Week 7 - Respiration during exercise (p2) Flashcards

1
Q

What are the 3 phases of the ventilatory response to constant load stead-state exercise?

A
  • Phase 1: Immediate increase in Ve
  • Phase 2: Exponential increase in Ve
  • Phase 3: Plateau
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2
Q

Define hypernoea.

A

is defined as PaCO2 (arterial carbon dioxide) regulation due to proportional changes in alveolar
ventilation (Va) and metabolic rate (VCO2)

PaCO2 = VCO2/Va

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3
Q

What happens to ventilation during incremental exercise as opposed to steady-state exercise?

A

increases linearly with exercise intensity until a point commonly referred to as the “ventilatory threshold” (Tvent) or lactate/anaerobic threshold, after which ventilation increases exponentially, resulting in hyperventilation (decreases PaCo2 - arterial CO2)

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4
Q

When does ventilatory threshold occur?

A

50-75% of peak workload (Vo2 peak)

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5
Q

Exercise-induced arterial hypoxaemia (EIAH) - Define it and outline who it occurs in?

A

Is defined as a reduction in PaO2 of ≥10 mmHg from rest.

Occurs in highly trained males (50%) during heavy exercise and
the majority of females regardless of fitness or exercise intensity

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6
Q

How did original theory explain why exercise-induced arterial hypoxaemia occurs?

A

It’s because ventilatory demand exceeds capacity - Demand versus Capacity Theory.

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7
Q

3 causes of EIAH

A
  1. Diffusion limitation: those with high cardiac output (trained) have a reduced diffusion time for gases to be exchanged (due to transit time of RBC increased).
  2. Ventilation-perfusion (V/Q) mismatch (most significant cause): mismatch between amount of air breathing in and amount of blood passing through pulmonary circulation. More perfusion than air reduces amount of diffusion.
  3. Relative hypoventilation: due to ventilatory demand being greater than capacity, may not be able to increase ventilation sufficiently. PACO2 stays high.
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8
Q

Changes in breathing patterns during exercise - At the ONSET of exercise, what are changes in ventilation largely achieved by?

A

Increased tidal volume

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9
Q

Changes in breathing patterns during exercise - During heavy exercise, what happens to tidal volume? What are further increases in ventilation achieved by?

A

Tidal volume plateaus and further increases in ventilation are achieved by increased breathing frequency

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10
Q

Even during maximal exercise, tidal volume does not exceed ..% of vital capacity.

A

60%

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11
Q

Changes in breathing patterns during exercise - What 3 values are well maintained until heavy exercise? What happens during higher intensities?

A

Arterial PO2, PCO2, and pH

Hyperventilation at high intensities result in arterial C02 decreases, decrease pH (more acidic)

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12
Q

Equation for work - applied to breathing.

A

Applied equation: pressure x volume

Respiratory muscle work can exceed 500 J/min and up to 500 mL O2/min.

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13
Q

What is total work?

A

the sum of elastic, flow-resistive, and inertial forces.

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14
Q

Oesophageal pressure (Poes)

A

is an estimate of pleural pressure (around the lungs) and can be used to calculate the mechanical work of breathing during exercise

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15
Q

Control of ventilation - Where are respiratory central pattern generators located?

A

within the brainstem (pons and medulla)

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16
Q

Control of ventilation - What are the 3 main groups of neurons involved in respiratory control?

A

o Ventral respiratory group (inspiratory and expiratory)
o Dorsal respiratory group (inspiratory)
o Pontine respiratory group (modulatory)

17
Q

Control of ventilation - What is the 3-compartment model?

A

Sensors (input) –> central controller (output) –> effectors

Central controller - pons, medulla, other parts of brain
Sensors - chemoreceptors, lung, and other receptors
Effectors - respiratory muscles (diaphragm)

18
Q

In terms of the control of ventilation, what are the two types of motor outputs that change alveolar ventilation?

A

Resistance muscles (cricoarytenoid) and pump muscles (diaphragm)

19
Q

In terms of the control of ventilation, what are the two divisions and 5 types of inputs to the central controller (brainstem)?

A

Feedback inputs
- Peripheral chemoreceptors
- Central chemoreceptors

Feedforward inputs
- Muscle afferents (peripheral neurogenic)
- CO2 flow (peripheral neurogenic)
- Central command (central neurogenic)

20
Q

Where are the peripheral chemoreceptors located?

A

aortic arch and carotid body

21
Q

What is the role of carotid bodies?

A

peripheral chemoreceptors that are sensitive to changes in arterial pH, PCO2, PO2

22
Q

What are the roles of peripheral chemoreceptors? What does decreased PaO2 result in?

A

Detect changes in PaO2 and PaCO2 perfusing systemic and cerebral circulation.

Relays sensory information to the medulla via vagus and glossopharyngeal nerves.

Decrease PaO2 stimulates them to increase ventilation.

23
Q

What other stimuli activate peripheral chemoreceptors?

A

temperature, adrenaline, and C02

24
Q

Central chemoreceptors

  • Where are they located?
  • What is their role?
  • What does an increase in PaCO2 result in?
A
  • Primarily in the ventral surface of the medulla, known as the retrotrapezoid nucleus (RTN).
  • Detect changes in PaCO2 and H+ in cerebral spinal fluid.
  • An increase in PaCO2 will stimulate an increase in ventilation.
25
Q

Chemoreceptor feedback

A
  1. Chemoreceptors detect error signals (disturbances to blood-gas homeostasis).
  2. Central and peripheral chemoreceptors increase afferent
    input to the brainstem in response to increasing PaCO2 or decreasing PaO2 or pH.
  3. Premotor neurons in the dorsal respiratory group are activated
  4. Inspiratory muscle contract, increasing VE.
  5. Changes in VE elicit changes in PaO2, PaCO2 and pH, thus restoring blood-gas balance.
26
Q

What are the ventilatory responses to…
a) 02
b) C02

A

a) curvilinear
b) linear

27
Q

Small changes in (a) PaCO2 OR PaO2 elicit much greater changes in ventilation versus (b) PaCO2 OR PaO2

A

(a) PaC02
(b) Pa02

28
Q

Why does hypoxaemia not elicit substantial increases in ventilation?

A

as you decrease PO2, the saturation doesn’t change much so ventilation stays the same - this is until 60mm Hg

29
Q

Ventilatory control during moderate-intensity exercise - What is the main input for ventilatory control?

A

Feedforward input response - peripheral and central chemoreceptors don’t contribute as arterial PO2 and PCO2 are well maintained.

  • Both central and peripheral neurogenic stimuli play a major role in exercise hypernoea.
  • Peripheral chemoreceptors “fine-tune” breathing.
30
Q

Ventilatory control during heavy and severe exercise - What is the main input?

A

both feedback and feedforward inputs drive the ventilatory response

31
Q

Does CO2 drive breathing during heavy exercise?

A

NO - it falls during heavy and severe exercise which inhibits breathing.

Metabolite accumulation (H+ and K+) stimulates breathing as well as increased body temperature and augmented muscle afferent input.

32
Q

What are the effects of endurance training on ventilation?

A

can reduce ventilation at any given exercise intensity

33
Q

What are the chronic training adaptations that improve aerobic capacity?

A

o ↓ metabolite accumulation
o ↓ afferent feedback
o ↓ ventilatory drive

34
Q

Do the lungs adapt to exercise training?

A

No - respiratory muscles may become stronger and more fatigue resistant but airways and lungs do not get bigger nor does diffusing capacities change.

35
Q

What are the 5 ways in which the pulmonary system may limit exercise performance?

A
  1. Exercise-induced arterial hypoxaemia (EIAH)
  2. Exercise-induced laryngeal obstruction (EILO)
  3. Expiratory flow limitation
  4. Respiratory muscle fatigue
  5. Intrathoracic pressure effects on cardiac output
36
Q

What increase more during mild to moderate exercise - Tidal volume or Breathing frequency?

A

Tidal volume

37
Q

During a graded exercise test, the increase in ventilation during the transition from rest to moderate exercise is achieved by?

A

an increase in both breathing frequency and tidal volume

38
Q

Why are changes in breathing patterns during exercise important?

A

1) To ensure the optimal mechanics of breathing are realized during exercise
2) Increased TV ensures that dead space ventilation remains small
3) Designed to reduce the risk of respiratory muscle fatigue