No... your version of ISS and the VPM formula are not related..... your version of ISS is one giant number .... goes against the rules and concepts of parallel mono-exponential models, duplicates data, has no concept of relative stress, un-calibrated, not verified.
I'll address this first, because it becomes relevant below. As I pointed out, it is not "my" concept; it is a very simple construct employed by the world's leading decompression modelling team to interpret the NEDU study, and it is at the core of VPM and several US Navy algorithms. There is only one "version"; it is a simple integral of supersaturation and time, and it is obvious to anyone reading this thread that time matters. It takes time for bubbles to form, so after a dive if you are supersaturated for 1 hour, that is way worse than one minute.
You have railed so strongly against this very simple fact because the integral of supersaturation and time is a metric that exposes the flaws of excessive deep stopping more clearly than any other. As for "going against the rules of mono-exponential models", this is just nonsense as Dr Doolette has explained to you before. Compartments are just mathematical constructs, not the reality of physiology, and it is perfectly valid (indeed necessary) to sum supersaturation across compartments in order to appreciate decompression status. Though it will not (unfortunately) be obvious to many readers here, this "going against the rules" notion is as stark (and scary) an illustration of your lack of understanding of decompression physiology as your recent claim that exercise and tissue perfusion does not affect decompression.
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On to the issues of this thread:
I don't have any information on O2 bio-markers causes and bio-physics interactions.... not my job.
That is not a very solid platform for opening this thread with a post that concluded:
"The elevated ppO2 extra time at 21 and 18m, causes extra off gassing and lowering of stress mid dive, thanks to higher ppO2 pressures, but it comes at the cost of elevated inflammatory markers".
In drawing this conclusion, you completely failed to explain how an air dive with low oxygen exposure but moderate decompression stress produced the same pattern of inflammatory activation as the UTD-RD profile. This observation was cited by the authors in their explanation of why they did not believe your version of events, but you simply ignored it. If you are going to analyse a scientific paper and publicly contest the conclusions of the authors, it is extremely dishonest to just ignore cogent arguments made in their published manuscript against your position.
You have repeatedly ignored my challenges to explain why you interpreted the data in a scientific paper differently to the authors, and "
I don't have any information, not my job" is the best answer you can come up with.
- For the bio-marker changes, you cannot demonstrate or show any relevance to supersaturation whatsoever?
- No math or graph to show whatsoever.
The following figure kindly provided by UWSojourner shows a comparison of integral supersaturation between the two tested profiles. There are two other profiles in the diagram, which we will discuss later, but for now just focus on the UTD-RD profile and the GF 30/85 profile. In the little boxes at the top of each bar RT = run time in minutes, and the numbers represent the integral supersaturation in millibar-minutes associated with that profile.
The first thing to note is that Ross's claim that
"the UTD-RD plan has less gas pressure (supersaturation) stress levels over the whole dive" is wrong (or misleading at the very least). The surface supersaturation (when bubbles are forming) in the UTD-RD profile is about 10% higher. This seems a subtle difference, but it is in the right direction for explaining the result. A similar comparison in the NEDU study showed about an 18% difference between the two profiles, and that was sufficient to produce higher bubble counts and a significant difference in DCS rates. 10% is a smaller difference and it is not surprising that we consequently see a less dramatic result. But remember, these supersaturation calculations are just numbers, not physiology. The true differences could be more (or less) but with the comments about oxygen made previously in mind, decompression stress remains the most plausible explanation.
Now look at the other two bars (the VPM 6.2 and GF 50/54 ones). Those show the supersaturation stress if you use VPM on high enough conservatism or a GF profile with parameters chosen to produce the
same decompression time as the UTD-RD. Dan-P, you might want to pay close attention to this.
We have always said that having two approaches with different total decompression times was not the best design for a study attempting to see whether distribution of stops shallow or deep makes a difference. As a corollary, we have also said that 30/85 was not the optimal comparator for UTD-RD in this study (mainly be cause it over-emphasises deep stops too). The diagram provides a stark demonstration of what happens if you choose decompression profiles
of the same length but with less emphasis on deep stops. Even VPM does substantially better, though Ross cannot claim any victory here because he has opined (incorrectly I might add) in the past that VPM used on high conservatism (eg VPM-B 6.2 as illustrated here) is outside the model parameters. But look what happens if you choose a GF decompression designed to be the same length as the UTD-RD profile. There is a dramatic reduction in decompression stress.
I would just like to thank UWSojourner for going to the trouble of producing this figure (and others which I have not used here).
Simon M