Why do you breathe hard with you run?

You breathe hard to increase both oxygen delivery to the blood and to remove excess carbon dioxide building up in the blood. The primary signal for this comes from the carotid bodies (chemosensors in the carotid arteries) and the hypothalamus, which detect blood pH and PCO2. They also detect PO2, but that signal is much less robust to increase or decrease breathing rate than pH and PCO2. Metabolic work produces more CO2 and other metabolic wastes which increses blood PCO2 and decreases blood pH.

The reason you continue to breathe hard after exercise (to repay "the oxygen debt") has been the source of great controversy in exercise physiology for decades. I have not kept up with the current literature on it, but as I understand it, the remaining elevation in breating is to continue to blow off CO2 in an effort to bring blood pH back to within the very narry limits that the carotid bodies and hypothalamic sensors approve of. Even though CO2 production post exercise might not be as high as during exercise, other metabolic wastes are reducing blood pH, and by ridding CO2 carbonic acid can be removed from the blood, thus pushing blood pH toward the normal of 7.4.

I hope that answers your question.

You breathe hard when you run? If you are experiencing and rise in temperature, difficulty breathing, or fatigue while running you should seek a medical expert immediatly.

Is that even a real question?

Breathng rate primarily increases because of CO2, getting oxygen in isn't the primary mechanism.

unknowingly wrote:

Breathng rate primarily increases because of CO2, getting oxygen in isn't the primary mechanism.

However, 02 and C02 are intimately related, so you won't be releasing any C02 with a corresponding intake of 02.

indebted to oxygen wrote:

However, 02 and C02 are intimately related, so you won't be releasing any C02 without a corresponding intake of 02.

Sorry, correction.

However....

While linked, we know that Oxygen uptake and ventillation diverge from there pretty steady increase at some point around Lactate Threshold. At this point ventilation increases to a greater extent than oxygen uptake. WHY? B/c of CO2...

Also, CO2 release occurs before O2 is even needed. CO2 release occurs during the Krebs cycle, which occurs before the ETC.

More detail.

Increased respiration is caqused by an increase in the stimulus sent to the inspiratory center located in the medulla oblongata. This area is stimulated by CO2 and H+ buildup in the blood.

If you want to get even more complex, you have central(spinal fluid) and peripheral(blood) chemoreceptors. Centrallly, pCO2 and H+ are the stimulators. Peripherally, H+ pO2, pCO2+ are the stimulators.

In addition there are proprioceptors that increase breathing rate before exercise even begins. These are going to be both a consequence of hormones (i.e. epi/norepi) and mechanical movement.

In summary, lots of crap affects breahting, and there are many many other factors not discussed. BUT the primary reason for increased respiration is an increase in CO2.

You're off a little on your understanding of oxygen uptake kinetics. You can produce various metabolic wastes and excess CO2 without driving down PO2 in the blood. Your breating will increase to get the CO2 out, and while more O2 will be coming into the alveoli of the lungs, it will not all necessarily be taken into the blood. Only if there is a driving force, meaning a concentration or pressure difference, will more oxygen than normal go into the blood.

The blood has a massive store of O2 in the form of oxyhemoglobin inside the red blood cells. The sensors in the carotid bodies and hypothalamus do not detect Hb oxygen saturation. They detect PO2, which is the partial pressure of O2 dissolved in the fluid portion of the blood. On the other hand, the primary method of CO2 transport in the blood is via dissolution into the fluid. Actually CO2 will dissolve into the water, but will react with water for form carbonic acid via the carbonic anhydrase reaction. The CA then dissociates into H+ (acid) and HCO3- (bicarbonate). The acid from this reaction is usually kept withing the RBCs while the bicarb is let out to serve as the primary acid buffer of the blood. Release of any metabolic acid will create H+, which binds to the bicarb, and by simple thermodynamic law pushes that reversible reaction back to the left, favoring the production of CO2 in the blood. Then, breathing will increase to get rid of it. Anyway, the point I'm making is that CO2 and its intimate partner pH are very closely monitored by the chemosensors in the body, and they are the driving force for breathing rate and depth.

Interesting fact about carbon monoxide (CO). The reason it kills you so easily and painlessly is that it binds to the Fe atom at the center of hemoglobin irreversibly, displacing O2. However, it does not affect the PO2 in the fluid portion of the blood becuase usually when you're inhaling CO, you have plenty of available O2 also. Therefore, breathing rate does not increase, you do not sense distress, and you simply "fall asleep" to die.

+1 ! well played, homey.

So, hang on a sec. given the primary function is elimination of waste (~C02), and the sensing mechanism is triggered by reduction of P02 (not hemoglobic 02). But P02 would effectively decrease as hemoglobic 02 is utilized, correct? So there is a distinct relationship between C02 removed and 02 intake (via P02 absorption and eventually hemoglobic 02), with hemoglobic 02 creating a buffer (which is why you probably don't start breathing hard immediately, and continue to breath hard for a period afterwards). Correct?

NO. There's some miscommunication here. The primary sensor is blood PCO2 and pH. CO2 and pH are exquisitely controlled. PO2 is detected but it takes a massive drop in O2 saturation in arterial blood to cause PO2 to drop enough to induce changes in breathing.

Sorry if the all the Hb talk was distracting. The point of that was that breathing rates can change up and down even at rest due to changes in PCO2 or pH and will not affect Hb O2 saturation or plasma PO2. O2 carried by the blood and CO2 carried by the blood are mostly exclusive of each other. Yes, pH can affect O2 dissociation from Hb, but they are essentially parallel systems for carrying gasses in the same medium. The rise or fall in one does not necessarily predicate the rise or fall in the other.

Take home message: The primary stimuli for increased breating rate and depth during exercise are incresed PCO2 and decreased pH.

Why is it that the body does not care so much about O2 levels and has relatively slow hypoxic responses (~days), but CO2 must be very tightly and immediately controlled via ventilation (~seconds)?

Because you're tired.

unknowingly wrote:

Also, CO2 release occurs before O2 is even needed. CO2 release occurs during the Krebs cycle, which occurs before the ETC.

Only in a textbook. In real cells these both occur continually. This isn't an assembly line. The reactants and products are moving in and out of many many other reactions as well. Also not sure what this statement has to do with CO2 or O2 levels regulating breathing rate.

zibba wrote:

Why is it that the body does not care so much about O2 levels and has relatively slow hypoxic responses (~days), but CO2 must be very tightly and immediately controlled via ventilation (~seconds)?

The markers that trigger breathing are waste markers, probably because it's more urgent to start getting rid of waste products than it is to replenish stores (makes sense, if you didn't have sufficient energy and 02 stores to do work, you couldn't do anything).

That said, 02 stores won't last long without replacement, however since (hard) breathing is already triggered it kinda takes care of itself.