by Claes E.G. Lundgren, MD, PhD
Center for Research and Education in Special Environments, State University of New York at Buffalo, NY, USA
The title of my talk may be too ambitious, especially when it comes to the future, because, after all, as the Danish humorist Storm Pedersen said many years ago, “Predictions are hard to make, especially about the future.”I think what lies in the future in terms of research on breath-hold diving physiology will come out of our discussions here, so it all rests with you. As for the past, I will dwell a bit on what conventional wisdom has said about safety and possibilities when it comes to breath-hold diving (commonly referred to as freediving), and we will see how reality has come about to set those predictions or those ideas straight. As for the current, it will be the material that will be presented by all of you here.Breath-Hold Diving Depth Records
Figure 1: Comparison of improvements in the no-limits breath-hold diving records and Olympic 200 m running records over a 50- to 60-year period (modified from ref. 1).
Now, some of you may have seen one version of this diagram before. This time I have added something that I think is quite astounding. When you reflect on the immense increase in diving depths for maximal breath-hold dives that has progressed from the mid- to late forties, when dives reached down to maybe 30 or 40 m, to the most recent record that I am aware of, which is 209 m (686 ft), it is more than a 700% increase in performance. Now, for comparison, look at the Olympic records. I have chosen, because there was a fair number of data available, the Olympic records for 200 m runs, which has progressed along this line. Now you have, of course, to pay attention to the time scale for the runs, which is in seconds. So we have from 1950, about 20.6 s, to the most recent 1995 record, which is about 19.4 s, a five percent improvement. I do not know that there is any other athletic activity that can show the same improvement in records as deep breath-hold diving. And all the time happening in the face of, we have to admit it, scientists predicting, that the limits would be much, much less than what the divers have shown us.
It does force us to recognize that there is a credibility problem to some extent between us in the labs and the divers who are spearheading the progress in the field. And it is an unfortunate problem, because we do feel that communication is extremely important.
For those who are on the diving side more than on the laboratory side, I would like to emphasize that the reason that the apparently too restrictive limits were proposed at one time or another was that they were based on insights and knowledge that had been gained, not by studying divers, but by studying lung physiology in healthy, non-diving people and patients. And the other reason, of course, was that since much of this was driven by physicians, there would be an overriding concern of not encouraging activities that might do harm.
On the other hand, as I will elaborate a bit on, there are some observations and predictions that I think the divers should take into consideration when it comes to potentially noxious effects of extreme diving. And we will hear a fair amount about that as we go on.
One of the first concerns was the possibility that the pressure and chest and lung compression would do harm. Consider a dive to 200 m (656 ft). And just for those of you who may not have pondered the finer points of this before, let us look at somebody going from the surface starting out with, let us say, a total lung volume of 9 L down to this record depth of currently 200 m. At 200 m the gas in the lungs has been compressed to less than 0.5 L (that is more than one liter less than the normal residual volume). For simplicity we can disregard small effects of oxygen and CO2 exchange. Going from 9.0 L to 0.4 L is a tremendous compression. And the question that for the longest time concerned researchers was, of course, while air certainly is compressed in the lungs and therefore the lungs should be compressed, what about the chest wall and the discrepancy in compressibility between the chest wall and the lungs? The chest wall in humans is certainly not as compressible as it is in, for instance, the diving mammals where the chest wall is less developed, less stiff.
So, going down, let us look at the predictions as they used to be. The following numbers are for measurements we did in an expert breath-hold diver diving in the wet-pot of our hyperbaric chamber. His vital capacity was 7.4 L, his residual volume was 2.2 L, for a total lung capacity of 9.6 L. If one predicts, as the rule was not too many years ago, the maximally safe diving depth based on the ratio between the total lung capacity to residual volume (this assumes, of course, that the diver inhaled maximally before diving) then 9.6/2.2 ~ 4.4, that is a compression to 4.4 ATA. Thus, the prediction from this data would be for his safe maximum depth to be 34 m (112 ft). Well, when we put this data together, he had done a dive to 133 m (436 ft), which makes for a compression of the lung air down to 0.67 L. Yet, his residual volume measured at the surface was 2.2 L. So there is a discrepancy of 2.2 -0.67 = ~1.5 L that has to be explained. And the explanation is, to a large extent, that blood fills the void, so to speak, between the chest wall and the lung.
As a matter of fact, we have recordings by pneumography taking external measures of the chest volume in another well-known breath-hold diver, Enzo Majorca – and when I mention names in this presentation, it is with the consent of the person in question – Enzo did dives in our wet pot, one dive to 55 m (180 ft) and another to 50 m (164 ft) while we measured the chest volume (Figure 2).
Figure 2: Submersed breath-hold dives to 55 m (180 ft) in water at 35°C (95°F) and to 50 m (164 ft) at 25°C (77°F) in hyperbaric chamber performed by Enzo Majorca. Difference between calculated compression of lung gas and measured reduction in chest volume shown as volume of blood (area above zero volume line) redistributed from periphery into chest (Figure courtesy Drs. D. Warkander, M. Ferrigno, C. Lundgren).
Furthermore, since we knew the volume of air he had in his lungs when he started the dive we could calculate the compression of that air as he descended to gradually greater pressure. The idea was to compare the volume of that air with the chest volume. Both of these graphs are designed the same way. This is the time/depth profile down to and up from 55 m (180 ft). You have the smooth line showing what is predicted in terms of compression of the air in the lung as he goes down. It is maximally compressed at the ‘bottom.’ And then as he goes up, it expands again. Contrast that with the actually measured reduction in chest volume and you can see that there is a considerable discrepancy between the chest volume line and the lung-gas volume line.
We have set off this difference up here as a volume of blood redistributed. In this particular dive, it is in the order of one liter of blood entering the chest, entering the space, so to speak, between the chest and the lung. In reality, of course, it is distending the volume of the blood vessels in the chest. This was Enzo’s second dive, down to 50 m (164 ft). It produced a redistribution of about 1.5 L of blood to his chest.
Now, what explains the larger volume of blood shift that is, one and a half liter at the lesser pressure at 50 m (164 ft) than the one liter shift at 55 m (180 ft)? That is probably answered by the difference in water temperatures, 25°C (77°F) at 50 m water versus 35°C (95°F) at 55 m (180 ft). The effect of the colder water was, in all likelihood, to cause constriction of peripheral blood vessels so as to shift more blood from the periphery into the chest than in the relatively warm water.
Thus, there is, without doubt, a very considerable distension of the blood vessels in the chest during breath-hold diving. The question then worrying the researchers is: can that be safe? Is really the human pulmonary vasculature designed to accept such tremendous volumes of blood? It is clearly very unnatural, compared to the situation of normal life on dry land.
Figure 3: Schematic of the lungs and the distribution of blood that can be moved from the periphery into the blood vessels of the chest. A hypothetic u-tube manometer compares the gas pressure in the lung with the water pressure surrounding the chest (chest wall not shown). TLC is total lung capacity and VC, i.e., the vital capacity represents the compressible part of the chest and lungs; residual volume (RV) is the incompressible part; ITBV is intrathoracic blood volume and ETBV is extrathoracic blood volume. A: the situation after inhalation to TLC before dive with small ITBV and because of recoil of chest and lungs a positive pressure in lung; B: beginning of dive with partial compression of chest and some increase in ITBV, pressure equilibrated between lung air and water; C: At this depth the chest-wall-lung system has reached RV and cannot be compressed more from the outside so additional blood is moved (‘sucked in’) from the ETBV to the ITBV and pressure equilibrium is maintained; D: with increasing depth lung gas pressure is lagging behind water pressure drawing in more blood because of limited distensibility and full pressure equilibrium is not reached, i.e., blood pressure in the vessels is higher than air pressure on the outside of the vessels which may burst (Figure reproduced from ref. 1 with permission).
This is fine for theory but is over-distension of blood vessels in the lung and bleeding something really to be concerned about? One of the first positive demonstrations of intrapulmonary hemorrhage was presented by Boussuges and co-workers in France when a diver had done repetitive dives to about 20 m (66 ft) during the day, started coughing up blood. He had a chest x-ray taken and pulmonary lavage was also performed and confirmed that he had blood in the alveoli. So it is definitively a potential risk. The remarkable thing is that there are people who can go down to considerable depth apparently without any problems. And we have accounts of divers who bleed at 20 m or 30 m (66 or 98 ft). It is still a medical mystery why there is this difference because some of those individuals have been subject to extensive diagnostic procedures without the bleeding source being found.
There is one medical condition that has been suggested as a possible explanation in these cases of bleeding after diving, and that is called the Osler disease, which is a condition with blood vessel malformations that can be located in many different areas of the body, from the skin to the gastrointestinal tract, and certainly in the lungs. These are somewhat akin to varicose veins. They are actually located in the transition from arteries to veins, and may be weak points in, in this case, the pulmonary blood circulation that could perhaps more easily rupture than the rest of the vascular bed.
There is other pathology which we will hear more about. Not too long ago it was claimed that there are some natural divers who dive very, very safely, although very intensively, and those are in particular, the Korean and Japanese Ama, who, it was at one time said, almost never suffered any ill consequences from the diving. As we will hear later, the reality is sometimes quite different. Japanese breath-hold divers have been diagnosed with severe brain lesions, most likely caused by decompression trauma (2)
As it comes to oxygen usage and the risk of hypoxia during breath-hold diving, predictions again based on conventional physiological wisdom fall considerably short of what reality and current breath-hold divers are teaching us. Without going into all the fine details, let me just say that if you assume a normal total lung capacity, say, of 6.5 L, and look at how much oxygen is available for metabolism without risking severe oxygen lack, and if you hyperventilate before the dive, you may have something in the order of 14 percent of that gas volume available as oxygen. That comes out to about 900 mL of oxygen in your lungs available for metabolism before you get down to an oxygen pressure of 30 mm Hg – this is at the surface now – at which point you should lose consciousness.
Those 900 mL would last, assuming a standard resting oxygen consumption of 300 mL·min-1, for three minutes. Then, the doctor says, you are going to lose consciousness from hypoxia. Yet, the current static apnea record, held by Tom Sieta, is not three minutes but an astounding 8:58 min:s. So, explanations? Well, one thing that breath-hold divers do that does help a bit in terms of increasing the lung oxygen store is glossopharyngeal breathing. However, that can only increase breath-holding time another half minute or so.
Then there is the improved storage capacity of the blood for oxygen after a series of dives because of an infusion into the circulation of erythrocytes from the spleen (3) with some potential to store extra oxygen, although I believe it is a rather modest effect. There is also the question whether the oxygen usage of the diver is not 300 mL·min-1 but perhaps something less, in which case, of course, the stores would last longer. Now, this brings us to the well-known phenomenon of the diving response. Here illustrated by recordings in Rossana Majorca in dives in our chamber to 50 m underwater. She had graciously accepted to have an arterial catheter put into an artery in her arm for continuous blood pressure recording and we also recorded her electrocardiogram (Figure 4).
Figure 4: Rossana Majorca’s submersed dive in water at 25°C to 50 m (164 ft) in hyperbaric chamber. Recordings (against time) from top to bottom: electrocardiogram (ECG), invasively measured arterial blood pressure, depth profile and breath-hold dive duration. For comments see text. (Figure used with permission from ref. 4).
What is striking here, first of course, is that this was a somewhat stressful or at least exciting moment where she was compressed underwater in the chamber at a relatively rapid rate. There was some tachycardia and a slightly raised blood pressure of 180/110 mm Hg or so in the beginning. When the dive starts, however, something quite remarkable happens. In this young, healthy woman with otherwise normal resting blood pressure but who is now in a diving situation, the blood pressure shoots up to this amazing level, the diastolic blood pressure at 190 mm Hg, and the systolic pressure can be extrapolated to be about 280 mm Hg. Absolutely amazing. Then comes the diving bradycardia and the pressure comes down. This is physiologically very interesting because it is being debated and I do not claim that a couple of recordings that we have done in Rossana and her farther, showing exactly the same thing, are conclusive proof that this is the primary mechanism in the diving response. But it suggests that the rise in blood pressure is an important factor that causes the slowing of the heart. It would do so by triggering the pressor reflex from the pressor receptors in the arteries and causing reduction in sympathetic tone and lowering of peripheral resistance and, as you can see, slowing the heart rate and therefore causing a drop in the cardiac output which would lead to the reduction in blood pressure. Then, at the end of the ascent, you see the circulation picking up and pressure getting back to where it was at the start.
Now, here are parts of ECG recordings in Enzo, Patricia and Rossana Majorca performing submersed dives in our chamber (Figure 5). The dives caused marked slowing of the heart and ventricular extrasystoles and we recorded heart rates of 8-10 beats·min-1 which looked very dramatic but only lasted for a very short time: tenths of seconds
Figure 5. ECG recordings during submersed descending dives in hyperbaric chamber in EM (A) to 50 m, PM (B) to 40 m and RM (C) to 50 m; top tracing recorded before dive and lower tracing at depth indicated (Figure used with permission from ref. 5).
This irregularity in heartbeat has also been observed by others and is apparently not of great concern in an absolutely healthy person but it may be a different thing in somebody with a heart condition – more about that in a while. But first something about the significance of the diving bradycardia, that is, the slowing of the heart
Figure 6: Diving response in terms of heart rate reduction (HR) vs. duration of maximal effort breath-holds during face immersion in cool water. Groups 1 to 3 were experienced breath-hold divers, Group 4 was scuba divers and Groups 5 to 9 were non-divers. Diving bradycardia was more pronounced and breath-holding time was longer in divers, but less so in older individuals (Group 2, Ama) (Figure used with permission from ref. 6).
It shows very nicely that the more pronounced the diving bradycardia is in divers the longer they can hold their breath. In other words, it suggests that the diving response is beneficial for diving performance.
I wish I could put in here another group, which would, however, be very hard to do the proper experiments in, and that is little children, babies or toddlers who have been trained to swim underwater, which they gladly do, if trained correctly. They have quite a vigorous diving response, although, of course, you can never test to see what their maximum breath-holding duration is. What makes this so fascinating is that nature apparently has given kids – this ability to react in a very appropriate fashion to a situation of threatening suffocation. Why so? Well, in the process of being born you are indeed, for a relative brief period of time, subjected to an enforced hypoxia that can become extremely severe. It starts when the child passes the birth canal and the chest is kept in a very firm grip so that it cannot expand even after the face has broken through, and the umbilical cord is also compressed. The face has broken through and is cooled by the outside air and a profound diving response develops. It can actually last for minutes after full delivery. This is nature’s carefully tested and through evolution developed method of protecting against dangerous hypoxia in the process of birth.
The diving response is actually found almost throughout the entire animal kingdom, certainly among vertebrates. It has even been demonstrated in slugs and in fish (Figure 7).
Figure 7: Hypoxic stress generated in cod fish lifted out of its aquarium results in bradycardia and anaerobic metabolism which is remedied when the fish is put back in the water (Reprinted with permission from ref. 7).
Look at the heart rate. What shall we call it, diving bradycardia? A clear, strong bradycardia, normal heartbeat being restored when it is put back into the water. Note also the increases in blood and muscle lactate after the hypoxic episode. It is equivalent to our situation being dipped underwater when the fish is pulled up on the dry. And it might serve survival in this case. So it is a reaction, the diving response that has been found valuable throughout the animal kingdom for survival.
I talked about the possibility that in us, humans, the rather modest oxygen stores in the lungs, in the blood, and some little in the tissues would last longer because of reduced oxygen usage in divers. Here are some measurements we did, again in the three Majorcas, some years ago. They did breath- holds in a dry environment in the laboratory (Figure 8).
Figure 8: On the horizontal axis is the breath-holding time. They held for something in the order of four to five minutes. The vertical axis shows oxygen uptake. This is based on analysis of the oxygen content in the lung air in repeated breath-holds. So each point here is where the breath-hold on command was broken and a sample of the lung air was taken to analyze how much of the oxygen had disappeared. Clearly, oxygen uptake from the lung is growing as they hold their breath, but at a slower and slower pace, especially when you compare it to the normal resting oxygen consumption, which is represented by these straight lines, you can see that they definitely use less when they hold their breath. The straight lines represent oxygen uptake when breathed quietly, and we just measured oxygen consumption in the normal way. And here (open circles) are age and sex-matched non-diving controls, in whom oxygen consumption, when they hold their breath, just reproduces their normal oxygen consumption when breathing. (Used with permission from ref. 8).
So certainly these divers were a breed apart, but what this figure illustrates applies to breath-hold divers in general. And recordings in several laboratories have now shown that if you look at the oxygen content in blood measured as oxygen saturation during divers’ breath-holds it falls at a much slower pace than in non-divers.
Another aspect of adaptation to breath-hold diving that probably is primarily due to training, is shown here again in our favorite subjects, the Majorcas (Figure 9).
Figure 9: Recording of relationship between spontaneous lung ventilation (vertical axis) and end-tidal CO2 pressure (horizontal axis) increased by inhalation of stepwise increased CO2 concentrations in an O2-CO2-N2 mixture. Open symbols: three expert breath-hold divers; filled symbols: age and sex matched non-divers (reprinted from ref. 9 with permission from Elsevier).
Recorded in the laboratory is their breathing in response to step-wise increases in CO2 in inhaled air. As the resulting CO2 pressure in their lungs (horizontal axis) and arterial blood increases they react with increased ventilation (vertical axis), according to this pattern. In other words, this is an expression of their ventilatory CO2 sensitivity; the age-matched, non-diving controls were much more sensitive. You can see much steeper rise in the stimulation from the CO2 of the breathing in the non- divers. So the breath-hold divers are less sensitive to CO2 build-up, good and bad. They can hold their breath longer, but also face an increased risk, of course, of running into hypoxia, an aspect that will be dealt with in various presentations to come.
I am getting back to the observation of irregular heart-beat during breath-hold diving, Figure 10. Our divers made two dives each in our dive chamber, one to 50 m (164 ft), one to 40 m (131 ft), and here is another to 50 m. There is an important difference between the two dives that each one did. One dive was in cool water (25°C/77°F) and one in thermoneutral water (35°C/95°F). Note the dive profiles to either 40 or 50 m.
Figure 10. Relative occurrence of arrhythmias at depth vs. time during submersed breath- hold dives, performed by three experienced divers (EM, PM, RM), in a hyperbaric chamber. Measurements were averaged over 10 s intervals. Note the higher incidence of arrhythmias in cool water (25°C/77°F) than in thermoneutral (35°C/95°F) water (Figure used with permission from ref. 4).
And what we have put down here is the frequency of normal (sinus) heartbeats. That is to say, relative occurrence of normal heartbeats and various types of arrhythmias. We have some abnormal beats emerging from not the normal source for heartbeat, namely the sinus node, but from various other locations and with different patterns and we have tied those (black squares) together with the dotted lines in the figure. So the lines delineate the bulk of abnormal heartbeats over the periods of time that the dives lasted. Note that the areas in the figures representing the amount, so to speak, of abnormal beats are much larger in the dives in cool water than in the dives in thermoneutral water. So what we are looking at here is a heartbeat pattern which is abnormal for healthy individuals during their every- day life but which is brought about as part of the diving response. This has, as I mentioned before been reported by other researchers but the distinction between the effects of cold and warmer water has not been made earlier. So of what consequence is it? Probably none in the healthy individual. But I would like to suggest that, in persons with heart conditions, maybe unknown, this could be the trigger of potentially fatal arrhythmias. And there are certainly cases heard of where somebody does a dive and for no clear reason dies in that dive. On autopsy they may not show any serious cardiovascular disease, but you would not expect that necessarily, if it is a fatal arrhythmia, such as ventricular fibrillation.
Now, much of our discussion about the effects of breath-hold diving in terms of clinical risks is concentrated on the question of hypoxic damage. And we will hear more about that in the coming presentations. I would just like to raise the question here: is there possibly a similar risk for divers subjecting themselves to repeated episodes of rather severe hypoxia especially as it happens in static apnea as there appears to be in persons suffering from sleep apnea. There is a recent study (10) which has shown cognitive deficits in sleep apnea patients. Admittedly, the hypoxic periods in sleep apnea are much more frequent than the hypoxia exposures in breath-hold divers but it is worth noting that many repetitive insults can even if, after each acute episode not much is noticed, accumulate damage.
Ladies and gentlemen: thank you for your attention – the floor is all yours and we are very much looking forward to hear about the science and practice of breath-hold diving , today and in the future.
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UNIDENTIFIED SPEAKER: I was intrigued by the CO2 response curves. And it seems that everybody is breaking around 55 mm Hg approximately. So there must be some change in the release of CO2 into the circulation, otherwise it would not be all breaking at the same point.
DR. LUNDGREN: Good point. And to the extent that we accept the idea of reduced metabolism, of course, you could have an extended breath-hold without necessarily breaking at a higher point. But there is, from Carl Schaffer’s work many, many years back some studies in which he recorded ventilatory sensitivity to CO2 and showed that in submarine escape tank instructors it was the same phenomenon. And it was clearly a training-related phenomenon where they lost it when they went on other duties for three or four weeks. And when they came back, they were normal in terms of their CO2 sensitivity.
UNIDENTIFIED SPEAKER: It must be that there is decreased metabolism but increased CO2, otherwise, the breaking points would be different.
DR. LUNDGREN: That is correct.
DR. MUTH: We made measures and we could show by arterial drawn blood gases that the CO2 does not increase because of various reasons. There is, on the one hand, the effect of the diving response, but on the other hand, you have a very strong effect by the old day effect, which says de-oxygenized hemoglobin can take up CO2. And thus, the CO2, the PCO2 does not rise. So, in our measurements you could clearly see that the PO2 rises with depth, as predicted, and falls down by using of the body, but the CO2 curve was more or less on the same level.
Another story is that the competitive apnea divers deny doing hyperventilation, but they all do yoga. If you take arterial blood gases just before they go for their dive, you will see PCO2 levels around 28 to 29 mm Hg. So this contributes to the effect as well.
DR. LUNDGREN: Another aspect of the body’s CO2 handling in diving which we have studied and not been able to fully explain, is the very clear increase in the body’s ability to store – other than the blood – to store CO2, when you are surrounded by water, and probably related to changes in distribution of blood flow just by being submersed. So there are several aspects to this question of how the body handles the CO2 economy, if you will, in breath-holding and immersion.
DR. RISBERG: That might put an end to the diving reflex, because I think it is a bit simplified. I think the mechanism might be a bit different. The reason I am saying that is an experiment we did many, many years ago, and I hope that someone finally will repeat it.
We had divers that performed a deep saturation dive for a moment. And we measured their maximum breath-hold time and their diving response in terms of bradycardia before they did that dive and after. And our hypothesis was that their CO2 sensitivity would be reduced because of reading of the dense scales.
What happened was that their CO2 sensitivity was increased. Their breath-hold time increased significantly. And they had no diving response for up to a month after that saturation dive. So there obviously must be other mechanisms involved probably related to some kind of adaptation maybe in the sensitivity of, we speculated it could change the sensitivity of the breathing muscles or the muscles of the thorax that had a different input, would be one possible explanation.
I hope that that experiment can be repeated because it could determine the mechanism for the bradycardia. It is a bit more complex than normally stated based on that one single experiment.
I also want to make a point about the statement that it is not beneficial to have repeated hypoxias. We have done this experimentally in animals, by looking at the effect of repeated hypoxias to a height of 3,000 m [9,842 ft] two hours a day for six weeks. And we found a significant improvement in epithelial functioning if you do that. So there are various aspects to this.
DR. LUNDGREN: I suppose it would be somewhat difficult to do cognitive functioning in those animals. Be that as it may, as far as the point about the changes in the saturation divers, that is very interesting, although I am sure you are aware that one cannot necessarily say that the mechanisms modified by the saturation dive necessarily applied to people who never do saturation dives. But it is an interesting observation.
NOTE: To access the entire proceedings of the UHMS DAN 2006 Breath-hold Proceedings, visit Divers Alert Network.
In: Lindholm P, Pollock NW, Lundgren CEG, eds. Breath-hold diving. Proceedings of the Undersea and Hyperbaric Medical Society/Divers Alert Network 2006 June 20-21 Workshop. Durham, NC: Divers Alert Network; 2006.