cwb once bubbled...
Let me start by saying "Thanks for your detailed comments".
You're welcome. I hope my replies are not confusing. Its not easy to accurately represent the physiology without jargon.
It looks like there were studies across wide ppO2 ranges. While the document here doesn't contain the abstract, I still found it interesting. Extension of O2 tolerance by Intermittent Exposure
This paper and other excellent links mentioned below, continue to build on work Lambertsen summarized in 1988. Where provided, consider the reference section of papers in your links. An interested reader may buy the 4th edition [ to save money] or for $150 the 2003 5th ed. of Bennett & Elliott's "Physiology and Medicine of Diving" to provide a wider, if not thorough, perspective than just isolated papers.
Remember, the context of Irvine's dives aren't those with "simple" 30 minutes bottom time. Rather, on his record-setting push he had 420 minutes of BT @ 300ft and a 7 hour deco schedule. 150 minutes of the deco is done on 100% O2 @ 30ft (in a trough).
Maximum Deco
Worse case OTU in 'maximum deco' is ~ 1,300 units, about 2 recompression chamber rides. This results at worse, 10% reduction in VC [assuming no benefit from normoxic breaks], at best it was 1-2%. An unpleasant, but non-lethal exposure. Without physiologic studies done on Irvine before or after "maximum deco," its hard to make claims on its safety beyond he survived. What damage to his lungs occured after the schedule? did lungs fully recover? By OTU analysis its likely he did well, but hard data would be better.
What maybe 'record setting' about "maximum deco" is the aggressiveness of the schedule and the extent of the cave penetration. It could be a superb data point for the validation of bubble decompression theory, but NOT of some superhuman resistance to 02 toxicity.
For reference, Irvine was using 12 minutes on 100% O2, and 6 minutes on backgas (11/65).
Perhaps some of the "recovery" ratios are derivations based upon studies regarding "Recovery" Equations.Pulmonary & CNS O2 Toxicity & Estimation Parameters
Arieli's paper is fine tuning an equation to fit curves for existing VC reduction and recovery data spanning ~ 30 years, and adds more data point with their own Israeli studies. The basic curves were established by Lambertsen, Clark and others, again summarized in the 1988 paper or any diving physiology text. Arieli measures recovery via vital capacity, which is just one measure of 02 pulmonary toxicity. The 2002 Arieli paper changed [I'm recalling from memory, so there may be errors here]:
dVC% = .0082 x hours^2 x [ppO2 in ATA] ^ 4.57
In 1994 [ see the references] his estimate was:
dVC% = .0115 x hours^1.85 x [pp02 in ATA] ^ 4.56
The recovery rate is not critical, since most recovery is in ~ 24 hours.
I think that Irvines' actual dive parameters bear out your references of "critical concern" regarding extended O2 exposures. 100% O2 @ 30ft has a PP of how much? ;-)
The "critical concern" I raise is not tolerating a pp02 of 1.9 at 30' but that Irvine teaches that the air breaks are part of the calculated 02 time. If a schedule states an 02 deco is 20 minutes and you take a 5 min backgas break, Irvine effective states you do 15 minutes of 02 and 5 minutes of backgas and that = 20 min of 02. In the 12min 02 and 6 min backgas break in 'maximum deco', the 30' stop is effectively reduced from 150min of 02 to only 75 minutes. This causes a large reduction in pp02 exposure. The explanation for how this might work is in my prior post.
It would seem to me that the discomfiture or burning sensation in the lungs is an indication that the lungs are already reacting to the prolonged high ppO2 event. While gas exchange may not be directly effected by VC (VC seems to be one of the most consistent measurable markers of O2 exposure insult), there is, however, tracking of negative effect on CO exchange after high ATA O2 exposures. It would seem inline that other pulmonary gas exchanges would be impaired as well. An earlier post indicated "no known experimental evidence" that gas exchange is effected. Perhaps this study touches on that.
Effects of Prolonged O2 Exposure
Pulmonary toxicity begins when exposure pp02 > 0.5 ATA. The rate of injury increases with increased pp02 and time on this pp02. Diving air or nitrox, this means 02 related injury begins once dives are beyond 46' [ diving per se causes a persistent reduction in VC over years, and this maybe one of its mechanisms.] So, even before deco, injury has begun. In reference to Mr. Irvine's dive of 420 minutes bottom time at pp02 1.1, there is certain to be marked injury, as the studies you linked show changes at pp02 of 1.0 and up.
DLCO is a sensitive marker for damage, and corroborated by the increase in (A-a)D02 which takes several days to normalize. Since lung injury was already initiated simply by diving past the critical depth, say 46', not to mention prolonged stay at depth, then the only thing gas breaks do is minimize further damage. If reduction in "efficiency" can be avoided by not having pulmonary injury, its too late, its already done.