Literature DB >> 28464406

Sustained apnea induces endothelial activation.

Lars Eichhorn1, Ramona Dolscheid-Pommerich2, Felix Erdfelder1, Muhammad Ajmal Ayub3, Theresa Schmitz4, Nikos Werner4, Felix Jansen4.   

Abstract

BACKGROUND: Apnea diving has gained worldwide popularity, even though the pathophysiological consequences of this challenging sport on the human body are poorly investigated and understood. This study aims to assess the influence of sustained apnea in healthy volunteers on circulating microparticles (MPs) and microRNAs (miRs), which are established biomarkers reflecting vascular function. HYPOTHESIS: Short intermittent hypoxia due to voluntary breath-holding affects circulating levels of endothelial cell-derived MPs (EMPs) and endothelial cell-derived miRs.
METHODS: Under dry laboratory conditions, 10 trained apneic divers performed maximal breath-hold. Venous blood samples were taken, once before and at 4 defined points in time after apnea. Samples were analyzed for circulating EMPs and endothelial miRs.
RESULTS: Average apnea time was 329 seconds (±103), and SpO2 at the end of apnea was 79% (±12). Apnea was associated with a time-dependent increase of circulating endothelial cell-derived EMPs and endothelial miRs. Levels of circulating EMPs in the bloodstream reached a peak 4 hours after the apnea period and returned to baseline levels after 24 hours. Circulating miR-126 levels were elevated at all time points after a single voluntary maximal apnea, whereas miR-26 levels were elevated significantly only after 30 minutes and 4 hours. Also miR-21 and miR-92 levels increased, but did not reach the level of significance.
CONCLUSIONS: Even a single maximal breath-hold induces acute endothelial activation and should be performed with great caution by subjects with preexisting vascular diseases. Voluntary apnea might be used as a model to simulate changes in endothelial function caused by hypoxia in humans.
© 2017 Wiley Periodicals, Inc.

Entities:  

Keywords:  Apnea; Breath-hold; Circulating Microparticles; Vascular Function

Mesh:

Substances:

Year:  2017        PMID: 28464406      PMCID: PMC6490346          DOI: 10.1002/clc.22720

Source DB:  PubMed          Journal:  Clin Cardiol        ISSN: 0160-9289            Impact factor:   2.882


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