hey spfoto, I can answer this mate
Ok first of all there are different mechanism of adaption in regards to changing the affinity of hemoglobin to O2/ CO2 or changing your respiratory mechanism when your body comes under respiratory stress.
For example, as you move to higher altitudes, lower altitudes, practice apnea, under other changes of air pressure etc...
Now for the first thing: You want to decrease the affinity of Hb (hemoglobin) to O2. That means you have more unloading of O2 in your tissue (think of this again: if O2 is tightly bound to Hb, you will unload less O2 to your peripheral tissues, and therefore that could even lead to necrosis in extreme conditions. At the same time, your lung are still functioning normally so you are still loading your Hb with oxygen in your lungs. So as expected, that results in increased partial pressure of O2 in your blood. Note that this all happens within an integrated feedback mechanism. You have different receptors in your systems and organs (e.g: receptor in your carotid artery etc...) that sense change in your arterial gases O2/ CO2.
Now I hope i didnt make it too complex: think again this way: you are taking a deep dive and hold your breath. As you are running out of O2 (your body is consumming it and you depleting whatever reserve left in your blood/lung), then CO2 increases. CO2 increase also causes some change in your blood pH (respiratory acidosis), as CO2 can dissolve and becomes a weak acid HCO3-, that all alert a feedback system that wants to make Hb less tightly bound to O2 so that it gives off any O2 left to it, and provided you take a breath again, you want to as quickly to counteract that previous effect. (Now that was for a short term mechanism), and also as a respiratory mechanism, you will even involuntary hyperventilate; that is you will take fast and deep breathes (like try to hold your breath for as much as you can till your hands cant hold it anymore and see what i mean

). For a long term mechanism (e.g: moving to a high altitude), the first way of adaption will be respiratory hyperventilation. If that doesn't happen one can risk hypoxemia, because changes in Hb affinity takes some time to happen effectively. After few days of the new stress introduced to your body, you will effectively produce a substance called 2,3-DPG (diphosphoglycerate) which stabilize Hb in the deoxygenated state (or T-state) which therefore means that it will makes it release more O2 to your tissue, and in turn you counteract the effect of reduced partial pressure of O2 in the air (as you moved to high altitude).
Note also that the hematocrit/and blood Hb concentration can itself change due to different strains or exercise happening. A particular interesting finding is that I noticed in most smokers (with no COPD or other chest diseases), their level of Hb is on the average higher than non-smoker (normal values should be btw 12-16Hb although that can also vary). Note that the magnitude and duration of change depends on the length/magnitude also of the introduced stress. So the longer the stress, the longer the adaptation period and the longer the recovery to the normal state. The opposite holds true also.
So in brief, I hope i didn't confuse you more. Just let me briefly summarize you in a nutshell the basic mechanism of adaption to hypoxemia/low oxygen conditions:
1- respiratory: Hyperventilation: by hyperventilating (fast deep breathes - note that this is very different than fast shallow breathes), you increase O2 in your blood, and increase the pH of the blood as well (increase in pH means decrease in acidity of blood, due to decrease of arterial pCO2 which means less CO2 in arteries and as I said before, CO2 is a weak acid and which other than normal quantities will cause flunctuation of blood pH).
2- Hemoglobin affinity to O2: That should decrease as well (note that this doesnt mean that Hb is binding to less O2 in the lung, but simply that Hb is giving off more O2 in the blood). Several factors will cause this:
- Increase in pCO2 and decrease in pH: That leads to decreased affinity of Hb to O2
- Increase in temperature: Which typically accompanies highly active tissues and exercising skeletal muscles, also make Hb less tightly bound to O2 so that more of O2 is released to tissues.
- Increase in 2,3-DPG: That typically takes a bit longer time to be fully effective (few days), and this substance which is a result of glycolysis in red blood cells facilitates the dissociation of O2 from Hb in the tissues.
Now just an interesting thing: I think this is a well known thing: CO (carbon monoxide poisoning): How it works? Basically very simple mechanism: Binds very tightly to Hb (250times more stronger than O2 binds to Hb), but that doesnt stop here: it also causes Hb to also bind to whatever left of O2 stronger than normal state, and the result: No O2 unloading to tissues, so your organs start suffocating even before you realize it!!!
I hope that was useful and not too confusing.
Regards
