Abstract
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.
Acknowledgement
We thank Victor Liman, Åsa Källén, Monica Christiansson, Sara Hullberg and Dzemila Secic for skillful technical assistance. We also thank Jonas Roberts, Ida Franzén and Gisela Malmgård for their assistance in collecting the blood samples.
Declaration of interest
MG, PS, UA and RL report no conflicts of interest. NN is an employee at UmanDiagnostics. DHW is an employee at Quanterix Corporation. KB and HZ are co-founders of Brain Biomarker Solutions, a University of Gothenburg-based platform company.