Objectives: Repeated exposure to hyperbaric pressure and decompression during diving induces unique physiological challenges for the cardiovascular system. The vascular endothelium plays a critical role in maintaining vascular homeostasis through regulating vascular tone, nitric oxide (NO) bioavailability, inflammatory responses, and oxidative balance. Previous investigations have shown that acute hyperbaric exposure may impair endothelial function through oxidative stress, inflammatory activation, and intravascular bubble formation; however, the long-term effects of repeated diving exposure on endothelial health remain unclear. Therefore, this review was conducted to summarize current evidence regarding alterations in endothelial function following repeated hyperbaric exposure in divers and to describe the underlying molecular mechanisms involved in endothelial injury and vascular adaptation. This review aimed to evaluate the effects of repeated hyperbaric exposure on endothelial function in divers and to summarize the potential mechanisms associated with endothelial dysfunction and vascular adaptation.


Methods: A comprehensive literature search was performed in PubMed, ScienceDirect, and Scopus databases using combinations of relevant keywords, including "endothelial function," "diving," "hyperbaric exposure," "decompression," "oxidative stress," "endothelial microparticles (EMPs)," "nitric oxide (NO)," and "heat shock proteins (HSPs)." The review focused on human and animal studies that assessed objective markers of endothelial function following hyperbaric exposure or diving activities.


Results: Current evidence indicates that acute hyperbaric exposure and decompression are associated with increased circulating gas bubbles, oxidative stress, inflammatory activation, and transient endothelial dysfunction. Reduced flow-mediated dilation (FMD) and increased endothelial microparticles (EMPs) have been reported following deep and repetitive diving exposures. Experimental studies have demonstrated enhanced oxidative responses after simulated deep dives, including alterations in lipid peroxidation and antioxidant activity. However, repeated diving training may induce adaptive responses, including decreased bubble formation and improved tolerance to hyperbaric stress, without necessarily causing persistent endothelial impairment. These responses appear to involve regulation of NO bioavailability, heat shock protein (HSP) expression, oxidative pathways, and vascular protective mechanisms.


Conclusions: Repeated hyperbaric exposure induces a complex interaction between endothelial stress and physiological adaptation. Although acute diving-related stress may cause temporary endothelial dysfunction, long-term repetitive exposure may promote protective vascular adaptations. Further longitudinal investigations are required to determine the long-term cardiovascular consequences of these adaptations in professional divers.