31. Respiratory Adaptations

Question 1

What is the relationship of the substantial changes that occur in the blood concentrations of lactic acid and bicarbonate? How do these relate to CO2 production and ventilation during progressive high intensity exercise?

Answer 1

• Lecture 30 slide 12/16
• Bicarbonate acts as a buffer to lactic acid
• Bicarbonate (Na+HCO3) & lactate-H+ → carbonic acid (H2CO3) → CO2 and H2O

Question 2

What effect does training have on lactate accumulation? Significance?

Answer 2

• Training delays onset of rapid H+Lactate- accumulation to higher work intensities
• Higher % of new, increased VO2max can be used for sustained workloads

Question 3

What are improvements in VO2max w/ exercise training mostly due to? What doesn’t change?

Answer 3

• Circulatory and muscle tissue adaptations

- Lung doesn’t change = same # alveoli, same surface area

Question 4

What are the only structures that undergo pulmonary adaptation?

Answer 4

Skeletal muscles of ventilation

Question 5

How do changes in end-tidal CO2 and O2 at near maximal exercise provide evidence that the lung is not the limiting factor in VO2max?

Answer 5

• CO2 production = primary stimulus for breathing
• Tissue level adaptations due to endurance training reduce amount of CO2 produced at any given workload –> adapted muscle release less signal to drive ventilations –> breathe less at any given workload
• Training reiieves the lung

Question 6

What are the tissue level adaptations in the working muscle due to endurance training? Significance?

Answer 6

• Less anaerobic metabolism throughout the work
• Faster o2 uptake kinetics (smaller O2 deficit)
• Shift in aerobic fuel substrate away from CHO towards fats
• *reduce need to breathe

Question 7

Which humans can outwork their lung, extracting more O2 from the blood than the lung can replace?

Answer 7

Some elite endurance athletes at near maximal work may remove more oxygen from their blood than can be replaced by pulmonary diffusion across the alveolar/capillary interface, due to the very diminished transit time of blood through the pulmonary capillaries

Question 8

What is the goal of ventilation?

Answer 8

We ventilate at levels sufficient to:

• clear all additional CO2
• hold alveolar and arterial CO2 constant

Question 9

T/F: the adaptation to aerobic training includes large increases in the lung’s diffusing capacity and in pulmonary ventilatory volumes such as vital capacity

Answer 9

False: maximal pulmonary flow rates & volumes don’t change w/ aerobic training

Question 10

How can regular aerobic training result in the subjective impression that breathing is somehow improved, less taxing, or easier?

Answer 10

• Training effect
• Training relieves lung –> less breathing during same workload
• Lung is able to reserve more of its function for higher workloads

Question 11

VO2 = Q x (a-V)O2. Which elements of this equation account for the increase in VO2max seen w/ regular endurance training

Answer 11

• Improved Qmax, SVmax

- Increased (a-V)O2 difference (better tissue extraction of O2 by working muscle

Question 12

Cite and explain 2 diff pieces of evidence during exercise which indicate that CO2 may be a greater stimulus and driver of ventilation than O2.

Answer 12

1. Relationship between pulmonary ventilation and rates of pulmonary CO2 excretion and O2 uptake in awake sheep
   - CO2 production is a far better predictor of breathing level than O2 uptake when the 2 are artificially and separately varied using heart/lung machine
   - brain seems to be tracking/regulating CO2 more closely than O2
2. Paralyzed cat w/ all muscle depolarization and peripheral feedback blocked
   - fictive locomotion stimulates walking neurons
   - w/in 1 sec of stimulation: depth and rate of phrenic nerve (to diaphragm) activity increases 30% + activation of brain’s motor center simultaneously co-activates ventilation
   - cat breathes faster & deeper

Question 13

Why is it so difficult to quantify what each source of ventilatory drive contributes to the eucapneic hyperpnea of exercise?

Answer 13

• No single source of ventilatory drive can account for the 15-20 fold exercise hyperpnea
• Lesions of any single source of ventilatory drive fail to impair hyperpnea

Question 14

What evidence indicates that multiple, redundant mechanisms regulate exercise hyperpnea?

Answer 14

• Central command is primary (brain’s motor cortex coactivates ventilation)
• Redundant modulation by peripheral mechanisms
• building up CO2 in arterial system is backup