Physiology of deep closed circuit rebreather mixed gas diving: vascular gas emboli and biological changes during a week-long liveaboard safari

Costantino Balestra; Clément Lévêque; Simona Mrakic-Sposta; Alessandra Vezzoli; Pierre Wauthy; Peter Germonpré; Frauke Tillmans; François Guerrero; Pierre Lafère

doi:10.3389/fphys.2024.1395846

Physiology of deep closed circuit rebreather mixed gas diving: vascular gas emboli and biological changes during a week-long liveaboard safari

Front Physiol. 2024 Apr 10:15:1395846. doi: 10.3389/fphys.2024.1395846. eCollection 2024.

Authors

Costantino Balestra^#^{1

2

3}, Clément Lévêque¹, Simona Mrakic-Sposta⁴, Alessandra Vezzoli⁴, Pierre Wauthy⁵, Peter Germonpré^{1

3

6}, Frauke Tillmans⁷, François Guerrero⁸, Pierre Lafère^#^{1

3

8}

Affiliations

¹ Environmental, Occupational, Aging (Integrative) Physiology Laboratory, Haute Ecole Bruxelles-Brabant (HE2B), Brussels, Belgium.
² Physical Activity Teaching Unit, Motor Sciences Department, Université Libre de Bruxelles (ULB), Brussels, Belgium.
³ DAN Europe Research Division (Roseto-Brussels), Brussels, Belgium.
⁴ Institute of Clinical Physiology, National Research Council (CNR), Milan, Italy.
⁵ Department of Cardiac Surgery, CHU Brugmann, Université Libre de Bruxelles (ULB), Brussels, Belgium.
⁶ Centre for Hyperbaric Oxygen Therapy, Queen Astrid Military Hospital, Brussels, Belgium.
⁷ Divers Alert Network, Durham, NC, United States.
⁸ Laboratoire ORPHY EA 4324, University Brest, Brest, France.

^# Contributed equally.

Abstract

Introduction: Diving decompression theory hypothesizes inflammatory processes as a source of micronuclei which could increase related risks. Therefore, we tested 10 healthy, male divers. They performed 6-8 dives with a maximum of two dives per day at depths ranging from 21 to 122 msw with CCR mixed gas diving. Methods: Post-dive VGE were counted by echocardiography. Saliva and urine samples were taken before and after each dive to evaluate inflammation: ROS production, lipid peroxidation (8-iso-PGF2), DNA damage (8-OH-dG), cytokines (TNF-α, IL-6, and neopterin). Results: VGE exhibits a progressive reduction followed by an increase (p < 0.0001) which parallels inflammation responses. Indeed, ROS, 8-iso-PGF2, IL-6 and neopterin increases from 0.19 ± 0.02 to 1.13 ± 0.09 μmol.min^-1 (p < 0.001); 199.8 ± 55.9 to 632.7 ± 73.3 ng.mg^-1 creatinine (p < 0.0001); 2.35 ± 0.54 to 19.5 ± 2.96 pg.mL^-1 (p < 0.001); and 93.7 ± 11.2 to 299 ± 25.9 μmol·mol^-1 creatinine (p = 0.005), respectively. The variation after each dive was held constant around 158.3% ± 6.9% (p = 0.021); 151.4% ± 5.7% (p < 0.0001); 176.3% ± 11.9% (p < 0.0001); and 160.1% ± 5.6% (p < 0.001), respectively. Discussion: When oxy-inflammation reaches a certain level, it exceeds hormetic coping mechanisms allowing second-generation micronuclei substantiated by an increase of VGE after an initial continuous decrease consistent with a depletion of "first generation" pre-existing micronuclei.

Keywords: acute phase; decompression physiology; hormesis; human; oxyinflammation; reactive oxygen species (ROS); vascular gas emboli (VGE).

Grants and funding

The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This research received financial support from DAN Europe and DAN USA (grant N° Apocalyptrip 2023 DAN-ISEK-2023-CBal). The sponsors had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and the decision to submit the manuscript for publication.