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Respiratory Quotient

Thread Status: Hello , There was no answer in this thread for more than 60 days.
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Pezman

We pee deep. Ew!
Sep 24, 2002
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Eric Fattah mentioned in a recent post something to the effect that the metabolic path for fats and proteins used o2 at 70% the rate of the metabolic path for carbohydrates (I presume that this is per unit of energy produced). Since we have a lot of physicians, physiologists etc. lurking around here, I was hoping someone could help unravel this.

I did find that fats and proteins cause a reduction in Respiratory Quotient, where RQ=(CO2/O2)/unit_time, the reason being that lipids and proteins are less oxidated and therefore require more O2 per mole of CO2 generated. In fact, the RQ was as low as 0.7, which matches the 70% figure that Eric mentioned (RQ for metabolizing carbohydrates is 1.0)

RQ itself does not seem to be any kind of indicator for how long you can go w/o o2, but it seems reasonable to think that it might be tied to respiratory drive -- lowering the rate of C02 production should prolong the amount time that you can tolerate apnea. I realize that this is a ratio here, not an absolute rate, and that RQ says nothing about the rate of Co2 production per se, but the whole topic made me wonder about a few things.

  • Are you more likely to black out when you're using lipolysis as your primary energy source?
  • Are you likely to pull off the best statics in the morning, since most of your energy is coming from lipolysis (and you're metabolic rate is low)
  • My understanding is that ketosis lowers metabolic rate amd it wouldobviously lower RV, so is it desirable to get into ketosis before doing statics?
  • I guess that a carb-heavy diet would increase respiratory drive and be bad for statics?
 
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I have done extensive experiments in pure fat burning (RQ=0.70), and pure carb burning (RQ=1.00), and I even built a indirect calorimeter to measure my respiratory quotient.

Bottom line is that at least for me, all apnea is best performed in pure carb burning mode. Static is most affected by this, for complicated reasons.

The only time pure fat burning is beneficial is when diving in extreme cold conditions, where thermogenesis is needed. Non-shivering thermogenesis requires free fatty acids in the blood, present primarily during lipolytic metabolism (i.e. RQ=.70).

I've read other posts from DB members saying their statics suffered when on low carb diets. Buring carbs is more O2 efficient, and produces more CO2. CO2 is what keeps you conscious at the end of the static, so you need as much as possible.


Eric Fattah
BC, Canada
 
I've read other posts from DB members saying their statics suffered when on low carb diets. Buring carbs is more O2 efficient, and produces more CO2. CO2 is what keeps you conscious at the end of the static, so you need as much as possible.

HI Eric, could you explain why the CO2 is responsible to our conscience in the end of static ? thanks Karol
 
I'm not Eric but I'll try to asnwer. :)

There are a few factors that change hemoglobin's affinity to O2, one of them is blood Ph (acidity/alkalinity). As the blood turns more acidic it tends to give away it's O2 (to the tissues in this case) more easily. So if you are more acidic you will stay conscious at lower blood saturation levels.
CO2 changes the blood Ph levels. CO2 is also responsible for some of our dive response as well.

To make it more clear, this is what is known as the blood O2 dissociation curve, you can see that you have higher PO2 at lower saturation rate when you are more acidic.

ODC_3.jpg

clip_image062.jpg
 
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In addition to shifting the Hb-O2 curve, CO2 also vasodilates your blood vessels. In this way, it dilates the blood vessels in your brain, forcing more blood into your brain (and thus forcing more O2 into your brain).

Lack of CO2 causes vasoconstriction. This is why you black out when you hyperventilate, because the vessels in your brain constrict.
 
another great physiology thread,

Thanks Eric and Michael for the answers and of course, someone had to ask the intelligent question, so thank you Pezman.
 
efattah said:
Bottom line is that at least for me, all apnea is best performed in pure carb burning mode. Static is most affected by this, for complicated reasons.
Same with me - eating something like pasta or cereal some time before training produces the best results, but I have to also not eat anything for about 3 or 4 hours before the actual training.

Lucia
 
Michael
Thanks for the interesting charts. They're new to me and I'm not sure that I can 'translate' them properly. If I take sea level in inches and convert to mm, I end up with 760. If that's right, PO2 at sea level is about 160 and 100 mm on your charts is 13% O2 by volume or 21% O2 at 2500 meters altitude. Did I get it close?
My only experience was at 7000 meters and the samba came fast while I was seated and performing a simple task, but I know that trained guides can work at the top of the world. How low can a trained diver go on a static?
The chart also raises a question about affinity. If it is lowered, it will give off O2 easier, but won't that make it harder to get O2 from the lungs. Seems that it would balance out.
Aloha
Bill
 
Bill said:
My only experience was at 7000 meters and the samba came fast while I was seated and performing a simple task
I thought you meant 7000 meters dynamic distance or depth for a moment! That would explain the samba...

Lucia
 
Bill,

You want high affinity at the start, to get O2 from the lungs. Once there is little or no O2 in the lungs, (at the end), you want low affinity so the hemoglobin gives up the O2.

This is why CO2 buildup is convenient. Low CO2 at the start means high affinity, high CO2 at the end means low affinity. This is called the bohr effect, and in seals & marine mammals, the CHANGE in affinity is much bigger, from the start to the end, because they have a higher 'bohr' effect. Interestingly, training can change your bohr effect.
 
Bill said:
Michael
Thanks for the interesting charts. They're new to me and I'm not sure that I can 'translate' them properly.
You're welcome. :)
That mm Hg might have thrown you off to think it's PO2 in the air but that's just another unit conversion for Atmopsheres as you just used.
That is not PO2 in air, that's arterial PO2 (PaO2) and Blood O2 saturation. It all takes place inside the body.
I'm sure it's clearer now, but just incase... :)

Arterial partial pressure of O2 is what really indicates how much oxygen is available for the tissues to take. The more O2 you have in your blood (=saturation in this case) and the less affinity your blood has to O2 (the curve), the higher PaO2 you will have. Hence the name of the table - "blood O2 dissociation table".

Example extrapolated fron the second table:
If I have 80% blood O2 saturation and my pH is 7.6 then my PaO2 will be about 40mm Hg. On the other hand, if my blood pH will be 7.2 then my PaO2 will be about 60mm Hg. That means more O2 available for the tissues. It shows that given all other stuff identical the more acidic blood will keep the person conscious longer.
efattah said:
in seals & marine mammals, the CHANGE in affinity is much bigger, from the start to the end, because they have a higher 'bohr' effect. Interestingly, training can change your bohr effect.
I assume that the trained response is that the body secretes more DPG enzyme to the blood (that reduces hemoglobin's affinity). If I'm not mistaken DPG secretion is proportional to raised blood acidity so that might be the whole reason behind this curve but I'm not sure. Does anyone know if hemoglibon changes affinity as a direct cause of pH change even without DPG?
 
Thanks Michael. I was hoping that I could draw some conclusions from the table that would show how blood saturation tracked O2 in the lungs and how low they were at the end of a static. I understand the chart now.
Aloha
Bill
 
If training increased your 2,3-DPG, then it would permanently change your affinity, rather than your bohr effect.

2,3-DPG affects affinity, not bohr effect.

So, the change in bohr effect after training is more likely to due structural changes in the hemoglobin itself, or perhaps the RBC's...
 
efattah said:
If training increased your 2,3-DPG, then it would permanently change your affinity, rather than your bohr effect.

2,3-DPG affects affinity, not bohr effect.

So, the change in bohr effect after training is more likely to due structural changes in the hemoglobin itself, or perhaps the RBC's...
Kinda missed the bohr effect there for a second, thought it was something else. :eek:
Still, increased DPG secretion as a response to a rise in blood acidity is not permanent.
I'm just speculating though, either could be true.
 
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