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Can apnea cause brain damage?

Thread Status: Hello , There was no answer in this thread for more than 60 days.
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Johan, other than S100B are there any other markers that can be measured in order to determine possible damage?
 
Glenn, just keep commenting my research! Even though I consider myself as a freediver (although not competitive), I am more of a physiologist/researcher. Ideas for new studies are often initiated by discussions with more expert freedivers than myself. I wish that funding and time could allow for more of them to be completed...

The reason for starting this thread was that I wanted the study to be discussed here. It was not to point fingers and saying that apnea is bad for you (and me).

/Johan
 
Johan, other than S100B are there any other markers that can be measured in order to determine possible damage?

Yes, there are other markers as well. Neuron-specific enolase (NSE), glial fibrillary acid protein (GFAP) and creatinine phosphokinase isoenzyme BB (CK-BB) are examples. These have been studied in other conditions. I have no further information at this time about these markers and apnea.

/Johan
 
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Of course, I disagree. There may very well be important subjective differences between the immersed and dry condition (when you are used to lying in water it feels different lying on your back and trying a max apnea). However, from what we have seen in previous studies involving both immersed and dry apneas and for the purpose of this study, the physiological differences are unimportant.

/Johan

The study analyzes physiological consequence of dry supine breath holding (like sleep apnea), not apnea diving. There are similarities, there are dissimilarities.
 
I guess this is the long version of the article described in the workschop proceedings from DAN in 2006.

Some comments on the S100B findings:

As noted earlier, there also have been found increased amounts of S100B in other sports, and there might be an association with stress. It might be interesting to see what happens with S100B when freedivers are doing sub-maximal cycling tests. I would be curious to know if there would be a significant difference.

Unless I am misreading the table, it seems that the control group S100B levels seems to drop on avarage to almost 80%. Is there an explanation for this finding?

Two divers show different S100B levels compared with the other divers. Where there any significant differences in other parameters, like blood pressure, heart rate and arterial oxygen?

From previous study's it seems that the cerebral artery's diameter changes a lot in a short time. First the artery constricts due hypocapna. Second its dilate during hypoxia.* This might influence the blood-brain barrier structure. Has there been any research on hyperventilation and S100B levels? I wonder if there would be a correlation between S100B and the change in diameter of the cerebral artery.

I also have done some small experiments with glucose and also found hyperglycemia. There was even a marked hyperglycemia after fasting for over 16 hours. I wonder if there is an relation with the found hyperglycemia in drowning victims. It has been suggested that hyperglycemia is correlated with increased levels of catecholamines and worse neurological outcome.**

I think we have (at least) two possibilities.

1.Extreme breath-holding isn't as relaxing as we think it is.
2.Extreme breath-holding does cause an temporal increase in the death of brain neurons.

I personally assume that we are more stressed as we think we are. My highest hyperglycemia levels where found with the most stressing dives. Dry breath-holds showed a higher hyperglycemia compared with wet breath-holds. However this was an experiment with only a single subject.

We shouldn't rule out the possibility of brain damage either. Ridgway's research does show some serious flaws. It was retrospective, consisted of freedivers with a large difference in years of experience, a large difference in amount of negative neurological events, and an the participants had a higher IQ the average individual.

It wouldn't surprise me if we would discover that competitive freediving is just as damaging as kicking a football with your head. This shouldn't be however reason to discourage freediving. It might just require us to look more into the positive effects of recreational freediving.

Just my 0.2 cents,

Rik

* Palada. Respiratory Physiology & Neurobiology 157 (2007) 374–381
** D. Warner, J. Knape, Brain Resucitation in the drowning victim. From: J.J.L.M. Bierens (Ed.) Handbook on Drowning, Springer, 2006. pg. 444
 
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The study analyzes physiological consequence of dry supine breath holding (like sleep apnea), not apnea diving. There are similarities, there are dissimilarities.

Yes, but for the purpose of this study, the physiological differences are not important.

/Johan
 
I came up with 2 theories :)

1. Perhaps the excess S100B is not coming from the brain at all, but is being produced by the body?

2. When the mamillian diving reflex kicks in, circulation is re-routed to the brain. Perhaps the holes in the bbb remain the same size, but the increased circulation allows more stuff to escape than normal?

I will see what else I can think up.
 
Unless I am misreading the table, it seems that the control group S100B levels seems to drop on avarage to almost 80%. Is there an explanation for this finding?

Rik, you are right. The control group has a small decrease in S100B. Contributing factors for this tendency could relate to both the inactivity and the fact that the individuals assumed a horizontal position. E.g., a shift in position from standing to supine leads to an expansion of plasma volume, reducing the concentration of serum S100B. Also, when arriving at the laboratory and assuming a supine position, thereby being completely at rest, the basal release of S100B into the blood is probably reduced, increasing the relative importance of elimination of S100B (taking place in the kidneys) and leading to a small decrease in serum S100B. We assume that the breath-hold divers would have followed the time course of the controls, had they not performed any apneas.

Two divers show different S100B levels compared with the other divers. Where there any significant differences in other parameters, like blood pressure, heart rate and arterial oxygen?

No, we have no precise explanation for this. We would probably need a much larger group of divers to be able to address such variations in the results.

From previous study's it seems that the cerebral artery's diameter changes a lot in a short time. First the artery constricts due hypocapna. Second its dilate during hypoxia.* This might influence the blood-brain barrier structure. Has there been any research on hyperventilation and S100B levels? I wonder if there would be a correlation between S100B and the change in diameter of the cerebral artery.

No, I am not aware of any such studies. It would certainly be interesting.

/Johan
 
So it is an invalidated apnea diving physiological study IMO, but a valid dry supine apnea physiological study.

OK, that's you opinion. I can just state that I am confident in that the results from this model can be used to make conclusions regarding the static apnea condition involving immersion (in addition to the obvious situation involving dry training).

We have of course "validated" the model, performing experiments on the same subjects in both a pool and in the laboratory. The "validation" experiments in the lab involved both resting and exercise apneas, showing us that responses were comparable to those observed in static and dynamic apneas in the pool. One reason for using the laboratory model is that several of the instruments we use are not "water-proof", unfortunately.

/Johan
 
1. Perhaps the excess S100B is not coming from the brain at all, but is being produced by the body?

S100B is specific to brain tissue to such an extent that any other source than the brain can be excluded.

2. When the mamillian diving reflex kicks in, circulation is re-routed to the brain. Perhaps the holes in the bbb remain the same size, but the increased circulation allows more stuff to escape than normal?

It is wrong to state that the blood-brain barrier has "holes", at least not for molecules of the size of S100B. The endothelial cells that line the blood vessels in the brain are normally attached to each other with "tight junctions", forming a barrier so that large molecules such as proteins cannot pass from the brain into the blood between the cells (there are other factors of importance as well). In addition, proteins, such as S100B, do not pass directly through the cell membrane. That's why there under normal conditions is a very low concentration of S100B in the blood. For the S100B to increase in the blood to the extent we observed, the barrier function must be compromised, changes in blood flow will not be enough.

/Johan
 
OK, that's you opinion. I can just state that I am confident in that the results from this model can be used to make conclusions regarding the static apnea condition involving immersion (in addition to the obvious situation involving dry training).

We have of course "validated" the model, performing experiments on the same subjects in both a pool and in the laboratory. The "validation" experiments in the lab involved both resting and exercise apneas, showing us that responses were comparable to those observed in static and dynamic apneas in the pool. One reason for using the laboratory model is that several of the instruments we use are not "water-proof", unfortunately.

/Johan

Thank you for your response, Johan.
Cheers.
 
C'mon, get to the important stuff. So how much longer will my Daddy have to hold his breath before he forgets about the money he loaned me to buy my car?

Extreme static apnea results in abnormal physiology. No argument there. Clinical significance? Well, I can vouch for my father's IQ and continued ability to embarass me at chess. My mother may have some input on the "brain damage" part however ;-)
 
Oh, and Johan... I'm interested in serotonin and norepinephrine fluctuations in freedivers. We have a lot of data on the clinical significance of THOSE chemicals and some anecdotal evidence of possible issues in divers. Thoughts?

--Lorraine, former undergrad in the psychobiology department at UC Irvine :)
 
Oh, and Johan... I'm interested in serotonin and norepinephrine fluctuations in freedivers. We have a lot of data on the clinical significance of THOSE chemicals and some anecdotal evidence of possible issues in divers. Thoughts?

--Lorraine, former undergrad in the psychobiology department at UC Irvine :)

Well, if you are thinking about those chemicals and the connection with e.g. depression, I have no specific thoughts (not really within my field). Any research going on in that area with regards to apnea? If so, that would be very interesting.

/Johan
 
C.M. Muth spoke about the possibility that depression could be a long therm effect of freediving at the Ulm Apnoe tauchen Workschop in 2002 or 2003.

Unless I am mistaken, this was based on what happened with Jacques Mayol.
 
C.M. Muth spoke about the possibility that depression could be a long therm effect of freediving at the Ulm Apnoe tauchen Workschop in 2002 or 2003.

Unless I am mistaken, this was based on what happened with Jacques Mayol.

Eep!

The whole reason I freedive is because it takes my mind off of my depression...
 
Eep!

The whole reason I freedive is because it takes my mind off of my depression...

I don't know if freediving causes depressions. Jacques Mayol had a difficult life. To my knowledge, there are no other (former) world record holders who have suffered from depressions, like Jacques Mayol did.

And we shouldn't confuse competitive breath-holding with recreational freediving.
 
Yes I know, I'm just saying.

And besides that, correlation and causation are 2 different things.
 
I dive with several guys - I swear have brain damage! example: ILDiver, Unirdna, Wreckrunner and Jon. to name a few. ;)


Very interesting thread to read! Thanks.
 
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