• Welcome to the DeeperBlue.com Forums, the largest online community dedicated to Freediving, Scuba Diving and Spearfishing. To gain full access to the DeeperBlue.com Forums you must register for a free account. As a registered member you will be able to:

    • Join over 44,280+ fellow diving enthusiasts from around the world on this forum
    • Participate in and browse from over 516,210+ posts.
    • Communicate privately with other divers from around the world.
    • Post your own photos or view from 7,441+ user submitted images.
    • All this and much more...

    You can gain access to all this absolutely free when you register for an account, so sign up today!

Bet you cant answer this?

Thread Status: Hello , There was no answer in this thread for more than 60 days.
It can take a long time to get an up-to-date response or contact with relevant users.

spfoto

Its not fat its fuel.
Mar 3, 2007
66
29
108
Hemoglobin does all the fetching and carrying in respect of the O2 and C02 and lives for about 120 day. Now when pushed to the limit does the hemoglobin live longer or die sooner? If the life span of hemoglobin changes due to training hard and the lack of training do the glands/organs that produce hemoglobin have a memory of what “type” of hemoglobin to produces when we are or ant in training?
Or have I missed the point……….
 
You might want to move this thread to 'advanced training & techniques' or something.
I don't believe there are different types of hemoglobin, the structure of hemoglobin is pretty well-defined. (look at the structure at rcsb.org) But I might be wrong, never looked deeply into the effect of training on molecular physiology.
 
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 :) :) :)
 
  • Like
Reactions: trux and sanso
Excellent post, GetawayFK! Although you did not really address the question directly, the answer was quite informative anyway. Since you seem to be an expert in the area, I use the thread to ask you little bit more (moderators please feel free to move it to the general freediving forum. BTW, I think DB deserves to have a separate sub-forum specifically for freediving physiology, medical, and scientific topics - such threads are not unusual here and it wouldn't be bad having all those interesting posts nicely together in one place).

So, GetawayFK, while most people here know that hyperventilation is dangerous and even counterproductive for freediving, there was so far only little information about the impact of altitude adoption (or the use of hypoxic tents) on breath-holding. I wonder if there was any deeper study made.

From what I understood, the 2,3-DPG's ability to stabilize Hb in the T-state, although it is working well for moderate hypoxic states, especially if the ventilation of air in lungs is assured (even if with lower O2 content), it may be quite counterproductive for breath holding: when the level of O2 in lungs drops below certain level, due to Hb stabilized by 2,3-DPG in the deoxygenated state, blood won't be able to get the remaining O2 the freediver holds in his lungs. At least it won't be able to pull from the lungs as much remaining O2 as it could without 2,3-DPG. Am I right here?

Also, what's the longterm health effect of having higher Hb levels (or higher 2,3-DPG). I've been already searching some information about possible negative health effects of Hb, but so far I did not find a lot of interesting documents. Just some information about higher blood viscosity and hence possibly faster wearing out of the organism, but I think there may be more behind it. It is clear that there are considerable positive effects of altitude trainings or hypoxic tent therapies for top sportsmen, but since such positive effects are rarely without some trade-off, I wonder what the real disadvantages and dangers of the hypoxic adoption are. Faster aging perhaps? Do you have any more info here?
 
Hey trux I will get to your question shortly afterwhile as Ive to go now.

Anyway, within your lung, there is a residual volume and within your whole respiratory system there is also whats called "dead space". You can't use whatever volume is in there as the residual volume is simply the amount of air left after a forceful expiration so that your lung doesn't collapse and the dead volume is the volume that air will occupy at any time in your respiratory system. Residual volume can greatly varie (e.g: in asthma or COPD it can occupies up to 60% of your functional volume) etc...

I'll get to your question later.

See ya
 
Anyway, within your lung, there is a residual volume and within your whole respiratory system there is also whats called "dead space". You can't use whatever volume is in there as the residual volume is simply the amount of air left after a forceful expiration so that your lung doesn't collapse and the dead volume is the volume that air will occupy at any time in your respiratory system. Residual volume can greatly varie (e.g: in asthma or COPD it can occupies up to 60% of your functional volume) etc...
I think you misunderstood my comment, GetawayFK. I did not speak about the residual lung volume. I was speaking about the gas exchange in lungs during a prolonged apnea and about O2 remaining in the air held by lungs (and not just in the residual volume). Quite oppositely I referred to the state when you have your lungs filled to the maximum or even over it (by packing / glossopharyngeal insufflation).

I meant the late state of apnea when the level of O2 in the air in lungs drops to low level. In this state the ability of Hb to bind the remaining O2 drops too because the difference of PaO2 in blood and in the gas contained in lungs is insufficient for efficient gas exchange. The effect is further amplified by the lower binding of Hb due to high acidity (high CO2), which on one hand facilitates unloading of O2 for consumption in tissue, but on the other hand it makes it difficult to bind any O2 from the air in lungs if the PaO2 gradient is not sufficient for efficient recharging. I repeat that I do not speak about the well studied and documented cases of altitude adoption - there, due to the continual ventilation, the level of O2 in lungs remains the same, so 2,3-DPG indeed has positive effect, because it facilitates O2 unloading, without significantly impacting the recharging.

However, in the moment there is no ventilation (as it is the case in a long apnea), the PaO2 in lungs permanently drops (and PaCO2 raises), making it more and more difficult for Hb to use the remaining O2 gas in lungs. And I assume that due to the 2,3-DPG's property of stabilizing the de-oxygenated state of Hb, this situation comes earlier (at higher O2 levels in air of the lungs) than it would be the case with just normal/low 2,3-DPG level.

So in fact, although 2,3-DPG is quite beneficial for altitude or hypoxic adoption with continual ventilation, I suspect it is not the case for breath holding. Fortunately, the increased 2,3-DPG is not the only part of altitude adoption - I believe that for breath-holding the increase of hemoglobin is much more important, since it increases the O2 binding capacity without increasing the minimal O2 level for efficient gas exchange.
 
Last edited:
Well friend I thin there are 6 different types of hemoglobin & each one has a different globin chain -- and the chains each are coded by different genes which are "turned off or "turned on" during the different stages of development. The first 3 mos of embryonic development Hemoglobin Portland is produced(blood cells are produced in the yolk sac at this stage). As the red blood cell making (erythropoiesis) changes to the liver and the spleen-- hemoglobin F appears. when erythropoiesis shifts to the bone marrow during the first year of life, the adult hemoglobins (Hb A and Hb A2) begin to be produced.
 
DeeperBlue.com - The Worlds Largest Community Dedicated To Freediving, Scuba Diving and Spearfishing

ABOUT US

ISSN 1469-865X | Copyright © 1996 - 2025 deeperblue.net limited.

DeeperBlue.com is the World's Largest Community dedicated to Freediving, Scuba Diving, Ocean Advocacy and Diving Travel.

We've been dedicated to bringing you the freshest news, features and discussions from around the underwater world since 1996.

ADVERT