Exercise Physiology III: The Urge to Breathe

This post is going to be kind of incomplete as we ran out of time (the first half of this lecture was basically the back end of Exercise Physiology II). As such, I'll just write about all of the stuff that we have learned about, and when we learn the rest, I'll update this post. Updated now :)

Describe and understand normal chemoreceptor control of ventilation

See previous post: Control of Ventilation

Describe and understand what happens to blood gasses during exercise

During exercise, venous PCO2 increases, but arterial PCO2 remains fairly steady. If anything, arterial PCO2 decreases a bit. This indicates that all excess CO2 produced during exercise is removed in the first pass through the lungs. The other consequence of this is that it suggests that chemoreceptors are probably not the main drivers of an increase in ventilation during exercise, as chemoreceptors are located in the arterial system, not the venous system.

Describe and understand what happens to blood gasses during exercise in the absence of normal chemoreceptor input

To study whether or not CO2 sensitivity is actually important during exercise, children with central congenital hypoventilation syndrome (CCHS) have been studied. Children with CCHS are insensitive to CO2, and while they breathe normally when awake, they stop breathing when asleep. Despite this, children with CCHS still have increased ventilation during exercise. The increase in ventilation is increased to a greater extent in fast than in slow exercise (matched for work rate), suggesting that mechanoreceptors detecting limb movements might be responsible in exercise.

Describe and understand alternative ventilator stimuli during exercise

Ventilation increases to a fairly large extent at the beginning of exercise. It has been suggested that this may be due to central command, as well as mechanoreceptors. The initial rise in Ve is larger in trained than in untrained individuals. Ventilation then gradually increases during exercise, which may be due to metaboreceptors, which are chemoreceptors in the muscle.

Describe and understand the alveolar gas equation and how ventilation and chemoreceptor input are causes and effects of each other 

The alveolar gas equation discussed in this lecture was different to the equation discussed in other units. Why not make things simple when you can make them confusing, right?

Anyway, the equation discussed in this lecture was as follows:

P_aCO₂ = K (V_CO2/V_A)
where P_aCO₂ is the arterial partial pressure of CO₂, and I think V_CO2 and V_A are the ventilation rates for carbon dioxide and for alveolar air, respectively.

As discussed previously, P_aCO₂ affects ventilation via the action of chemoreceptors. Conversely, ventilation can affect P_aCO₂, as higher ventilation rates result in lower partial pressures of CO₂, and vice versa. P_aCO₂ vs. ventilation and ventilation vs. P_aCO₂ can be graphed simultaneously (sort of like the cardiac and vascular function curves), and the equilibrium point is where the two curves intersect.

Describe and understand how work intensity and muscle fibre type recruitment affects the relationship between VE and VCO2

As mentioned here, type I fibres are activated at all intensity levels. As intensity increases, type IIa and IIb fibres are also activated. Type II fibres, especially IIb fibres, rely a lot on anaerobic respiration (e.g. glycolysis) to produce energy. One of the main downsides of glycolysis production is that lactic acid is produced. We do have a buffering system to reduce lactate levels, but this produces carbon dioxide, increasing ventilation:

Lactic acid + Carbonic acid <--> Water + Carbon Dioxide

Because of this buffering system, respiration increases more rapidly following the Onset of Blood Lactate Accumulation (OBLA), which occurs when blood lactate levels are around 4mM. Eventually, this buffering system is pushed to its limit, and the pH starts to decrease. The decrease in pH (increase in H+ ions) drives ventilation further, causing an even steeper increase in ventilation rate.

Describe and understand some experiments designed to investigate the phenomenon of ‘central command’ in ventilator control 

In the first experiment, researchers attached a vibrator to the bicep muscle tendon. This stimulated reflex contraction of the bicep via the muscle tendon reflex. While the muscle tendon reflex was stimulating the bicep, not as much input from the brain was required to lift a weight (as compared to participants who didn't have the vibrator). When central command required was reduced, ventilation also decreased.

The second experiment had a similar setup to the first experiment, but in the second experiment, participants were asked to use their tricep muscle to pull something down to lift a weight via a pulley system, rather than use their bicep to lift something up. As the vibrator was still attached to the bicep muscle, the muscle reflex actually made it harder to contract the tricep (as the bicep and tricep are antagonistic muscles). Therefore, in this setup, participants with the vibrator needed more input from the brain in order to lift the weight. When central command required was increased, ventilation also increased.