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Updated: Jul 15, 2026

Training Rats to Voluntarily Dive Underwater: Investigations of the Mammalian Diving Response
Published on: November 12, 2014
Prophylactic statins as a possible method to decrease bubble formation in diving
Christopher A Duplessis1, David Fothergill, Derek Schwaller
1Naval Submarine Medical Research Laboratory, Groton, CT 06349-5900, USA.
Introduction:
Nitric oxide (NO) may decrease bubble formation in diving. Statin medications are attractive potential options to increase NO. Statins exhibit a proven safety profile, and possess a myriad of pleiotropic properties improving vascular endothelial function. Additionally, statin-mediated lipid reduction may reduce bubble generation via alterations in plasma surface tension. We investigated the efficacy of atorvastatin as a pharmacological intervention to reduce the risk of bubble formation after diving, a surrogate for decompression sickness (DCS).
Methods:
There were 16 trained military divers who completed a provacative hyperbaric chamber dive protocol after taking either 80-mg of atorvastatin or placebo for 4 d. Subjects completed the alternate medication regimen no sooner than 2 wk. After each dive, subjects were subjected to precordial trans-thoracic echocardiographic exams via standardized protocols. Bubbles were graded via a non-parametric, ordinal grading system and statistically analyzed via Wilcoxon signed-rank tests.
Results:
We found no within subject differences for the maximum bubble grade scores (z = 0.00, p = 1.00, n=16). Low-density lipoprotein (LDL), and total cholesterol (TC) levels decreased significantly (107.6 +/- 26.2 to 79.3 +/- 21.9 mg x dl(-1) and 175 +/- 20.9 to 147 +/- 22.4 mg x dl(-1), respectively) 1-2 wk post statin administration. Age, bioelectrical impedance (BEI), TC, LDL, potassium, and calcium demonstrated positive correlations to placebo bubble grades.
Discussion:
Prophylactic 80-mg atorvastatin administration for 4 d failed to reduce the number of intravascular bubbles observed following a 60-ft, 80-min dry chamber dive despite significant acute reductions in lipid levels. Several hypotheses may explain why statins failed to decrease bubble volume: (1) differential influence of statins on the venous vs. arterial vasculature; (2) failure to elicit an improvement in endothelial function and, therefore, the hypothesized endothelial conditioning in younger patients possessing normal baseline; and (3) the ordinal grading system encompassing a substantial variation in bubble volume (bubbles Scm(-2)).
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