Depending on what theories you identify with, there's a suggestion that post-dive fatigue (
decompression stress /
sub-
clinical DCS) results from complement system (
immune) activation to micro-emboli (
micro-
bubbles) perfusion in the body.
Medicine has proven that micro-emboli are indeed recognized as antigens and activate the complement system.
A number of aspects from immune response can cause fatigue or malaise.. such as the release of serotonin or increased hemoconcentration....and/or if an immune-response is limited to the brain/CNS compartment (
believed to be separated from the rest of the body - see: Does the brain possess an independent immune compartment?).
I won't even mention issues of protein clotting and brain lesions..
(
see my article Subclinical DCS, Decompression Stress and Post-Dive Fatigue for full details)
So, if we're to believe that micro-emboli are the cause of
undeserved post-dive fatigue, then we have to look at
all the aspects that promote micro-emboli creation and longevity.
GF settings play a role in managing the micro-bubble process:
- - - GF-Lo (
is suggested to) control initial bubble formation and rapid resolution. Whereby:
Pamb + Bubble Surface Tension > Pinternal
causes bubbles to collapse.
--- GF-Hi (i
s suggested to) resolve remaining bubbles, especially if high differential is created across the bubble surface using richer O2 mixes, and is time dependant...as the process of bubble collapse is now diffusion based.
Ascent rates are also important. Creating a rapid increase in P
amb is hypothesised to resolve bubbles at an early stage. Inert gas tissue pressure elevates quicker than inert gas can diffuse into a bubble. This crushes the bubble.
Too slow ascents from bottom depth (
to first stop) may exacerbate bubble longevity. A slower rise in P
amb could allow inert gas to dissolve into bubbles at a rate equal, or closer to, the elevation of inert gas tissue pressure. Thus, bubbles would collapse slower, or not at all.
Many novice technical divers do struggle to maintain precise 9-10m per minute ascents...
So... it's a case of 'prevention' or quick-resolution (
deep factors) versus 'cure' or slow-resolution (
shallow factors).
When it comes to the scale of complement (
immune) system reaction, I'd suggest that the degree of response would be dictated by the number of bubbles PLUS the amount of time they persist in the body.
It could be that delaying the resolution of micro-emboli until the shallow deco phase is not timely enough to prevent complement system activation.
Once an inmuno-response is activated, and if allowed to become severe enough, the diver could still experience fatigue/malaise even after very effective shallow decompression.
If not resolved satisfactorily on the deepest stops, the time of micro-emboli persistence, and consequent severity of complement system activation, will be greatly influenced by the intermediate deco stop schedule.
Once reaching O2 deco (
assuming O2 is utilised), we might assume that more effective micro-emboli resolution starts to occur due to the oxygen window effect.
However, by that time, the damage may already be done. You could potentially surface 'clean', but already be suffering blood-chemistry and/or CNS compartment effects from the intermediate-late stage processes of an immuno-reaction that was triggered in the ascent phase of the dive.
It should also be noted that there is a theory that frequent exposure to micro-emboli initiated complement system activation creates a desensitising effect.
It's possible that if someone dives very frequently then the immuno-reaction to micro-emboli becomes less severe, or even ceases altogether (see
Diver0001's comment on pg1).
Resolving bubbles in the shallow deco phase may not be entirely successful in preventing complement system activation. Allowing micro-emboli to resolve naturally post-dive is, of course, even less successful.
VPM-B is a dual-phase model. It calculates deeper deco based specifically on mathematics that model predicted micro-emboli growth/shrinkage. Thus it gives deeper stops based on a 'sweet spot' where bubble surface tension causes shrinkage.
At the same time, VPM-B functions as a content model (dissolved gas) and accounts for slower tissue saturation - calculating subsequent deco stops accordingly.
Buhlmann ZH-L16 is a
pure content model. However, the addition of GF allows us to replicate the deeper profiles (via GF-Lo) we'd recognise from VPM-B or other bubble models.
At the same time, we can dictate (via GF-Hi) the overall deco time - primarily allocated to shallower stops.
When it comes to GF selection, I think there is NO ideal or singular perfect universal setting.
For a start, it is dependent on the dive depth. A perceived beneficial GF-Lo in the 40-60m range is unlikely to have the same benefits in the 60-90m range etc etc.
We also have to consider GF-Lo in relation to breathing gas at first stop depth. This accounts for the potential to create a better diffusion gradient through has switches.
Of course, there also has to be some consideration for the need to prevent excessive overall deco by removing helium and/or nitrogen as early as possible. Bottom gas deco stops are inherently inefficient.
We have a situation where GF optimisation (
determined by post-dive observation of vitality/fatigue) can/should vary on each dive, according to the dive parameters, for each diver... and can vary even for the same diver dependant on their recent diving habits.
The only real solution, as I see it, is for a slower process of trial and error experimentation; monitoring post-dive fatigue/vitality in relation to a myriad of possible influencing factors.
Sometimes, there's just no substitute for experience