Holding your breath might just adversely affect your brain. So, don't ever try it again - not even for fun.
A study conducted by researchers in Sweden found that divers who held their breath for several minutes had elevated levels of a protein that can signal brain damage.
Although the appearance of the protein, S100B, was transient, it leaves open the question of whether lengthy apnea (breath-holding) can damage the brain over the long term.
"The results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system, and may have cumulative effects," the researchers said.
The researchers said that the release of S100B into the blood suggests that holding one's breath for a long time disrupts the blood-brain barrier.
However, the concern is that repetitive exposures to severe hypoxia (lowered oxygen supply), such as that experienced by individuals training and competing in static apnea diving events, could cause neurological damage over time.
Nine competitive breath-hold divers (eight men and one woman) participated in this study, along with six individuals who had limited experience with breath-hold diving. The nine competitive divers formed the experimental group, while the non-divers acted as the controls.
The researchers found that the average breath-hold time was 5 minutes 35 seconds. The longest was 6 minutes 43 seconds and the shortest was 4 minutes 41 seconds.
They found that the marker for brain damage, S100B, rose in seven of the nine divers, the controls showed no change in S100B, on average, S100B rose 37 percent within 10 minutes after the apnea ended, S100B levels returned to normal within two hours for all the participants, and the divers showed signs of asphyxia, that is, blood oxygen levels fell, while carbon dioxide levels rose.
The S100B levels, while elevated, were well below levels associated with brain injury. In brain-injured patients, the presence of S100B in the blood can increase by several hundred percent.
In addition, the elevation of S100B was more transient in the divers, compared to people who suffered brain injury. The divers had a quick return to normal, while S100B levels peak in 24 hours in brain-injured patients.
The transient nature of the increase in S100B among the divers probably indicates the blood-brain barrier has been compromised, allowing the protein to escape from the fluid in the brain into the circulation.
The blood-brain barrier controls what passes between the brain and the circulation. S100B would normally remain in the brain.
The study has been published in the Journal of Applied Physiology.