See, I argue in my blog post linked above that this point is separate from their experimental study. In the theoretical part they compare profiles to a model. And we don't know how much that model corresponds to the reality of bubble formation in tissue. It's not a conclusion from their experiments at all.
My point again in terms of applicability and practicality to take from the NEDU Study is: you have to determine how much deco stress your Slow Tissues are willing to take if you want to do multiple decompression dives per day consecutively for a week or more, as in Expedition Technical Diving,
for whatever particular deco model algorithm you decide to use. If you're feeling very tired by the third consecutive day with a few latent indistinct musculoskeletal "transitory aches & pains" in your limbs/joints, then you have sub-clinical DCS -you're not effectively doing enough shallow stop O2 decompression time to washout out residual inert gas in the venous blood & slow tissues. (Take a day off to further reduce deco stress, and try diving again the day after).
The real essence of the NEDU Study and the vital parameters to consider are the bottom time and depth of fast & slow tissues' on-gassing exposure, and effective final decompression relief of surfacing Slow Tissue supersaturation to prevent pathological DCS bubble formation. The Fast Tissues are a lot more robust & tolerant than we once thought (because of their greater blood vessel vasculature & perfusion?), and therefore prescribed deep stops to protect them from inert gas supersaturation are not as critical as preventing further Slow Tissues on-gassing and later supersaturation upon surfacing.
Some more Simon Mitchell snippets (sifting through the Deep Stops Increases DCS thread again):
...I am saying (based largely on the results of the NEDU study) that transient high / peak supersaturation in
fast tissues does not seem to matter as much as we thought it might, and therefore that protecting fast tissues from supersaturation early in the ascent by using deep stops does not seem as effective as assumed by bubble models. This is especially so when it comes at the cost of increased supersaturation (both in terms of peak levels and
duration) in slower tissues later in the ascent. The NEDU study is telling us that this is where the problems seem to come from.
@Kevrumbo asks:
. . .
Explain from a physiological basis why allowing supersaturation of Fast Tissues in this instance is less risky to those tissues and results in a lower overall incidence of DCS in the shallow stops trials of the NEDU Study. . . ?
Hello Kev,
The bubble models and the deep stop approach were originally promoted on the basis that they were more successful at controlling bubble formation. The attempts to evaluate this notion in decompression dives in humans that I am aware of have shown that gas content models (or decompression procedures that have backed off deep stops to some extent) actually produce less bubbles when measured after surfacing. Neal Pollock presented some fascinating work they have been doing at the inner space event at a NOAA / AAUS rebreather diving forum I attended last week. Hopefully this will find its way into the literature at some point soon. In any event, the more we investigate it, the more the "control bubbles by deep stopping" concept appears to need reconsideration. What this is suggesting is that the bubbles are coming from the slower tissues that absorb more inert gas during the deep stops. It also implies that the faster tissues that deep stops attempt to protect from supersaturation are less prone to bubble formation when they become supersaturated.
You are seeking a physiological explanation for this, and while I can't be definitive, I would suggest that it makes sense that a tissue washing inert gas out quickly might be less prone to bubble formation and growth than a tissue with slower inert gas kinetics where the supersaturation persists for longer (there's that time integral again).
Simon M
Deep Stops Increases DCS