CNS\O2 Toxicity and Exercise

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SkimFisher

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I'm taking my Nitrox (PADI) class next week and I've read the book and have some questions about CNS/O2 toxicity. The book says that "heavy exercise" can predispose a diver to CNS/O2 toxicity, but it doesn't really say how or why.

1.) What is considered "heavy exercise"? I'm not a triathlete, but I hit the gym 5 days a week and do a fair amount of running/swimming.

2.) What's a more in depth explanation of the relationship between the two? The book is pretty vague.

Thanks! :D
 
Here's an article that you may find helpful...

Tales from the Wet Side - Hedging the Bet Against CNS Oxygen Toxicity

While it relates more to DCI and post-dive exercise there's an excellent article "Juggling Physical Exercise and Diving" (Neal Pollock - Alert Diver) DAN Divers Alert Network : Juggling Physical Exercise and Diving

I asked DAN a similar question regarding what constitutes "heavy exercise" and the answer was not definitive but they did not have a problem with me running a 5K the day after doing 2 relatively shallow (40fsw) 45 minute dives on EAN32.
 
I asked DAN a similar question regarding what constitutes "heavy exercise" and the answer was not definitive but they did not have a problem with me running a 5K the day after doing 2 relatively shallow (40fsw) 45 minute dives on EAN32.

I sure hope not. I run 4 days a week. If had to not run for a day before and a day after diving then I'd never be able to manage it all. The only time I stop running for diving is on a dive holiday when I'm diving several times a day for a week.

Locally I never run for 6 hours after diving (or a day if I'm doing OW days with new divers :)) but I'll run just before and make sure my profiles are tame. The real message shouldn't be that running is bad, teh real message should be that pushing the NDL's if you run is bad.... Everything in moderation.

R..
 
Very informative. Thanks for the links. I wish PADI would have expounded on the subject. They make it sound in the book like you have to avoid the gym at all cost if you don't want to die. I've also talked to a few divers who believe just that.
 
I believe Dr. Deco had a post recently about research showing that pre-dive exercise is not as harmful as was once thought, although post-dive exertion is still contraindicated (something I think about each time I heave myself up some awful ladder to get back on the boat).

My suspicion is that the comment about heavy exercise predisposing to O2 toxicity is referring to exertion DURING the dive.
 
I believe Dr. Deco had a post recently about research showing that pre-dive exercise is not as harmful as was once thought, although post-dive exertion is still contraindicated (something I think about each time I heave myself up some awful ladder to get back on the boat).

My suspicion is that the comment about heavy exercise predisposing to O2 toxicity is referring to exertion DURING the dive.

I think Lynne pretty well hit the nail on the head. Somewhere in the dim recesses of my memory, I recall something from the WKPP stating that mild to moderate exercise 24 hours pre dive could actually be beneficial in off gassing.

Strenuous exercise immediately following a dive should be avoided. Spend a few minutes (3-5) on the surface before climbing aboard ladders, lugging gear, etc. if at all possible. I'd also avoid doing any type of workout for exercise for at least several hours post dive.

Heavy exercise during a dive can cause a buildup of CO2, which others have associated with increasing the effects of several problems.
 
The book says that "heavy exercise" can predispose a diver to CNS/O2 toxicity, but it doesn't really say how or why.
DCS and CNS/pulmonary O2 toxicity are completely different beasts. I think that some responses in this thread have focused more on the association between exercise and DCS.

To be honest, the mechanisms of CNS and pulmonary oxygen toxicity are still unknown. IMO, one of the most interesting hypothesized mechanisms is one which involves nitric oxide (NO) signaling. If you're up for the academic legwork, I'd suggest learning all you can about how NO works, what enzymes (nitric oxide synthase) produce it, where those enzymes are located, how expression of those enzymes changes with exercise, the effect of NO on neuronal functioning, and how NO affects other very important cellular processes (stem cell differentiation, cell death, etc.). The Wikipedia page on NO is a little thin, but it's probably worth a quick read anyway. A lot of interesting research on NO is going on right now. (Do a PubMed search if you don't believe me.) It's cutting edge stuff that goes way beyond what any scuba instructional agency would ever include in course materials. This shouldn't be too surprising since we still don't know enough to make informed recommendations on diving practices based on NO research. Give it a few years, though, and things will change. You'll see.

You asked about how exercise can be linked to CNS and pulmonary oxygen toxicity. Based on what I've read, here's how I would make the connection...

Many studies have shown that exercise can increase NO production in blood vessels. NO has the effect of relaxing endothelium (muscular lining of blood vessels). This is most likely how mediators of NO (nitroglycerin pills) function in the context of coronary artery disease. So it would seem that when it comes to cardiovascular health NO is a "good" thing. However, that's not a complete picture of how NO functions in the entire human body.

NO has very important functions in the CNS as well -- some good and some bad. Just as in peripheral blood vessels, NO causes vasodilation in CNS blood vessels. This has important physiological implications that I won't get into here. In addition, researchers have found that, in the brain, breakdown of NO by the enzyme superoxide dismutase can produce a radical oxygen species (ROS) known as peroxynitrite, which is actually toxic to neurons. There is a positive correlation between levels of brain peroxynitrite and seizures associated with hyperbaric oxygen treatment.

Prolonged NO production in the lungs results in diffuse tissue damage (pervasive inflammation) due to breakdown of the "alveolar-capillary barrier," possibly related to the generation of ROS. This eventually causes fluid in the lungs (pulmonary edema) and consequently impairs gas exchange. It should be noted that under normobaric conditions, NO effects predominate in the lungs, whereas under hyperbaric conditions, CNS NO effects are seen.

Given all this mechanistic info regarding how CNS and pulmonary oxygen toxicity proceeds, it begs the question how exercise can impact any of these processes. I speculate that the key here is the generation of ROS. With exercise, more oxygen flux occurs on a metabolic level and consequently more ROS are produced. Over time and with increased training, the body can upregulate enzymes which help keep the ROS safely in check. There are likely differential limits on the extent of upregulation of such enzymes (blood vessels vs. lung tissue vs. brain tissue). If those "good" enzymes are overwhelmed, it's not difficult to imagine the ROS running amok. This could explain the complicated relationship between the timing/extent of exercise training and CNS/pulmonary oxygen toxicity. Put simply...Too much exercise in the short-term can be bad, but exercise training over the long-haul can be good.

Here's a link to a nice article on the relationship between NO, exercise, and cardiovascular disease.

Allen et al. wrote a very nice mini-review of how NO is implicated in oxygen toxicity. I've linked directly to a PDF version of this article, which unfortunately lacks the figures. The text alone, however, contains a lot of good info.

As with most things in science, this post probably raises more questions than it answers. At the very least, I hope you find it entertaining. :D
 
I assumed they were referring to the possibility of increased CO2 production, which could increase the risk of a CNS hit.
 
I assumed they were referring to the possibility of increased CO2 production, which could increase the risk of a CNS hit.
Increased CO2 production is an expected byproduct of an increased metabolic rate during exercise. It's entirely possible that increased levels of CO2 are coincident with increased probability of a CNS hit, yet have nothing at all to do with causation of that hit. The literature seems to point to oxidative stress as the true culprit.
 

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