Breath-hold safety divers exhibit pulmonary stress but not decompression strain

Breath-hold (BH) diving induces hypoxia-reoxygenation cycles and hydrostatic stress. Although decompression illness is traditionally associated with compressed-gas diving, neurological events have been reported after repetitive BH dives. The decompression stress, pulmonary effects, and inflammatory responses in BH safety divers (BHSDs) remain unclear.

Fourteen BHSDs (11 males, 3 females; 35±6 years) performed 174 dives (mean depth 18.8 ± 12.3m). Vascular gas emboli (VGE) were assessed by echocardiography, pulmonary B-lines by lung ultrasound, salivary IL-6 and TNF-α by ELISA, and hydration by bioimpedance spectroscopy. Measurements were collected pre- and post-dive over two competition days and at 24-h and 48-h recovery. Linear and generalized linear mixed-effects models with Holm-corrected contrasts were used.

No VGE were detected. Pulmonary B-lines increased significantly post-dive on Day 1 (rate ratio = 1.60; p = 0.037) and Day 2 (RR = 2.30; p = 0.0008), returning below baseline at 48-h recovery (RR = 0.25; p = 0.0003). Salivary IL-6 peaked at 24-h recovery (+6.52pg.mL^-1; p < 0.0001), remaining elevated at 48h (p < 0.0001). TNF-α rose from Day 2, reaching 25.16pg.mL⁻¹ at 48-h recovery (p < 0.0001) with no return toward baseline. Hydration remained stable (p = 0.69).

A moderate inflammatory signal was observed up to two days following BH sessions. The BHSDs did not demonstrate any VGE but rather exhibited pulmonary B-lines consistent with the observed salivary inflammatory markers. Despite the absence of documented incidents or accidents, it is strongly recommended that BHSDs allocate additional days for recovery.