One Week Diving on Pure Oxygen: Vascular Function is Altered in Similar Fashion to Air Diving in Short Term Analyses yet a Unique Sustained Hyperemia Results from Hyperbaric Hyperoxia and Subsequent Intense Aerobic Exercise
Authors: Campbell James , Bergeron Elizabeth , Florian John 
Published: June 2021

Previous investigations in our laboratory reported altered vascular function after repeated dives with divers breathing AIR at 1.35 atmospheres absolute (ATA). Diving on pure oxygen (O2) vs. AIR affords the benefit of elimination of decompression pathophysiology upon assent, yet it may also promote deleterious pneumotoxic and neurotoxic effects due to the increasing hyperoxic dose delivered. Therefore, we investigated vascular function in healthy male subjects aged 31.3±1.8 years (mean±SEM) who dove for 6 hours at 1.35 atmospheres absolute of pure oxygen for 5 consecutive days. Findings were compared to previous air‐diving results (groups: O2, n=13; AIR, n=15)for measures of endothelial function via reactive hyperemia index (RHI), peripheral artery tone (augmentation index, AI), corrected AI per heart rate at 75 (AI_75), blood pressure (BP), heart rate (HR), and plasma volume (PV), all measured during supine rest. Results of SAS Procedure Mixed analyses (variables:before/after dive, dive day, and O2 vs air) indicate that pure oxygen diving is not significantly different from air diving (previous data collected) for the dependent variables RHI (p=0.51), HR (p=0.53), AI (p=0.55), AI_75 (p=0.31), and dPV (p=0.48). However, we re‐examined the manufacturer's suggested methods (Itamar Peripheral Arterial Tone technology) and found that baseline measurements of RHI data, signal amplitude before occlusion for each individual test, increased significantly in the O2 group when comparing dive day 1 pre to 24 hour follow‐up after the 5th day (460±92 to 1070±175 amplitude units; p<0.0001), whereas the air group had no such significant difference (505±105 to 653±83 au; p=0.211). The uniquely different event that occurred on every 5th day post‐dive in our protocol, versus days 1 through 4, was an 85% VO2 maximum run to exhaustion that perhaps promoted the sustained hyperemia when measured over 12 hours later in the O2 group. Closer analysis of before and after diving with baseline RHI data also revealed a strong pre/post factor (p<0.0001). Although there was no effect of gas (p=0.226), continuing this line of analysis (pre/post factor) in combination with the gas factor, the air group showed many significant hypoperfusion events pre vs post per dive day whereas O2 showed little significant hypoperfusion under the same circumstances (day 1 through 4, pre‐dive vs post‐dive, AIR: 504.8±104.6 vs 287.5±87.6 au; p=0.034, 584.9±98.3 vs 326.2±64.3 au; p=0.023, 526.0±89.3 vs 295.2±66.6 au; p=0.023, and 560.1±104.0 vs 347.2±106.3 au; p=0.30; and O2: 459.8±91.7 vs 297.2±89.3 au; p=0.15, 424.1±86.1 vs 294.7±84.1 au; p=0.25, 760.4±160.7 vs 286.8±58.3 au; p<0.0001, and 656.4±146.9 vs 437.1±94.1 au; p=0.068 respectively). These findings of short term decreases in blood flow following diving are supported by the literature for both loss of blood plasma during a dive and for the effects of hyperoxia. Most interestingly, our findings support claims of a previously unreported physiological phenomenon of a late‐phase hyperemia (24 hours post‐exposure or treatment) as a result of the diving environment of hyperbaric hyperoxia and subsequent intense aerobic exercise.

Support or Funding Information

Grant Funding: Office of Naval Research (ONR) Award Number N000141612112 and NAVSEA DSBDP N0002416WX02277.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.