NetDoc:
Why do deep stops work where slow ascents don't? Perhaps its a function of the half times. Blood and neural tissues have an incredibly SHORT halftime (about 5 minutes).
Good point, Pete. Thinking through what you wrote:
2/ If my N2 loading is such that I can go to half my max depth without incurring significant bubbling, then it is simple math to conclude that a slower ascent means I reach that deep stop depth with significantly less N2 loading (given that we are talking about fast tissues) than if we went up directly. So up until this point, a slow ascent is actually better.
So the interesting bit happens from the point of deep stop to the surface. A 5 min deep stop *may* result in the diver leaving D/2 (half his max depth) with less loading than a slow diver who keeps continuing upwards without stopping... but this is a funtion of how fast he came up in either case. Also, whether or not the controlling issue changes also plays a role.
Assuming that the controlling tissue doesnt change, a slow ascent should indeed work better. Taken to a hypothetical extreme, if there was a tissue with a superfast half-time, a slow ascent would result in the tissue pressure equalizing more or less in sync wih the divers ascent. Slow tissues are less likely to be affected. So, depending on the function, either there is an optimal range of controlling tissues where the above doesnt hold; or it doesnt hold at all; or the controlling tissue changes which puts the math far beyond my abilities.
Ok, not only did this NOT reach any conclusion, but I succeeded in confusing the hell out of myself as well. So that takes me to the next 2 points...
2/ Assuming it was simply a matter of half-times, even if slow ascents dont work as well as deep stops, they'd still work better than faster ascents + no deep stops. Which doesnt appear to be the case.
3/ A fundamental assumption in the article under discussion is that bubbles are a result of critical supersaturation. But critical supersaturation = DCS, and we are talking asymptomatic bubbles here, which occur even when critical supersaturation is not reached.
GIT, bless his sweet, stroke-loving self, had a different - and to my mind, a more logical explanation on deep stops help: his idea was that spending time at a give depth allows your blood to circulate through your lungs once, which gives your lungs a chance to control bubble build-up. This makes sense. I've used this when I've done nasty profiles, and it has been ok - I reckon atleast 2 or 3 times, it has saved me from getting bent.
Assuming bubble formation is a simple function of overall saturation (not *critical* supersaturation, where you exceed your tissue M-values), then the above findings would make sense: a slow ascent rate would actually increase overall N2 loading which would lead to greater bubbling; a slow ascent would also, by virtue of circulation, allow the body to control that bubbling. Too slow, and the increased N2 loading becomes dominant; too fast and inability to control the bubbling becomes important - so there is an "ideal" ascent rate, which would be somewhere between 5-15 m/min (18m/min -- too fast; 5m/min -- too slow). My guesstimate this would be somewhere in the 6-9 m/min.
I dont know where I am going with this... just thinking out "loud", I guess. Anyway, F1 is starting, time to pull out a beer and get comfy.
Vandit