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Increased serum levels of the brain damage marker S100B after apnea in trained breath-hold divers: a study including respiratory and cardiovascular observations

Andersson, Johan LU orcid ; Linér, Mats LU and Bjursten, Henrik LU (2009) In Journal of Applied Physiology 107(3). p.809-815
Abstract
The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., "static apnea" (average: 335 s, range: 281–403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O2 and CO2 (PaO2 and PaCO2) were 128 Torr and 20 Torr, respectively, at the start of... (More)
The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., "static apnea" (average: 335 s, range: 281–403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O2 and CO2 (PaO2 and PaCO2) were 128 Torr and 20 Torr, respectively, at the start of apnea. The degree of asphyxia at the end of apnea was considerable, with PaO2 and PaCO2 reaching 28 Torr and 45 Torr, respectively. The concentration of S100B in serum transiently increased from 0.066 µg/l at the start of apnea to 0.083 µg/l after the apnea (P < 0.05). The increase in S100B is attributed to the asphyxia or to other physiological responses to apnea, for example, increased blood pressure, and probably indicates a temporary opening of the blood-brain barrier. It is not possible to conclude that the observed increase in S100B levels in serum after a maximal-duration apnea reflects a serious injury to the brain, although the results raise concerns considering negative long-term effects. At the least, the results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system and do not preclude cumulative effects. (Less)
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author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
glucose, lactate, ionized calcium, hypoxia, hemoglobin
in
Journal of Applied Physiology
volume
107
issue
3
pages
809 - 815
publisher
American Physiological Society
external identifiers
  • wos:000269370700024
  • scopus:69749096910
  • pmid:19574501
ISSN
1522-1601
DOI
10.1152/japplphysiol.91434.2008
language
English
LU publication?
yes
id
14f1f0b5-9450-40c9-a646-73a81a8fdc92 (old id 1471959)
date added to LUP
2016-04-01 12:30:18
date last changed
2022-02-11 07:53:21
@article{14f1f0b5-9450-40c9-a646-73a81a8fdc92,
  abstract     = {{The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., "static apnea" (average: 335 s, range: 281–403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O2 and CO2 (PaO2 and PaCO2) were 128 Torr and 20 Torr, respectively, at the start of apnea. The degree of asphyxia at the end of apnea was considerable, with PaO2 and PaCO2 reaching 28 Torr and 45 Torr, respectively. The concentration of S100B in serum transiently increased from 0.066 µg/l at the start of apnea to 0.083 µg/l after the apnea (P &lt; 0.05). The increase in S100B is attributed to the asphyxia or to other physiological responses to apnea, for example, increased blood pressure, and probably indicates a temporary opening of the blood-brain barrier. It is not possible to conclude that the observed increase in S100B levels in serum after a maximal-duration apnea reflects a serious injury to the brain, although the results raise concerns considering negative long-term effects. At the least, the results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system and do not preclude cumulative effects.}},
  author       = {{Andersson, Johan and Linér, Mats and Bjursten, Henrik}},
  issn         = {{1522-1601}},
  keywords     = {{glucose; lactate; ionized calcium; hypoxia; hemoglobin}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{809--815}},
  publisher    = {{American Physiological Society}},
  series       = {{Journal of Applied Physiology}},
  title        = {{Increased serum levels of the brain damage marker S100B after apnea in trained breath-hold divers: a study including respiratory and cardiovascular observations}},
  url          = {{http://dx.doi.org/10.1152/japplphysiol.91434.2008}},
  doi          = {{10.1152/japplphysiol.91434.2008}},
  volume       = {{107}},
  year         = {{2009}},
}