Sustained apnea induces endothelial activation

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.

Vascular dysfunction following breath-hold diving

“…In both diving protocols, the alterations of endothelial reactivity were coupled by increased levels of EMPs (CD31+/41-), markers of endothelial apoptosis. Sustained and intermittent hypoxia (Eichhorn et al 2017;Lichtenauer et al 2015) could lead to increased rates of cellular stress. An increase in CD31+/annexin+ EMPs was observed in 14 healthy volunteers exposed to normobaric hypoxia in a chamber with oxygen saturation (SaO 2 ) reduced to 73% ± 10% (Lichtenauer et al 2015).…”

“…In a recent study, sustained static dry apnea induced endothelial activation with an increase in CD144 endothelial microparticles (EMPs) (Eichhorn et al 2017). This endothelial dysfunction was mainly caused by hypoxia and hypercapnia.…”

MicroRNA expression profile during different conditions of hypoxia

“…MiRNA-21 and miRNA-26a are both released from endothelial cells [ 21 , 22 ]. A previous study showed that both miRNA-21 and -26a are expressed after apnea process and speculated that hypoxia induces endothelial cell activation [ 23 , 24 ]. Our data are in line with these results even if demonstrated that while miR-26a level is higher in chronic hypoxia, miR-21 is more expressed in intermittent hypoxia.…”

Endothelial microvesicles in hypoxic hypoxia diseases

“…found that a time‐dependent increase of circulating EMVs which carry different miRNAs in apnoea and circulating miR‐126 levels were elevated at all time‐points after a single voluntary maximal apnoea, 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 . Serban et al.…”