does vasodilation and vasoconstriction both occur

A

must have a balance

  • vasodilation increases O2 delivery to working muscles
  • vasoconstriction maintains BP
71
Q

what would happen to MAP without vasoconstriction

A

MAP would plummet becuase of widespread vasodilation of other beds and increase in CO

72
Q

what controls CV response to exercise

A
  • autonomic nervous system

- local mechanisms

73
Q

role of autonomic nerves system in CV response to exercise

A
  • controls increase in HR, SV and vasoconstriction of inactive muscle and other orgas
74
Q

role of local mechanisms in CV response to exercise

A

controls increased vasodilation in working muscles

- e.g build up of muscle metabolites

75
Q

how is HR increased during exercise

A

ANS
combination of:
-reduced vagal/parasympathetic stimulation of SA node
- increase beta adrenergic sympathetic stimulation of SA node

76
Q

how is stroke volume increased in exercise

A

ANS

  • increased sympathetic activity to:
    • increase central venous pressure
    • increase ventricular contractility
77
Q

how does increased central venous pressure result in increased stroke volume

A

-decreased venous compliance
- increased atrial contractility
= force of contraction via frank starling mechanism

78
Q

CO during exercise

A

increased total CO, and additional blood flow carefully redirected to where it is needed

79
Q

role of vasodilation during exercise

A

at active muscle for oxygen delivery

at skin for thermoregulation

80
Q

role of vasoconstriction during exercise

A

of inactive muscles and other tissues to maintain BP

81
Q

what drives vasodilation in exercise

A

local mechanisms

82
Q

what rives vasoconstriction in exercise

A

widespread increase in sympathetic vascular tone (ANS)

83
Q

what controls the ANS in exercise

A

multiple mechanisms, hence complex response

  • feedforward via central command
  • reflex feedback via:
    • -metabolically and mechanically sensitive skeletally muscle afferents
      • arterial baroreceptor afferents

= coordinated autonomic adjustments to increase HR, SV, CO, BP and arterial resistance

84
Q

central command

A

concept that the higher brain simultaneously activates two seperate networks:

  • neuromotor control systems of active skeletal muscles
  • autonomic neural control of CV system & possible respiratory control centres
85
Q

theory of feedforward central command

A

theorised that the CV system can anticipate the demands of exercise and so is a feedforward control mechanism

86
Q

concept for feedforward

A
  • Krogh and Lindhard
  • HR and ventilation increase immediately with dynamic exercise
  • immediacy suggests not a feedback mechanism
87
Q

two methods for assessing feedforward CC theory

A
  • uncoupling motor drive of CC from muscle force/work

- identifying neurocircitry of CC

88
Q

Uncoupling motor drive of CC from muscle force/work

A

isometric handgrip exercise performed with and without neuromuscle block NMB, curare
- with NMB, attempted hand grip produced almost zero force as forearms effectively paralysed
- in these conditions, CC mechanism won’t be affected but there will be no neural feedback from muscle as no force produced
- NMB attempt resulted in similar HR response to normal contraction, but smaller increase in MSNA and MAP
= suggests that CC has greater role in regulation HR in these workloads

89
Q

curare

A

neuromuscular block

90
Q

NMB

A

neuromuscular block, e.g curare

91
Q

Identifying the neurocircuitry

A

cat was stimulated in the sub thalamic motor region
= increased BP during spontaneous locomotion
cat was the paralysed, therefore no neural feedback from muscle for movement
- cat stimulated again and there was a CV and respiratory response even though cat didn’t more

92
Q

summary of central command theory

A
  • feedforward thought to provide instant and gross matching or CR responses to metabolic needs
  • compelling but indirect evidence that CR system controlled by feedforward too
  • animal evidence strong
  • hard to obtain evidence in humans
  • evidence that other mechanisms also play a role
93
Q

reflex feedback control of CV response to exercise evidene

A

Alam and Smirk 1963 used PECO experiment to show that ANS is modulated by not just feedforward. PECO showed that metabolites trapped in muscle were driving an exercise pressor reflex EPR

94
Q

PECO

A

Post Exercise Circulatory Occlusions
animal studies demonstrated that group III and IVE afferents in muscle are responsible for EPR
- stimulating ventral roots results in muscle contraction and increased BP
- PECO sustains BP
-cutting dorsal root afferents abolishes the BP response (GI-IV)
- BUT selective blocking of thinly myelinated and non-myelenisted fibres (III-IV) via local anaesthetic did abolish the response
- Group III and IV afferents drive EPR

95
Q

which group fo afferents dove EPR

A

III and IV

96
Q

what is EPR

A

exercise pressor reflex

97
Q

anatomy of Group III afferents

A
  • thinly myelinated
  • largely mechanosensitive
  • passive muscle stretch in humans causes:
    • vagal withdrawal (PNA)
    • increases in HR
98
Q

PNA

A

parasympathetic neural activity

99
Q

SNA

A

sympathetic neural activity

100
Q

Anatomy of group IV afferent

A
  • non-myelinated
  • largely metabosensitive
  • PECO in humans results in
      • large insures in SNA and BP
      • effect on HR debated
101
Q

which fibres are metabosensitive

A

Grou IV

102
Q

which fibres are non myelinated

A

group IV

103
Q

Which fibres are mechanosensitive

A

Group III

104
Q

which fibres are thinly myelinated

A

Group III

105
Q

recent evidence for afferent feedback

A

injection of opiod agonist fentanyl inhibits feedback fro III and IV sensory efferents

reduced HR and MAP during cycling at different workloads
reduced ventilatory response despite similar VO2

106
Q

summary for afferent feedback mechanism

A
  • provide sensory feedback on conditions of working muscle
  • compelling evidence that CV system is partly controlled by skeletal muscle afferent feedback … and may drive respiratory response too
  • attractive mechanism bc accounts for rapid CR response at onset, along side CC, and how metabolic rate is matched
  • stimulation can results in increased SNA and reduced cardiac PNA = increased HR and BP
107
Q

vascular tone control mechanisms for muscle blood flow in exercise

A
  • neural
  • endothelial
  • hormonal
  • myogenic
  • metabolic
108
Q

neural vascular tone

A 
sympathetic adrenergic fibres:
- vasoconstrictor 
- alpha and beta 
sympathetic cholinergic fibres:
- vasodilator
109
Q

hormonal vascular tone

A

adrenaline and noradrenaline

110
Q

endothermic effects on vascular tone

A

Nitrix oxide
prostaglandins
EDHP factors

111
Q

myogenic effects on vascular tone

A

pressure response of vascular smooth muscle

112
Q

metabolic effects on vascular tone

A
  • potassium
  • adenosine
  • H+/pH
  • lactate
  • hypoxia
113
Q

peripheral resistance to blood flow is dependent on

A

radius of the vessel which is regulated by the tone of vascular smooth muscle

114
Q

what regulates the radiator of vessel

A

tone of vascular smooth muscle

115
Q

what initiates contraction in VSM

A

mechanical, electrical an chemical stimuli

116
Q

sympathetic control of muscular tone

A
  • sympathetic nerves innervate arteries and veins
  • most are adrenergic releasing noradrenaline for vasoconstriction
  • important for maintaining BP in exercise
  • local mechanisms predominate in the exercising muscle causing vasodilation
  • increase MSNA in active muscle keeps TPR in check so MABP doesn’t drop
117
Q

MSNA

A

muscle sympathetic nerve activity

118
Q

what do adrenergic sympathetic nerves release

A

Noradrenaline which stimulates a1 and a2 adrenergic receptors to mediate vasoconstriction

119
Q

metabolic control of muscular tone

A
  • metabolites act directly on the VSM to decrease tone by vasodilation
  • metabolites act indirectly by inhibiting SNA vasoconstriction, which further promotes vasodilation
120
Q

what organs have variable metabolic rate

A

heart, brain, skeletal muscle

121
Q

how is flow graded in organs with variable metabolic rate

A

flow is graded with tissue metabolism

122
Q

what is direct action of metabolites for muscular tone

A

directly act on vascular smooth muscle to decrease tone

123
Q

decreased tone

A

vasodilation

124
Q

what is the indirect action of metabolites for muscular tone

A

indirectly act, by inhibiting SNA mediated vasoconstriction which means vasodilation is promoted

125
Q

what are the metabolites that effect muscular tone

A

No one factor is sufficient on its own to account for all the increase in blood flow - cocktail effect
H+, K+, adenosine, lactate, AP etc

126
Q

endothelial control of muscle vascular tone

A

Nitric oxide and prostaglandins are released in response to:
- chemical stimuli like ATP and Ach
- frictional drag force of blood across the vessel surface (sheer stress)
= vessels dilate in response to increased blood flow

127
Q

interactions between metabolic and endothelial dilation , and sympathetic constriction

A
  • downstream: vasodilation occurs through metabolic factors

- upstream: vasodilation occurs by endothelial factors because metabolites cannot reach here

128
Q

increased muscle tension with constant muscle length

A

isometric/static exercise

129
Q

rhythmic cycles of contraction and relaxation with muscles changing length

A

dynamic exercise

130
Q

summary of CV response to Dynamic exercise

A
  • high demand for O2 = increased CO, by increased HR and SR
  • increased SV from increased SNA to the heart and increased venous return from muscle pump
  • decreased TPR due to active muscle vasodilation
  • increased systolic BP
  • same or slight lower diastoli BP
  • modest increase in MAP
131
Q

summary of CV response to isometric exercise

A

-modest demand for O2 results in small change in CO mainly from increased HR

  • reduced SV bc:
  • increased TPR from local vasodilation being overrides by sustained mechanical compassion of vessels and impeded venous return and blood flow
  • valsalva manoeuvre
  • increase SNA induces vasoconstriction in on active muscle
  • increased TPR
  • increased diastolic, stoic and MABP
132
Q

valsalva manoeuvre

A

closing mouth and holding nose and blowing helps restore normal heart rate if beating too fast
- causes build up of pressure

133
Q

phases of heavy weightlifting

A

I) mechanical compression of blood vessels cause rise in intramuscular pressure to up to 1000mgHg
II) valsalva manoeuvre
III) exercise pressor reflex
blood pressure can rise to extremes e.g 480/350mmHg

134
Q

what increases during dynamic exercise

A

HR, venous return, atrial filling and stroke volume

135
Q

where is increased CO redistributed

A

active working muscles

136
Q

what causes vascular beds of inactive tissues to dilate

A

local mediators / metabolites

137
Q

what helps maintain BP alongside increased CO

A

SNA

138
Q

why does isometric exercise have different CV response

A

mechanical compression of contracting muscle can override metabolic vasodilation

139
Q

CV response is regulated by

A

both feedforward CC and feedback reflex

Exercise & Environment (14 decks)

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