Blood biomarkers indicate mild neuroaxonal injury and increased amyloid β production after transient hypoxia during breath-hold diving
2016 (English)In: Brain Injury, ISSN 0269-9052, E-ISSN 1362-301X, Vol. 30, no 10, 1226-1230 p.Article in journal (Refereed) Published
Objective: To determine whether transient hypoxia during breath-hold diving causes neuronal damage or dysfunction or alters amyloid metabolism as measured by certain blood biomarkers.
Design: Sixteen divers competing in the national Swedish championship in breath-hold diving and five age-matched healthy control subjects were included. Blood samples were collected at baseline and over a course of 3 days where the divers competed in static apnea (STA), dynamic apnea without fins (DYN1) and dynamic apnea with fins (DYN2).
Main outcomes: Biomarkers reflecting brain injury and amyloid metabolism were analysed in serum (S-100β, NFL) and plasma (T-tau, Aβ42) using immunochemical methods.
Results: Compared to divers’ baseline, Aβ42 increased after the first event of static apnea (p = 0.0006). T-tau increased (p = 0.001) in STA vs baseline and decreased after one of the dynamic events, DYN2 (p = 0.03). Further, T-tau correlated with the length of the apneic time during STA (ρ = 0.7226, p = 0.004) and during DYN1 (ρ = 0.66, p = 0.01).
Conclusion: The findings suggest that transient hypoxia may acutely increase the levels of Aβ42 and T-tau in plasma of healthy adults, further supporting that general hypoxia may cause mild neuronal dysfunction or damage and stimulate Aβ production.
Place, publisher, year, edition, pages
Taylor & Francis, 2016. Vol. 30, no 10, 1226-1230 p.
Amyloid, breath-hold diving, tau, hypoxia, blood biomarkers, neuroaxonal injury
IdentifiersURN: urn:nbn:se:liu:diva-132561DOI: 10.1080/02699052.2016.1179792ISI: 000384324300009PubMedID: 27389622OAI: oai:DiVA.org:liu-132561DiVA: diva2:1046668