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Splenic contractions

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

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Dec 9, 2005
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Splenic contractions during breath-hold diving were already discussed here on DB several times. There are also number of studies about this topic - I have a dozen of them listed at spleen @ APNEA.cz

Few days ago, Elisabeth Kristoffersen published on her blog a new entry about her participation on the research of Erika Schagatay, a Swedish scientist from the Mid Sweden University, who is also the author of another older study listed in my database too.

However, I was rather surprised that Erika estimates the average increase of BHT (breath-hold time) to 20-30s. When calculating the possible effect of splenic contraction on the apnea time at humans, I do not see any possibility to get an improvement more than very few seconds (approx 2-4s in average). Since I guess that it may interest some of you, I posted a comment with the calculation on Elisabeth's blog, and am copying it below:


Personally, I am afraid that the breath-hold increase of 30s thanks to the splenic contraction is rather exaggerated. In the older study Erika found that in average the splenic contraction releases 49 ml of blood. Now the hematocrit is packed with the density twice so high as in arterial blood, so let's assume it corresponds to 100 ml. At ~5 l of blood in body, it would make about 2% hematocrit increase. That's consistent with the measurement from Erika's study (2.2% Hct increase).

However, spleen is used as a depository of old hematocrit, where it is then being destroyed. So quite likely this hematocrit released from the spleen has not the same oxygen transport capacity as new one. I wonder if this fact was taken in view in Erika's study.

Even if we speculate with the uncertain 2% increase of Hct, at the max breath-hold of 5 minutes (300s), the 2% would make only 6s. In fact even less, because although the higher Hct will allow saturating the blood with more oxygen during the breath-up, it won't help too much with pulling oxygen from lungs after the start of the apnea. Well, to certain extent the gas exchange with the dropping oxygen level in lungs during the apnea will be more efficient at higher Hct, but likely the difference will be much lower than the Hct increase. Blood pH will be a more important factor, so even with more Hct it won't allow much lower hypoxemia.

Considering the above mentioned facts, I am afraid that the splenic contraction will help with just some very few seconds (2-4s ?). I believe that the 20s or 30s observed in the study of Erika Schagatay can be only attributed to the other remaining factors of the progressing diving response (bradycardia, vasoconstriction, etc.), and unfortunately not to the splenic contraction.

I'd love though hearing from Erika or other experts on this topic. Of course, having the possibility to increase own breath-hold time by 30s thanks to the splenic contraction would be wonderful, but I am afraid it is just a dream originating probably in the studies of seals, who have indeed huge spleens containing several liters of blood highly packed with Hct.
 
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I think the 30 second increase due to splenic contraction is probably right.

This is mostly evidenced by several studies that compared people who had spleens, to people who were splenectomized (spleen removed). The subjects who had no spleens did not show improvement over successive breath-holds.

This gives strong evidence that the spleen is responsible for the increase in time. If so, then our model may be too simplistic to calculate the actual effect.

For example, the extra hemoglobin released by the spleen not only carries and stores oxygen, but also buffers CO2. Further, who knows what other chemicals or enzymes the spleen might release.
 
Yes, indeed, it is this study: Physiological and Genomic Consequences of Intermittent Hypoxia: Selected Contribution: Role of spleen emptying in prolonging apneas in humans -- Schagatay et al. 90 (4): 1623 -- Journal of Applied Physiology - by the same author (Erika Schagatay).

In that study, they measured higher increase of hematocrit at serial apneas, than in the other study of Erika Schagatay - +6.4% Hct (though just +3.3% more hemoglobin), and 17 s increase of the physiological breaking point of apnea, while there was no change in these values in the splenectomized group. You are probably right that there are other factors than just the increased Hct/Hb that play a role.

And from the discussion section in that document it looks the effect may be higher at trained subjects than at nondivers.

What disturbs me little bit on all those studies are the rather huge differences in the measured values. Also, for example the later study shows that the splenic contraction is fully reversed within 10 minutes of breathing, while in another study I read it takes 30 minutes to the spleen to reduce the contraction by 50%.
 
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Just a quick comment that if you measure HCT increase in serial apneas, you should take into account the diuresis effect. I mean if these were done for example on the period of one hour, personally I could loose up to 1-2 litres of fluid in that time doing max apneas. Certainly that shows in in the HCT levels as well?

Although "no change in splenectomized group" would contradict this.

(no I did not RTFA, just commenting in general - would not surprise me if this was factored out)
 
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Anyone have any idea of the oxygen satruation of the hemoglobin while it is in the spleen? The 2001 research paper referred to by Trux says that hematocrit and hempblobin increase rapidly during the first 10-12 minutes of a long dive.
It seems counterintuitive that this would be of any value unless the hemoglobin is already loaded with oxygen?
The same would go for FRC dives. Why change the oxygen carrying capacity (by increasing hemoglobin) unless there's a benefit?

Howard
 
I'd tell that the oxygen saturation of hemoglobin in spleen is relatively low, but that's not too important. The advantage of spleen contraction is not the direct injection of oxygen into the blood system, but rathter the increased stock and transport capacity. It helps better binding and transporting the oxygen remaining in lungs, and it helps with pre-charging hematocrit with O2 at the subsequent apnea. That's why the effect is much more pronounced at serial breath-holds.
 
I think that spleen hemoglobin is fully saturated with oxygen.

Otherwise seals would be in deep trouble. Seals are known to suntan on rocks for hours with heart rates of 120bpm. Then, they suddenly jump in the water, and the heart rate plunges to 10-20bpm, and the elephant seal releases 24L of blood stored in the spleen, during the dive, which may be the only dive.

Generally speaking, the dive reflex is something which is supposed to happen 'during the dive'. Seals do not need to do negative pressure 'warm up' dives to first contract the spleen, then oxygenate that blood during subsequent breathe-ups. Similarly, the high success rate of the no-warm up method used by WR holders like Will Trubridge and Tom Sietas supports that the spleen red cells are fully oxygenated.

The only evidence I have for that from my own experiments is the drastically different SaO2 vs. Time curve that is created from static apnea with or without warm up, using an oximeter. Using an oximeter, I can sometimes see the moment of splenic contraction, as my SaO2 will sometimes INCREASE in the middle of the breath-hold (but only if it is the 1st breath-hold) -- one must ask where does this oxygen come from...?
 
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Well, when I wrote that the hematocrit in spleen is relatively lowly saturated, I did not mean that is completely discharged, but that it is rather somewhere between the SaO2 and SvO2 (arterial and venous saturation). Additionally there is another factor reducing the maximal saturation - spleen is an organ stocking and destroying old and damaged hematocrit, so the stocked Hct may not be as efficient as fully functional hematocrit.

Depending on physical effort, and the breath-up prior the breath-hold, the venous oxygen saturation may be relatively high, and likely the saturation in spleen will be higher too.

At subjects measured in diverse studies (both divers and non-divers), the spleen continuously contracted over several serial apneas. However, although serial apneas with short recoveries lead to progressive reduction of the splenic volume, they may also lead to a slower increase of the venous oxygen saturation.

Splenic contraction is not directly related to diving reflex - facial immersion has no considerable impact on the strength of splenic contractions. It means, you can achieve good splenic contraction already during your dry preparation, and rather using the immersion shock to trigger good diving response.

This all together explains why the no warm-up approach may be successful, but it does not necessarily tell that the hematocrit in spleen is close to 100% saturated, or that there was no splenic contraction (and Hct release with subsequent oxygenation) before the actual performance.

At seals, the situation may be different. Unlike elephant seals with 24 liters of blood in the spleen, human spleen contains typically only 200 - 300 ml, and only part of it gets released to the body when contracted.

Furthermore the positive effect of the splenic contraction is not only the higher O2 stock, but as I wrote, also the increased transport capacity, and then also the higher CO2 buffering. All this together makes it little bit less important whether the Hct is fully saturated, or rather with only low O2 saturation (close to the venous saturation).

There is a simple and comprehensible document about splenic contractions with many graphs, explaining some of the details mentioned here:

http://www.baromedisin.no/NBF_arkiv/2007/Moete_1_07/Schagatay_2007.pdf
 
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Is there any real signal in my body, at the moment I have Splenic contraction? does the diafragm contraction has some thing to do with this point of splenic contraction? thanks
 
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