16. Respiratory responses to exercise Flashcards

1
Q

What is the key role of ventilation?

A

Maintain arterial O2 saturation and remove CO2.

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2
Q

How are breathing frequency and tidal volume affected during exercise?

A

They increase

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3
Q

What is the effect of heavy exercise on respiratory muscles?

A

They become significant consumers of oxygen, can fatigue and are a source of chemoreflex with effects on active muscle blood flow

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4
Q

What is involved in the regulation of ventilation during exercise? (4 main dot points here)

A

Involves:

  • central neural control
  • feedback from muscle afferents
  • mechanical feedback from lungs & limbs
  • humoral factors
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5
Q

What are the respiratory responses to exercise?

A

Primarily maintains arterial O2 saturation and CO2 removal. Impairment of exercise performance can occur through:

  • accumulation of CO2
  • decrease in arterial O2 saturation

Acid-base balance

  • hyperventilation ⇒ increase in CO2 production (consuming H+ and leading to alkalosis)
  • metabolic acid is a stimuli of breathing

Fluid & temperature balance

  • loss of heat & fluid in air that we breathe out
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6
Q

Ventilation during & after exercise

A

During exercise

  • gradual increase until it gets to max minute ventilation (inc. dead space & alveolar ventilation)

After exercise

  • rapid decrease (neuronal imput) followed by slower adjustment post-exercise (hormonal imput).
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7
Q

Ventilation during incremental exercise

A
  • Pre-VT1: Initially there is a linear relationship between ventilation and CO2, increase in CO2 production is from ox. metabolism.
  • B/w VT1-VT2: classical anaerobic threshold where CO2 is from both ox. metabolism and carbonic anhydrase reaction
  • Post-VT2: increases in CO2 is due to increases in adrenaline, heat, etc.
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8
Q

Arterial PO2 vs. mixed venous PO2

A

Arterial PO2 = 95-100 mmHg

Mixed venous PO2 = 40 mmHg

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9
Q

Arterial PCO2 vs. mixed venous PCO2

A

Arterial PCO2 = 40 mmHg

Mixed venous PCO2 = 46 mmHg

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10
Q

Arterial pH & HR during exercise

A

As HR is a proxy for exercise intensity, we can say that as exercise intensity increases the lungs are effective at maintaining a stable PO2.

PCO2 has no change/however can have decrease when you hyperventilate, and consequently, arterial pH increases too (more alkaline).

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11
Q

What happens to ventilation during prolonged exercise?

A

During prolonged ex, ventilation increases. The increase in ventilation is related to exercise intensity and is due to the increase in tidal volume, but also breathing frequency.

Over time, it’s the increase in breathing frequency that contributes to the progressive increase in ventilation.

  • compliance of lung/chest wall limits tidal volume drift

RESPIRATION = TIDAL VOLUME x BREATHING FREQUENCY

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12
Q

Pulmonary gas exchange during exercise

A

During exercise, there is:

  • increased O2 extraction
  • decreased mixed venous VO2
  • higher cardiac output
    • CO to lung is also higher since L & R side of heart pump at the same rate.
    • HR increases ⇒ decrease in time spent in pulmonary circulation OR high altitude means smaller diffusion gradient of oxygen
      ⇒ suboptimal oxygenation of blood
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13
Q

What causes exercise-induced arterial hypoxemia (EIAH)?

A

A-aDO2 (alveolar - arterial difference in oxygen):

  • V/Q ventilation perfusion ratio mismatch (mostly non human - affects horses more)
  • DIFFUSION LIMITATION: reach maximal CO, but transit time is too low to fully equilibrate gas exchange

Inadequate compensatory VE:

  • expiratory flow limitation

O2 dissociation curve shift

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14
Q

Relationship between exercise-induced arterial hypoxemia (EIAH) and locomotor muscle fatigue?

A

Decrease in arterial O2 saturation at higher intensities could have a significant negative effect on the performance of leg muscles

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15
Q

What is the transdiaphragmatic pressure?

A

It is the difference between the esophageal pressure and the gastric pressure.

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16
Q

How does the diaphragm contribute to air moving into lungs?

A

When the diaphragm contracts, a pressure difference is created between intrathoracic cavity and outside so air moves into the lungs.

17
Q

Does exercise induce diaphragmatic fatigue?

A

The diaphragm is stimulated by the phrenic nerve. It contains lots of ST fibres, capillaries, mt, and is very fatigue-resistant. Despite this, it can still fatigue with 15 min 90-95% VO2 max exercise.

18
Q

Why does the diaphragm fatigue?

A

It is working very hard, may increase to as much as 15% VO2 & CO during strenuous exercise.

This is because diaphragm is the only active muscle in inspiration, then as exercise intensity increases, expiration muscles can be recruited, these require O2 too.

19
Q

What can increased diaphragm & respiratory muscle activities result in?

A

At high intensities,

  • chemoreflexes from respiratory muscles
  • ⇒ sympathetically mediated vasoconstriction
  • ⇒reduced active muscle blood flow
20
Q

Respiratory muscle metaboreflex

A

Fatiguing contractions of the diaphragm expiratory and accessory respiratory muscles cause:

  • increased reflex activating metabolites
  • increased group IV phrenic afferent discharge

Therefore brain has reflex actions to vasoconstrict active muscle:

  • increased sympathetic efferent discharge, limb vasoconstriction
  • decreased O2 transport
  • increased locomotor muscle fatigue
  • brain intensifies effort perceptions
21
Q

Control of ventilation

A

Respiratory neurons in hindbrain (pons, some in medulla) respond to:

  • higher centres
  • central drive (PCO2, H+, pH) in extracellular fluid, CSF
  • chemoreceptors (PO2, PCO2, pH)
  • stretch receptors in heart
  • pain receptors
  • body temperature
  • hormones
  • thermoreceptors (skin)
  • pressure receptors
  • mechanoreceptors, chemoreceptors(?) in muscle
22
Q

What factors control exercise hyperpnea (ventilation increase)?

A
  • Motor cortical activation
    • same central command that increases cardiovascular response & HR also increases ventilation
  • Muscle afferents (spindles, type III & IV)
    • unmyelinated nerve endings tend to respond to mechanical stimuli
  • CO2 flux to the lung (chemoreceptor?)
  • Increased K+, H+, lactate
    • influence type 3&4 afferents and other chemoreceptors
  • Elevated catecholemines & temperature
    • contribute most at high intensities
  • No role for O2
    • no hypoxic drive during exercise
23
Q

Muscle group 3 & 4 afferents & exercise hyperpnea

A

40-45% of the total ventilation at 50, 100 & 150W is attributed to activation to type 3 & 4 afferents

In an experiment involving blockage of impulses of legs back to spinal cord (but not motor nerves to legs), showed important feedback mechanisms from contracting muscle telling brain & lungs how much O2 needed

24
Q

What are the effects on exercise ventilation following training?

A

Comparing trained vs untrained, same O2 uptake, but lower ventilation with trained subjects at the same power output, indicating increased O2 extraction.

  • Reduced blood lactate/H+
  • Lower plasma K+
  • Lower plasma catecholamines
  • Reduced activation of muscle afferents?
  • Reduced central drive?