Past Smoker

[Hydro-Mike]

Hello I'm new here and thought of a question that has been bugging me. I'm 44 and quit smoking about 6 years ago getting back into shape for the last 2. The question is has anyone heard of any problems about a history of smoking and taking up free diving. I'll quit sniveling/ just curious is all. Thanks

 

[devondave]

Hello Mike.
Welcome to db.
I have often wondered about the same thing.
As an ex-early twenties to thirties smoker (stupid,stupid,) sometimes I can't help thinking what might have been if I'd never started.
On the other hand there is not much that can be done about it now, so it's probably best to just carry on and do the best you can.

 

[Bill]

Hi Hydro, ditto on what Dave just said. Forty years ago, I moved to S. California, gave up smoking and started diving 1-2 times a week. If only I had started 20 years earlier, never smoked and took a trolley car to Palos Verdes to dive while I was still in grade school, like some of the super divers. At the rate I'm going, I may never be able to reach 80 meters. Maybe we should concentrate more on enjoying the journey.

 

[chrismar]

If it really has a permanent negative effect, I'd hate to think what some of the ex-smokers I know would be like if they hadn't. Suffice to say, there are world champions and world record holders that are ex-smokers, so you should be fine. Current smokers though, not so much.

 

[Mullins]

It's not like you need fast gas exchange for freediving anyway. There's no hurry!

 

[trux]

Fast indeed not, but efficient yes. Not during the entire apnea, but when in the final phase of your breath-hold, the less functional alveoli you have, the sooner you'll be critically hypoxic.

 

[Mullins]

Bit of elaboration here would be good Trux. Where would the inefficiency lie, i.e. where would O2 be lost in the process of extracting it from the lungs and delivering it to the brain? Heart having to beat harder due to high resistance in plaque-ridden arteries? Heart working needlessly to pump blood through non-functional alveoli?

Since the example you're giving presumably involves a subject reaching critical hypoxia while alveolar ppO2 remains relatively high, it sounds more like you are talking about speed/effectiveness of gas exchange rather than efficiency...?

 

[trux]

What I meant was, that during the major part of apnea you are perfectly right, because the speed, efficiency or effectiveness of lungs (or whatever you want to call it) is not at all critical, since the consumption of the body is minimal, hence even quite damaged lungs will likely work sufficiently to bring sufficient level of O2 to the brain. But when you approach the critical levels of O2 in the blood, efficient gas exchange begins to be critical. The gas exchange is slowed down due to low alveolar PO2 and due to high blood acidity. So on my mind it is logical that in this moment the bigger functional (undamaged) alveolar surface you have, the longer you can prolong the critical phase. Possibly the difference won't be any serious (assuming moderate alveolar damage), but still you will squeeze the last low O2 easier and saturate the hemoglobin better with large alveolar surface than with a small one.

 

[Mullins]

I thought there was very little gas exchange taking place towards the end of an apnea anyway, due to increased blood acidity. In the last few seconds there may be almost no gas exchange at all - instead you're just desaturating the blood until you BO. So while it's possible, I'm not convinced that having slow (ineffective) gas exchange would be a disadvantage in freediving.

I think it's pretty important to be careful about how the terms efficiency and effectiveness are used with regards to freediving. I often see people talking about how cardiovascular 'efficiency' aids freediving, for example, when most of what they're talking about is really effectiveness i.e. a high VO2 max - the ability to consume heaps of oxygen. Same goes for some of the sports physiology articles I've read - they talk about increasing cardiovascular efficiency in test subjects, then it turns out that O2 consumption goes up proportionately with power output, meaning that from our perspective there has been no increase in efficiency. Few studies would be interested in O2 efficiency specifically, because for them it's an inexhaustible resource.

Bit off-topic....

 

[KatFish]

Being an ex-smoker is no excuse. Kiwis Guy Brew (9 min + STA) and Kerian Hibbs (200 + DYN) are ex-smokers doing perfectly well in the sport.

 

[trux]

I thought there was very little gas exchange taking place towards the end of an apnea anyway, due to increased blood acidity...

Exactly. And that's the problem. As long as the gas exchange works fully, you do not need any healthy (efficient) alveoli. But in the moment the gas exchange drops due to the lower PAO2 and pH, the efficiency of the alveoli is crucial. Tobacco smoking is associated with a decrease in PaO2 and an increase in PA-aO2 gradient. In other words with the same PAO2 (partial alveolar pressure) you can only achieve smaller PaO2 (partial arterial pressure). Which clearly means you starve the brain of oxygen quicker than with healthy and efficient lungs. You simply do not use as much of oxygen in your lungs as you would with better working gas exchange through healthy lung tissue.

In the same time I agree that it's only one of many factors, and it does not prevent an ex-smoker becoming an excellent freediver. Smokers are on the other hand usually also more tolerant against hypercapnia, and possibly against hypoxia too, and there are other factors influencing the performance. So I agree with Kathryn that being an ex-smoker is no excuse

 

[Mullins]

But if gas exchange is minimal towards the end of apnea anyway and contributing little (or perhaps nothing) to the aterial saturation, reducing the rate further might not make much (or any) difference? I do see your point, but even if gas exchange makes a significant contribution towards the end of a breathhold I think the performance cost of smoking would depend heavily on how time-critical that exchange is.

ps you've, umm, used that 'efficiency' word again... Still not sure that smoking causes inefficiency with regards to O2 delivery. Sounds trivial, but I think the distinction is important.

 

[trux]

Dave, I do not understand why you can't see it. So let me show it on a concrete example. The following numbers are approximate, and may differ both at individuals as well as in different situations.

PAO2 = partial alveolar pressure of oxygen
PaO2 = partial arterial pressure of oxygen
PA-aO2 = difference between alveolar and arterial partial O2 pressure

Lets say that the hypoxic level of PaO2 resulting in a blackout is 25 mmHg at both subjects (perfectly healthy person and an ex-smoker with lung damage). We suppose same conditions and also same blood pH at both subjects in the final phase.

Lets assume the following:
- both subjects start with 100 mmHg PAO2 in lungs.
- the healthy freediver has PA-aO2 of 5 mmHg
- ex-smoker has PA-aO2 of 10 mmHg

It means the healthy subject will black out at the PAO2 of 25 + 5 = 30 mmHg
Ex-smoker will black out at the PAO2 of 25 + 10 = 35 mmHg

This means he does not use 5 mmHg of PAO2 of total 100 mm, hence 5%, that the healthy subject can use. Will the healthy subject really hold 5%longer? That's an entirely different question, but it is clear that the smoker has a disadvantage due to his less efficient lungs and gas exchange.

I am using the word efficient because it is exactly the word that needs to be used here. Efficiency is "the ratio of the output to the input of any system" (from Princeton University), and that describes exactly what we are speaking here about.

 

[Mullins]

The assumption you make in your example is that there is zero delay between pAO2 hitting its minimum value in the healthy subject, and his/her paO2 reaching 25mmHg. I think there may be a delay, due to the increasing strength of the Bohr effect. Sound feasible? I know that in this case there would still be limited time for gas exchange before reduction in pH curtailed it, as BO does in your example. But if the three-way system of pA02, pa02 and pH held arterial O2 demand stable for even a short period of time, the slower-exchange system could come very close to catching up, to the point where the difference is negligible.

Regarding efficiency - the ratio of (oxygen) output to input is the same in a lung with slow gas exchange, since no O2 is lost from the system. The variable here is rate of delivery, hence my use of the word 'effectiveness'. This is a known property of the lungs that you start from, whereas the 'efficiency' you cite is something you've arrived at after making assumptions about the effects this property has on the overall 'diver' system. Hope that makes sense.

Gee that sounded formal.

 

[trux]

The delay is actually irelevant, and it is not a sudden event, but a slow continuous process. The only thing that is important from this point of view is the volume of oxygen available for consumption. In the above example, at the healthy person it will be 100-30=70 mmHg (multiplied by the TLC). At the subject with lung dammage it will be 100-35=65mmHg (x TLC), hence less. Whether it diffuses slower or faster into the blood makes little difference (or at best a very speculative difference if any), but it is clear that the absolute volume of air available for consumption is lower.

The efficiency of the gas exchange: input = available O2; output = consumed O2
1) healthy person: output = 70 mmHg / input = 100 mmHg => 70%
2) ex-smoker: output = 65 mmHg / input = 100 mmHg => 65%

 

[Mullins]

What causes the differences in PA-aO2 in your example above, if not the different rates of diffusion?

 

[trux]

I did not tell that the rates of diffusion are identical. But the diffusion rate is not equal to consumption rate in the brain and body. It just slows down the blood saturation, where the debt then grows faster (dropping closer to the critical level). It won't have any impact on the total volume of oxygen available for cosumption, which will be simply less at the ex-smoker.

 

[Mullins]

So what is the cause of the difference in PA-aO2, i.e. 5mmHg vs 10mmHg in the two examples? I thought it was due to lower diffusion rate in smokers, assuming equal consumption on the arterial side for each subject.

Edit - oh, misread the original example somewhat. You're saying that 1. smokers would start with reduced arterial saturation and 2. maintain that 10mmHg difference all the way into hypoxia. In addition to questioning #2 as I've already done, I'm not sure about #1 since they'd be at rest prior to the breathhold. Would their arterial saturation really be lower while in this state?

 

[trux]

Yes, it is due to lower diffusion rate, and that again is due to worse alveolar permeability. But it does not mean that when it is lower, you simply wait a bit longer for the gradient to drop back to the normal PA-aO2 of a healthy individual.

 

[Mullins]

But the gradient would drop back to normal PA-a02 in time, IF saturation on the arterial side was kept effectively stable, e.g. by the increasing Bohr effect (decreasing saO2, decreasing oxyhaemoglobin affinity = potentially same effective alveolar:arterial gradient for a time). No?

After all, the PA-a02 difference is purely due to difference in diffusion rate assuming steady consumption. Take away the (effective) consumption and it'd level out.