Lecture 33 Flashcards

(33 cards)

1
Q

How does minute ventilation (VE) increase during exercise?

A

By increasing tidal volume and breathing frequency.

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2
Q

Breathing pattern in mild exercise?

A

Tidal volume increases first with small increases in frequency.

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3
Q

Breathing pattern in heavy exercise?

A

Tidal volume plateaus at ~50–60% VC; increases in VE come from frequency.

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4
Q

How is the initial increase in tidal volume achieved?

A

By lowering end-expiratory lung volume via activation of expiratory muscles.

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5
Q

How is further increase in tidal volume achieved?

A

By raising end-inspiratory lung volume via accessory inspiratory muscles.

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6
Q

Why increase tidal volume first?

A

Reduces dead space ventilation → improves alveolar ventilation (Vd/Vt falls).

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7
Q

Why is tidal volume limited to 50–60% of VC?

A

This range minimizes work of breathing and elastic load.

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8
Q

Why is reducing end-expiratory lung volume beneficial?

A

Lengthens diaphragm → allows optimal force generation; stores elastic energy.

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9
Q

What are the three phases of VE during submaximal exercise?

A

Phase 1 rapid rise, Phase 2 slow rise (~2–3 min), Phase 3 steady-state.

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10
Q

What is exercise hyperpnea?

A

Matched increase in ventilation proportional to metabolic rate in submaximal exercise.

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11
Q

Two major control theories for exercise breathing?

A

Feedforward (central command) and feedback mechanisms.

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12
Q

What supports feedforward control?

A

Initial rapid ventilation rise (Phase 1) is too fast for peripheral feedback.

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13
Q

Evidence from decorticate cat studies?

A

Respiration increases before locomotion → central command contributes to drive.

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14
Q

Key feedback mechanisms during exercise?

A

CO₂ production, chemoreceptors, Type III/IV afferents.

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15
Q

What do chemoreceptors sense?

A

CO₂, pH, and low O₂ (peripheral only).

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16
Q

Why are blood gases stable in submaximal exercise?

A

Ventilation closely matches metabolic demands.

17
Q

What are Type III & IV afferents?

A

Group III (mechanical) and IV (chemical) muscle afferents influencing breathing.

18
Q

Evidence for Type III/IV afferents?

A

Fentanyl blocking reduced VE, HR, and BP.

19
Q

Ventilation pattern summary for submaximal exercise?

A

Phase 1 neural, Phase 2 combined neural & feedback, Phase 3 steady-state matching metabolic rate.

20
Q

What is exercise hyperventilation?

A

Ventilation rises disproportionately above ~60–70% VO₂max.

21
Q

Why does hyperventilation occur above VT1?

A

Large CO₂ production from muscles triggers ventilatory drive.

22
Q

During heavy exercise, what happens to PaCO₂?

A

Falls 5–15+ mmHg below rest due to hyperventilation.

23
Q

Why does pH fall during maximal exercise?

A

ATP hydrolysis during cross-bridge cycling, NOT lactic acid.

24
Q

How does hyperventilation affect pH?

A

Reduces CO₂ → slows pH decline.

25
Does physical training increase lung structure?
Generally no; heart and muscles adapt more than lungs.
26
Which athletes may show lung adaptation?
Swimmers—repeated forced inspirations to TLC may increase lung volumes.
27
What airway adaptations may occur with training?
Repeated stretch may improve airway smooth muscle function.
28
Do children show respiratory adaptations?
Yes—high activity may accelerate lung growth pre‑puberty.
29
Why is the lung considered ‘overbuilt’?
Large diffusion surface and short diffusion distance allow adequate gas exchange even in exercise.
30
What is expiratory flow limitation?
When tidal expiratory flow reaches maximal flow-volume loop boundary.
31
What is dynamic hyperinflation?
End-expiratory lung volumes rise toward/above rest due to shortened expiration.
32
Consequences of dynamic hyperinflation?
Increases elastic work and fatigues inspiratory muscles by shortening them.
33
Sex differences in ventilatory constraints?
Women have ~17% smaller airway diameters → higher resistance and earlier limitations.