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Why do we blackout? Not how, WHY.

Thread Status: Hello , There was no answer in this thread for more than 90 days.
It can take a long time to get an up-to-date response or contact with relevant users.
efattah said:
Samba/LMC can happen from other types of blackout. I think the main issue is the timeframe. If the blackout happens more gradually, the glutamate level has more time to build up. If the blackout happens more suddenly (i.e. fainting or choking, from lack of blood flow to the brain), I think the glutamate doesn't have much time to build up.
Eric, thanks for explaining, that makes sense. :)

Fondueset said:
Slightly off track - but has anyone noticed improvements in static times breathing up through the nose vs mouth?
Yes, I mostly prefer to breathe through my nose. Of course, sometimes I have to breathe through my mouth, but I try not to if I don't have to. Breathing through my mouth makes me feel stressed.
 
Same here - though I manage it allright. I haven't blacked out since I was a kid - and don't generally push my dives very hard at all - since I'm nearly allways diving alone. But I have noticed intense relief just inhaling a bit from my mask - all out of proportion to the volume. I thought it was probably just psychological - but the sinus factor makes sense - and also explains why dives are generally better after a nasal breath up.
 
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To Naiads question, I think the lmc reaction varies with individuals or quite possibly, as Eric suggests, with different conditions. For example, I and several of my buddies experianced tunnel vision, loss of color vision as a result of fast repeditive spearfishing dives and hyperventilation (made us a lot more cautious). None of us got the shakes, that I know of. Apparently lots of other divers never get the visual symptoms. I've seen only two BO's, one guy got the shakes after he lost conciousness and the other never had a visible twitch. Same root cause though.

Connor
 
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Certainly it does vary between individuals. Maybe excessive hyperventilation makes it more likely for someone to blackout without any LMC?

Lucia
 
I also made the experience that it is depending an the "speed" the hypoxia sets in. At the Ambulance Service I actualy often saw spasms when people suffered hypoxia over a longer time increasingly.

Robert
 
I'm researching how the eyes and brain function during apnea diving, it's quite complex.

During BO, often vision darkens into tunnel vision with loss of color vision, do the eyelids always close then (involuntarily) or do they remain open?
At that time, are the pupils usually dilated or constricted?

The brain and the eyes are heavy consumers of both energy (from food) and oxygen. Too much oxygen can be dangerous.

Premature infants were once treated for breathing difficulties (due to under-developed lungs) with excess oxygen, this sometimes produced blindness.

I found some articles on neuroglobin, I'll copy them in the next post.
DDeden

efattah said:
I have read an entire book about brain hypoxia. From everything I read, it does not appear to be a defense mechanism at all. It is simply a matter of energy failure.

The neurons in the brain require certain electrical gradients in order to do their job as neurons. Maintaining the electrical gradient requires energy. The energy comes from ATP (adenosine triphosphate), which stores lots of energy in the phosphate chemical bond. The brain gets ATP from several sources, including:
1. Stored ATP in the brain (very small, enough for 3 second of consciousness)
2. Stored creatine phosphate in the brain (which can generate ATP, enough for 3 seconds of consciousness)
3. Burning O2 with glucose or ketone, generating ATP (requires oxygen supplied from the blood, as well as either glucose or ketone, also from the blood)
4. O2 stored in neuroglobin (very small --just discovered recently)

If #3 is cut off (from either holding your breath too long, or being strangled or choked), then you have enough energy from #1 and #2 to maintain consciousness for 6-7 seconds. This is why in the old days when people had their heads cut off (guillotine), they remained conscious for 6-7 seconds, and responded if you called their name by looking you in the eye (even after their head was cut off).

Once all these energy sources have been exhausted, there is no more ATP available. Burning glucose anaerobically (without O2) creates lactic acid very fast, and generates very little energy, enough for maybe 1 second of consciousness.

Once no energy is available, the neurons lose their electrical gradient and 'depolarize'. The process creates a chain reaction called 'anoxic depolarization'. When neurons no longer function, consciousness cannot be maintained, because the brain simply isn't working properly anymore.

The moment when blackout occurs depends on many variables, including blood pressure, hydration, brain creatine stores, carotid artery width, and so on. Because the moment of blackout can vary dramatically (either very early or very late), it seems even more likely that it isn't a defence mechanism. If it were a defense mechanism, then it would not be possible to develop tolerance to brain hypoxia and delay the blackout. If it were a defence mechanism, why not just black out nice and early to 'save' the organism?
 
The following are from a few articles on oxygen use and conservation in regards to physiology. Nitric Oxide (NO), Iron (Fe), Globins (Neuro- Cyto- Hemo- Myo-), and other chemicals are involved in O2 transport and use in the body.

Neuroglobin (Ngb), a globular heme protein expressed in the brain of vertebrates, binds oxygen reversibly, with an affinity comparable to myoglobin (Mb). Despite low sequence identity, the overall 3D fold of Ngb and Mb is very similar. Unlike in Mb, in Ngb the sixth coordination position of the heme iron is occupied by the distal histidine, in the absence of an exogenous ligand. Endogenous ligation has been proposed as a unique mechanism for affinity regulation and ligand discrimination in heme proteins. This peculiarity might be related to the still-unknown physiological function of Ngb. Here, we present the x-ray structure of CO-bound ferrous murine Ngb at 1.7 Å and a comparison with the 1.5-Å structure of ferric bis-histidine Ngb.

A vertebrate globin expressed in the brain. [Nature]
Burmester T, Weich B, Reinhardt S, Hankeln T. Institute of Zoology, Johannes Gutenberg University Mainz, Germany.

Haemoglobins and myoglobins constitute related protein families that function in oxygen transport and storage in humans and other vertebrates. Here we report the identification of a third globin type in man and mouse. This protein is predominantly expressed in the brain, and therefore we have called it neuroglobin. Mouse neuroglobin is a monomer with a high oxygen affinity (half saturation pressure, P50 approximately 2 torr). Analogous to myoglobin, neuroglobin may increase the availability of oxygen to brain tissue. The human neuroglobin gene (NGB), located on chromosome 14q24, has a unique exon-intron structure. Neuroglobin represents a distinct protein family that diverged early in metazoan evolution, probably before the Protostomia/Deuterostomia split.

Neuroglobin and cytoglobin. Fresh blood for the vertebrate globin family.
Pesce A, Bolognesi M, Bocedi A, Ascenzi P, Dewilde S, Moens L, Hankeln T, Burmester T.
Department of Physics-INFM and Center for Excellence in Biomedical
Research, University of Genova, Via Dodecaneso 33, I-16146 Genova, Italy.

Neuroglobin and the survival of the neuron
Martino Bolognesi

After cardiovascular disease and cancer, stroke and other hypoxia-related diseases are the third most common causes of death in many industrialised countries. In Europe, they represent the most important cause of morbidity and long-term disability imposing an enormous economic burden.The brain's response to hypoxia and ischemia, which helps determine the clinical outcome, is a complex pattern of events including the synthesis of neuroprotective proteins. These proteins help to counteract the adverse effects of hypoxia or ischemia by increasing anaerobic metabolism, tissue vascularity and 02 delivery or by the elimination of toxic compounds. Neuroglobin is an 02-binding protein suggested to enhance the 02 supply of the brain. We propose to study neuroglobin in normal and pathologic conditions in order to elucidate its role in the survival of the neuron under hypoxic and ischemic conditions. Neuroglobin and cytoglobin are two recently discovered members of the vertebrate globin family. Both are intracellular proteins endowed with hexacoordinated heme-Fe atoms, in their ferrous and ferric forms, and display O2 affinities comparable with that of myoglobin. Neuroglobin, which is predominantly expressed in nerve cells, is thought to protect neurons from hypoxic-ischemic injury. It is of ancient evolutionary origin, and is homologous to nerve globins of invertebrates.
Cytoglobin is expressed in many different tissues, although at varying levels. It shares common ancestry with myoglobin, and can be traced to early vertebrate evolution. The physiological roles of neuroglobin and cytoglobin are not completely understood. Although supplying cells with O2 is the likely function, it is also possible that both globins act as O2-consuming enzymes or as O2 sensors. Here, we review what is currently known about neuroglobin and cytoglobin in terms of their function, tissue distribution and relatedness to the well-known hemoglobin and myoglobin. Strikingly, the data reveal that O2 metabolism in cells is more complicated than was thought before, requiring unexpected O2-binding proteins with potentially novel functional features.

Neuroglobin, nitric oxide, and oxygen: Functional pathways and conformational changes
Maurizio Brunori *,Alessandro Giuffrè *, Karin Nienhaus G. Ulrich Nienhaus §, Francesca Maria Scandurra * and Beatrice Vallone **Department of Biochemical Sciences and Consiglio Nazionale delle Ricerche Institute of Molecular Biology and Pathology, University of Rome "La Sapienza," 00185 Rome, Italy; Department of Biophysics, University of Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany; and §Department of Physics, University of Illinois, 1110 West Green Street, Urbana, IL 61801. Edited by Britton Chance, University of Pennsylvania School of Medicine, Philadelphia, PA and approved April 21, 2005 (received for review November 24, 2004)

Neuroglobin (Ngb) is a globin expressed in the nervous system of humans and other organisms that is involved in the protection of the brain from ischemic damage. Despite considerable interest, however, the in vivo function of Ngb is still a conundrum. In this paper we report a number of kinetic experiments with O2 and NO that we have interpreted on the basis of the 3D structure of Ngb, now available for human and murine metNgb and murine NgbCO.
DDeden
 
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wet said:
During BO, often vision darkens into tunnel vision with loss of color vision, do the eyelids always close then (involuntarily) or do they remain open?
At that time, are the pupils usually dilated or constricted?
The eyes usually remain open, at least that is what I have seen happening, and what has happened to me. The pupils are probably dilated, at least that is what others have described, I haven't noticed that.
 
Interesting thread. Maybe we need to explore the exact physical makeup of a blackout. If it isn't a controlled emergency reaction, why does it occur with 25-30% of the total oxygen left?
Aloha
Bill
 
naiad said:
The eyes usually remain open, at least that is what I have seen happening, and what has happened to me. The pupils are probably dilated, at least that is what others have described, I haven't noticed that.

I had expected the eyelids to close nearly always. I haven't BO'd underwater, but during BO's and dead-faints in air, I think the lids close usually.

Here is an article on seals, shivering above water but not below, and connection to O2 and neuroglobin.

http://www.livescience.com/animalworld/061010_shivering_seals.html
While diving, hooded seals can handle oxygen levels so low they'd be
lethal to humans. Now scientists are beginning to understand how they
do it: The seals stop shivering and go with the chilly flow. By
switching off the shivers, which are designed to produce heat and keep
a body warm, the plunging seals chill their bodies, and even their
brains, to a point of hypothermia. When diving down to 3,280 feet
where oxygen is scarce, the chill lowers metabolism so the animals can
save on precious oxygen, explained Lars Folkow, of the University of
Tromso, Norway.

The finding, presented here this week at a meeting of the American
Physiological Society, could have implications for people who suffer
cardiac arrest, stroke or respiratory disorders, which rob the brain
of oxygen. The researchers monitored seals [image] as they dove in
tanks of water cooled to around 36 degrees Fahrenheit. Before, during
and after the dives, the scientists measured shivering, heart rate,
and brain and body temperatures of the seals. The seals shivered while
on the surface but stopped or nearly stopped shivering during dives,
even though their bodies continued to cool. Upon resurfacing, the
seals almost immediately started shivering again.

They also found the seals' brains cooled about 5 degrees during the
dives, a chilled state that requires less energy and oxygen while
reducing chances of brain damage from hypoxia. Seals are naturally
built to survive the extreme conditions of deep dives, spending 80 to
90 percent of their time at sea underwater. They can store four times
the amount of oxygen in their blood and muscles as humans, Folkow
said. So by not shivering—an activity that requires oxygen for fuel—
and slowing their metabolism, the animals extend the amount of time
they can survive on oxygen stores. Most of the time the stores may be
sufficient, as the seals typically take many short dives. But
sometimes seals in the wild can dive for so long that they use up
nearly all of their oxygen.

"If our brain would receive arterial blood with that little oxygen, we
would faint right away and we would probably experience brain damage,
and may even die," Folkow told LiveScience "Somehow they tolerate
hypoxia better," he said. "We don't know why." Folkow and his
colleagues speculate that the seals are equipped with more
neuroglobin, a brain protein that makes oxygen available to brain tissues.
 
Interesting. There is a definite tendency to stop shivering during apnea. If I get into a cold pool and start shivering, then do a static, I will stop shivering for the first 1:30-2:00. If I continue past this point it will start again. Also diving with empty lungs will immediately stop shivering. I tried this and it works. My diving ability is greatly reduced when I am cold, so I don't know how useful this is, or maybe some people are better than others.

I also didn't know that seals get seriously hypoxic during dives in the wild. I thought they would always stay well within their limits.
 
Question: Is it possible that a samba is a delayed shiver, but instead of the skin-muscles twitching, the deeper skeletal muscles twitch?

Is a samba more likely to occur when diver is overheated or superchilled? I know that temperature isn't the cause of a samba, but it might be a factor in its manifestation.

Shivering can be very mild (with goose pimples and slight teeth rattling) or very strong (jerking jaw & leg muscles involuntarily).

I don't think it's possible to shiver when overheated. If a samba can occur in a warm pool, then I think shivering isn't related to samba.
DDeden
 
Bill said:
Interesting thread. Maybe we need to explore the exact physical makeup of a blackout. If it isn't a controlled emergency reaction, why does it occur with 25-30% of the total oxygen left?
Aloha
Bill

I think the simplest explanation for this is to use an analogy. A portable CD player will die and cease to function even though the batteries still have about 20% of their power left. A certain threshold of power is needed to operate the device, below which the devices ceases to function, even in the presence of some limited energy reserve.

Everything I have studied leads me to believe that blackout is a total energy failure, not a protective mechanism.
 
wet said:
I don't think it's possible to shiver when overheated. If a samba can occur in a warm pool, then I think shivering isn't related to samba.
A samba certainly can occur in a warm pool, or during dry statics in a warm environment.

efattah said:
I think the simplest explanation for this is to use an analogy. A portable CD player will die and cease to function even though the batteries still have about 20% of their power left. A certain threshold of power is needed to operate the device, below which the devices ceases to function, even in the presence of some limited energy reserve.

Everything I have studied leads me to believe that blackout is a total energy failure, not a protective mechanism.
I agree. I don't see how it can be useful to blackout in water, unless there is someone else there to sort out the situation. It looks much more like a failure than a protective mechanism.

That reminds me - I need to get a battery for my diving watch. After a few weeks of not working very well, it has stopped altogether. :head
 
Thanks Eric. Batteries and electronics are easier to understand than the workings of the brain. The more I look into it (energy failure), the more it makes sense.
Aloha
Bill
 
efattah said:
As brain energy begins to decrease to critical levels, the GABA to glutamate ratio changes, in favour of glutamate. Glutamate then increases without limit. Glutamate is an excitatory neurotransmitter. When it becomes high, then 'random' electrical impulses in the brain are enough to make entire muscles shake.
Interesting. Goldfish have high levels of glutamate and glutamine, and they have a very high resistance to hypoxia.
 
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