Does Diving Damage the Brain?

It is well known that compressed gas diving may result in acute decompression sickness and cause permanent injury to the brain and spinal cord. However, the risk of possible injury to the brain in the absence of acute decompression illness is less clear. Because of the controversy over the subject, and the lack of definitive evidence, DAN recently enlisted the help of a group of industry respected experts to provide their insight into the subject and published the results in Alert Diver (1).

The agents of neurologic decompression injuries are gas bubbles (emboli) that occur in tissue, travel with venous blood and may pass from venous circulation into the arterial system. Detectable venous gas emboli are often present after a dive, but they are usually removed through pulmonary capillary filtration. When the emboli pass to the arterial side, they may block arterial flow, causing tissue hypoxia in watershed areas and sometimes damage. The risk of arterialization increases in divers with a large PFO, but it can also occur through pulmonary arteriovenous shunts when there is high load of VGE. For decades this has been raising concern that brain injuries in divers may be more prevalent than previously thought and could potentially occur without a manifestation of acute decompression illness.

bubblesA recent paper published by our colleagues Balestra and Germonpre (2) seems to provide a quite clear answer to the question. The two researchers recruited 200 recreational divers who had never had DCS, and then randomly selected from among them 50 divers for further studies. In addition, they maintained a control group of subjects who had never been diving, and another control group of subjects who had been exposed to neurotoxic solvents. The aim of the study was to establish whether divers have more asymptomatic brain injuries than non-divers, review how divers perform on psychometric tests in comparison to non-divers, and research the possible effect of the presence of a PFO.

Balestra and Germonpre(2) used magnetic resonance imaging (MRI) to evaluate subjects for signs of asymptomatic brain injuries (unidentified bright objects – UBOs), performed echocardiographic tests for PFOs, and gave the subjects a battery of four neuro-psychometric tests. Divers who did not complete all studies were excluded, but 42 of the initial 50 remained in the study.

A significant PFO was detected in 38% of divers. UBOs were detected in 5 (12%) divers. Importantly, there was no correlation between the presence of a PFO and the ending or extent of UBO’s. That is the good news: diving without acute decompression illness does not cause UBOs, which were of concern to many divers and researchers.

Neuro-psychometric testing, however, produced inferior results for divers in two tests in comparison to non-divers, and similar results in comparison to the group exposed to neurotoxic solvents. On two other tests, divers did significantly better than the solvent group. This was not correlated with the presence of PFO. In summary, it appears that divers with five or more years of experience and at least 200 dives, have decreased short term memory and visual-motor performance, which could be a bad news if further studies confirm it.

Another interesting point from this study is that the prevalence of PFOs among study subjects was higher than in general population. The authors hypothesize that this may be due to strenuous intra-thoracic pressure changing activities, such as those encountered in diving, which may “open-up” previously sealed or microscopically small PFO. However, there are many other everyday life situations that raise intrathoracic pressure in similar manner as some dive maneuvers. In our opinion, this finding is of concern when discussing the prevalence of PFO in DCS case series. Even divers without a history of DCS may have greater prevalence of PFO than the general population.

This paper is worth reading and is available for free online at:http://journal.frontiersin.org/article/10.3389/fpsyg.2016.00696/full

  1. Willey J. Effects of diving on brain. Alertdiveronline. http://www.alertdiver.com/Brain
  2. Balestra C and Germonpré P (2016) Correlation between Patent Foramen Ovale, Cerebral “Lesions” and Neuropsychometric Testing in Experienced Sports Divers: Does Diving Damage the Brain? Front. Psychol. 7:696. doi: 10.3389/fpsyg.2016.00696

BREATH-HOLD DIVING, CIRCULATING GAS BUBBLES, AND NEUROLOGICAL SYMPTOMS

Decompression sickness has been the suspected cause of the post-dive symptoms of brain injury in breath-hold divers for a long time, and the quest for the proof of culprit has been ongoing, but without success. In the meantime, many possible explanations of neurological symptoms in breath-hold divers were proposed, including in-situ bubble development, lung barotrauma and consequent gas embolization, atherosclerosis, small vessel disease, transitory extreme elevation of blood pressure, and repeated hypoxic injury.

Several researchers have studied venous gas emboli in breath-hold divers, but their results have been mixed. Spencer reported in 1972 positive finding of VGE in Ama divers of Japan after repetitive breath-hold diving. Lamaitre reported in 2009 finding of the lowest freediver-istock_webVGE grade in one out of twelve Ama divers.  On the other hand, Boussuges could not find any bubbles in ten divers diving repeatedly for two to six hours up to 34 meter depth. More details on those studies can be found in another post on this blog, in which I admit that clinical documentation of decompression sickness-like symptoms and signs appears supportive of a DCS diagnosis. The bulk of material presented by the researchers was, however, more circumstantial than crucial evidence.

Recently Cialoni and co-authors (1) published in UHMS a report about finding high grade bubbles in breath-hold divers lasting for 45 minutes post dive and declining over the following 90 minutes. This diver did not have any symptoms, but the bullets were flying around and there was a potential for arterialization of bubbles and, if the diver had a PFO, embolization of the brain. This outstanding finding, they explain, is a result of 14 deep dives (40 m) and long bottom times (141+-42 seconds), typical for advance spearfishing divers.

However, another outstanding circumstance is that these dives were conducted in warm water (33 0C; 91.4 0F), which was uniform throughout the water column, which is higher than usual water temperature where the spearfishing occur. It was shown previously that diving in warm water increases the bubble grade three-fold (2), and may increase an individual’s risk of DCS.

Regardless of the circumstances, the finding of Cialoni and coauthors is the proof of hypothesis that breath-hold diving may generate venous gas bubbles. The true relationship of VGE and post-dive neurological symptoms is not known. The VGE may not be necessary for cerebral decompression sickness. Finally, the DCS may not be the only cause of cerebral symptoms occurring after deep and repeated breath-hold dives. More investigation on the topic is necessary, and some studies are ongoing and we hope that more results will come soon.

References:

  1. Cialoni D., et al. Detection of venous gas emboli after repetitive breath-hold dives: case report. Undersea Hyperb Med 2016;43(4):449-455
  2. Dunford R. Hayward J. Venous gas bubble production following cold stress during a no-decompression dive. Undersea Biomed Res, 1981;8(1):41-49.
  3. Gerth WA. On diver thermal status and susceptibility to decompression sickness. Diving Hyperb Med. 2015 Sep;45(3):208.

How is Eustachian Dysfunction related to Inner Ear Barotrauma

Diving and Hyperbaric Medicine Volume 46 No. 2 June 2016

Normal Eustachian tube (ET) function is important for fitness to dive. Eustachian tube dysfunction may result with ear injury during diving. The most common diving injury related to Eustachian tube dysfunction is middle ear barotrauma, and less common but more grave is inner ear barotrauma (IEBt). While middle ear barotrauma usually heals well, inner ear barotrauma may cause permanent damage if not recognized and treated on time and thus, the prevention of IEBt is very important. The Diving and Hyperbaric Medicine Volume 46 No. 2 June 2016 brings three articles addressing these issues.

Kitayima and co-authors studied Eustachian tube function in 16 divers who experienced IEBt and in 20 healthy divers without history of IEBt. They correlated the function of Eustachian tube to the incidence of IEBt. They measured the opening pressure for ET, the divelab20161013maximum volume of the air in the middle ear and the speed at which the equalization occurs. In the ideal conditions, the pressure differential needed to open the ET in either direction is 200 to 650 daPa which corresponds to a pressure gradient caused by depth change of 20 – 65 cm or 8-26 inches. The maximum volume of air in middle ear varies from 0.2 to 0.9 ml. The paper describes three main type of ET based on the equalization characteristics: patulous (open) ET, normal ET and stenotic (narrowed) ET. The patulous ET is open permanently or it takes pressure differential of less than 200 daPa to open it. Normal ET is collapsed but it takes less than 650 daPa to open it and it fills or empties instantaneously. The stenotic ET takes larger pressure (up to 1200 daPa/120 cm H2O measured) to open it or it fills and empties very slowly.

In healthy divers without a history of IEBt, one third had slow equalizing ET but the pressure differential required was within normal range. They avoided IEBt so far, probably by practicing slow ascent but they often experienced alternobaric vertigo. Among divers with IEBt, most had dysfunctional ET requiring either greater pressure differential to open it and/or it took longer time to equalize. However, some divers with IEBt had normal ET function at the time of measurement. Divers with IEBt and perilymph fistula had more severe ET dysfunction. Authors suspect that excessive pressure caused by forceful Valsalva may have been the cause of IEBt in some divers and especially in those with normal opening pressures but who became impatient with equalization and blew to strongly.

Morvan and co-authors presented a series of 11 cases of perilymphatic fistula due to IEBt in scuba divers. The perilymphatic fistula is most severe form of IEBt but it diagnosis is not always obvious. Dizziness, hearing impairment and tinnitus after scuba diving indicate likely injury of inner ear but the cause may be either decompression sickness or barotrauma. Delayed onset, fluctuation and progressive deterioration of deafness point toward perilymph fistula. In either case, occurrence of cochlea-vestibular symptoms after a dive is an emergency. Early evaluation should be focused on decompression sickness and need for hyperbaric oxygen treatment which may prevent permanent damage to inner ear. Effort must be made to exclude perilymph fistula before recompression treatment. However, that is not always possible and divers with a fistula sometimes get treated but there is no indication so far that it is deleterious if necessary precautions are taken. If there is no improvement on recompression or if there is worsening of symptoms, the treatment should be aborted and perilymph fistula considered.

Guenzani and co-authors reported case histories of nine cases of inner ear decompression sickness (IEDCS) in recreational technical divers who were identified through an online questionnaire. The most common leading symptom in IEDCS was vertigo, reflecting affliction of vestibular part of inner ear. The deafness which dominates in IEBt was seen in only three cases reported in this paper. IEDCS occurred in isolation (4 cases) and with other DCS manifestations (5 cases). The symptoms occur during ascent or soon after. IEDCS occurs more often than IEBt and due to growing participation in technical diving we may see it even more often in the future.

Presentation of these three papers in the same volume, seem like a good opportunity to re-fresh our knowledge about inner ear injuries in diving. Early recognition and prompt treatment are important to reduce the risk of permanent damage to hearing and orientation in space.

References

  1. Kitajima N, Sugita-Kitajima A, Kitajima S. Quantitative analysis of inner ear barotrauma using a Eustachian tube function analyzer. Diving Hyperb Med. 2016;46(2):76-81.
  2. Morvan J-B, et al. Perilymphatic fistula after underwater diving: a series of 11 cases. Diving and Hyperbaric Medicine. 2016;46(2):72-75.
  3. Guenzani S, et al. Inner ear decompression sickness in nine trimix recreational divers. Diving and Hyperbaric Medicine. 2016;46(2):111-116.

Endothelial cell dysfunction in diving

The EUBS annual scientific conference in Geneva, September 2016 presented several papers about endothelial dysfunction in diving. The endothelium is the layer of cells on the inner surface of blood vessels. It is very active in regulation of local blood flow, self-repair, prevention of blood coagulation and inflammatory response to various insults. An important mediator in activities of endothelium is nitric oxide (NO) which regulates also the constriction and dilatation of vessels. This has been found affected by diving due to hyperoxia which limits the availability of NO and thus reduces ability of vessels to dilate following temporary occlusion (flow-mediated dilatation; FMD). Injury of endothelium, which can be caused by bubbles, results in increased quantities of released cell fragments called endothelial micro particles (EMPs). The study of possible roll of FMD and EMPs in diving is confounded by variety of stressors that contribute to their changes, like exercise and thermal stress. However, the potential to explain mechanisms of decompression illness keep these topics in the focus of scientists.

The group from the Second Military Medical University, Shanghai,(1) studied effects of bubbles in isolated endothelial cells (in vitro) and in vivo. They have shown that contact with bubbles increases the release of EMPs. They collected the EMPs and brought it in contact with normal endothelial cells without presence of bubbles. They also infused EMPs to live animal. In both cases, the EMPs caused further damage of endothelial function causing increased cell apoptosis (programmed death of cells), increased intracellular content of reactive oxygen species, decreased NO, increased cell permeability (leakage) and pro-inflammatory response.

The entire story of endothelial dysfunction and DCS sometimes is similar to the dilemma of chicken and egg: what is first, the bubbles that cause injury of endothelium, or the endothelial dysfunction that enhances occurrence of bubbles? This study verified that bubbles may cause endothelial injury but did not prove that it is the only possible scenario that occurs.

The same group presented another study that explored effects of endothelial protection on occurrence of DCS in animal model. They treated a group of animals with escin for seven days before dive exposure and compared outcomes in treated and in control group. Escin has been used for endothelial protection in various indications. In this experiment, animals that receive escin had less DCS and in case they got DCS the delay to onset of symptoms was longer and manifestations less severe. All other endothelial indices which they measured were improved.(2) The results support hypothesis that endothelial integrity is important for outcome of diving. However, this is not a proof that escin could be useful in protecting divers from DCS.

There were three studies presented that used FMD to measure decompression stress in divers.  Nicolas Renne and coauthors presented measured FMD 30 to 140 minutes after dive to 30 m (98 ft) for 20 minutes in a deep pool with warm water. The dive was within no-decompression limits (but not likely without bubbles, which was not reported in the abstract). They have found borderline reduction of FMD at 30 and 70 minutes post-dive, with a complete recovery at 140 minutes.(3)

Jean Pierre Imbert and coauthors measured FMD before and after saturation diving. The decompression did not result in any bubbles but the FMD was still reduced in average for 7% with a complete recovery within 12 hours. These results support hypothesis that bubbles and FMD are two independent dimensions of decompression stress where bubbles result mainly from the changes in pressure while FMD reduction results from hyperoxia.(4)

The third paper uses FMD to study effects of nitrox after a dive to 25 msw (82 fsw) for 40 minutes. They found that in comparison to air, nitrox results in less bubbles, increased peripheral pulmonary resistance, and a reduction in FMD. Again, the bubbles and FMD appeared to be two independent indices of DCS. However, it was unusual in this study that diving air to 25 m (82 ft), which exposes divers to 0.74 ATA partial pressure of oxygen, did not change at all the FMD.(5)

Both EMPs and FMD remain promising in the study of mechanisms of decompression sickness and we hope that the presented work at EUBS will find their way into peer reviewed scientific journals.

References

  1. Xuaxu Yu, Jiaju Xu, Weigang Xu. Bubble-induced endothelial microparticles promote endothelial dysfunction. Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;16
  2. Zhang Kunm Jiang Zhongxin, Ning Xiaowei, Weigang Xu. Protective effect of escin on decompression sickness in rats. Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;63
  3. Renne N, et all. Flow mediated dilatation evolution after a Nemo33 scuba dive. Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;83
  4. Imbert JP, Kiboub F, Balestra C. Measurement of the decompression stress during offshore saturation. Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;33
  5. Andre Zenske at all. Is nitrox dangerous for the recreational divers? Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;32

Can drinking wine provide benefits for divers?

Historically, alcohol was used to treat bends in Greek sponge divers. In the late 1980s attempts to verify the possible beneficial effects of ethanol on prevention of DCS led to prevailing opinions that there was no proven benefit and that divers should not drink and dive. On the other hand, the assumption that wine drinking has beneficial effects on general health is still propagated.

wine_shutterstock_85339912The so called “French paradox” fueled a search for possible healthful components in wine that, as some researchers posted, protect French people from heart disease despite their fat rich diet and high blood cholesterol levels. Tannins and phenolics, a large group of substances that together make up to 0.1% of wine mass and determine the color and the taste of wine, were identified as beneficial substances. The most intriguing and studied phenolic is resveratrol which is now also sold as a dietary supplement.

Studies of resveratrol in vitro (on cellular cultures or in various models of biochemical systems) have shown anti-oxidant and other effects that with basic biological processes may provide protection against aging, various diseases and death. Further animal studies appeared to confirm beneficial effects. Some of the suspected mechanisms involving resveratrol included functions of endothelial cells (inner lining of blood vessels) and platelets which are also affected in diving. If resveratrol could prevent endothelial cell dysfunction and platelet aggregation, it may help to avoid decompression sickness. Recent resveratrol studies claimed several additional health benefits that could be appealing to divers.

The first claim is that resveratrol has beneficial effects on
skeletal and cardiac muscle functions similar to what is seen with endurance exercise training.1  Wouldn’t it be nice to work on your fitness by relaxing and sipping wine after a long workday rather than going to the gym and sweating?

The second claim is that resveratrol improves brain perfusion and provides neuroprotection2, both of which may be helpful in reducing risk of decompression sickness. Why not drink wine before or after diving?

Unfortunately, there is only one problem with all these studies; the amount of resveratrolDelicious  portion of  fresh salmon fillet  with aromatic herbs, used is equivalent to drinking 50 to 3000 liters of wine per day. It is far more than is needed to get drunk. It’s enough to dive in. Thus, drinking red wine does not seem to be a practical prophylaxis of decompression sickness.

But don’t despair. Even French Paradox is not due to wine drinking as was believed forty years ago. Most population studies indicate that health and longevity may be associated with overall diet. The benefits of French diets appear to come from plenty of fresh vegetables, moderate caloric intake and physical activity rather than just from wine. The French diet has a lot in common with the so called Mediterranean Diet which is widely considered most favorable. In fact, in 2010 it was acknowledged by UNESCO as an Intangible Cultural Heritage of Humanity. (http://www.unesco.org/culture/ich/en/RL/mediterranean-diet-00884)

This story illustrates a common wisdom that there is no one single dietary supplement that could provide what mortals want. To stay healthy and fit for diving, adopt a healthy diet3 and, if you drink wine, limit yourself to one glass with your meal. More importantly, do not drink before the dive.

For quick orientation about healthy meal check MyPlate

http://health.gov/dietaryguidelines/2015/guidelines/chapter-3/strategies-for-action/#callout-myplate

 

References

  1. Dolinsky VW, Kelvin E. Jones EJ, Robinder S. Sidhu SS, Mark Haykowsky M, Michael P. Czubryt MP, Tessa Gordon T, and Jason Dyck   Improvements in skeletal muscle strength and cardiac function induced by resveratrol during exercise training contribute to enhanced exercise performance in rats. J Physiol 590.11 (2012) pp 2783–2799
  2. Otto MA. Resveratrol improves cerebral perfusion in type 2 diabetes. Clinical Endocrinology News Digital Network. January 17, 2016 http://www.clinicalendocrinologynews.com/specialty-focus/diabetes/single-article-page/wdc-resveratrol-improves-cerebral-perfusion-in-type-2-diabetes/1fe1ba3439a5ae9dc24b003d21793512.html
  3. US Department of Health and Human Services and US Department of Agriculture 2005 – 2020 Dietary Guidelines for Americans. 8th December 2015. Available at health.gov/dietaryguidelines/2015/guidelines/.

Scuba divers beware: sudden death is not always unannounced

CPR_2Sudden death in adults is often caused by an unexpected loss of pulse due to stop of heart pump (sudden cardiac arrest; SCA) followed shortly by a loss of consciousness and muscular power (collapse) without an external cause. SCA is a cause of over 550,000 deaths in USA including out-of-hospital and hospital patients. Regardless of circumstances, survival remains very low (7%). SCA affects people with and without history of previous heart disease. According to DAN fatality data, about one quarter to one third of scuba fatalities may be caused by SCA which, in addition, may be sealed by drowning.

Although cases of SCA progress rapidly the name does not imply that cardiac arrest occurs without warning signs. Medical professionals know that in some cases warning signs like chest pain and dyspnea precede SCA long enough to initiate pre-emptive intervention. We have also learned from the DAN scuba fatality monitoring program that in some divers death ascribed to SCA obvious warning signs were present before the fatal dive. How prevalent these warning signs are in the general SCA patient population was not known until a study done by Marion Eloi and coauthors published last December.

The study identified SCA patients from Portland, Oregon metropolitan area hospitals who had symptoms assessments done four weeks prior to the SCA event. Total of 839 patients were identified. The mean age of patients was 52 years and most were males (75%). Fifty-one percent of patients had at least one warning symptom. There was no difference in percentage of males and females with warning symptoms. The most common warning symptoms were chest pain and dyspnea. Men had more chest pain and women more dyspnea. Most SCA occurred while patients were at home. Warning symptoms occurred one hour before SCA and in many cases even 24 hours before. Only 19% with warning symptoms called the emergency medical services (911). Callers were more likely to be patients with a known history of heart disease. The mean response time between a 911 call and EMS arrival was seven minutes. Initially shockable rhythm was present in about fifty percent of the cases. Survival in those who call 911 was 32% in comparison to those who did not call.

The takCPR_3e home message is that chest pain and dyspnea in middle age and older individuals even without known heart disease history, should be recognized as a warning sign of a life threatening condition and patients should be prompted to seek emergency medical care before SCA occurs. Even in the best of circumstances, when emergency response is initiated after the occurrence of SCA, chances of survival are slim. However, a prompt reaction to warning signs may prevent SCA and in case it still occurs, it increases survival rate. Other symptoms that may precede SCA but are less specific are syncope, palpitations, abdominal complains and influenza-like symptoms. These symptoms may be difficult to recognize as warning signs of SCA without history of heart disease. For divers it is important not only to acknowledge likely cardiac symptoms (chest pain and dyspnea) and call 911 but also to abstain from diving in case they have any symptoms until they have a clearance from their diving physician.  Once SCA occurs, one does not have time to get surprised but those who act upon warning signs, may pre-empt sudden death.

 

References

Marijon E, et al. Warning Symptoms Are Associated With Survival From Sudden Cardiac ArrestCardiac Arrest. Ann Intern Med. 2016;164:23-29. doi:10.7326/M14-2342.

Participation in recreational scuba diving

Sports & Fitness Industry Association Report 2015

Every year the Sports & Fitness Industry Association (SFIA) releases a report that reviews participation data on various sports and recreational activities. The 2015 report pertains to 2014 participation data and is based on 10,778 online interviews (5,067 individuals and 5,711 households) among one million US online panel members. The survey asked about demographics and participation in various physical activities and sports.

Demographics of the survey participants included the following:

  • 49 percent male, 51 percent female
  • < age 18: 15 percent
  • > age 65: 17 percent
  • 77 percent Caucasian, 8 percent African American, 5 percent Asian/Pacific Islander, 8 percent Hispanic, 1 percent “other”
  • The results were calculated based on a U.S. population of 292,064,000 ages 6 and older. Various weighting techniques were applied. The sample provides a high level of confidence. A sport with a participation rate of 5 percent has a confidence interval of plus or minus 0.42 percentage points at the 95 percent confidence level. However, scuba diving participation was significantly smaller (1-1.1 percent of population)

According to this report, 3.145 million Americans (1.1 percent of population) participated in scuba diving once or more in 2014, which is a 0.9 percent decrease over 2013. However, the average participation for the last two years shows a 1.3 percent increase over the average for the previous five years.

There are 2.252 million casual participants in scuba diving (defined as making between one and seven dives per year) and 893,000 core participants (defined as making eight or more dives per year). Males make up 66 percent of casual and 74 percent of core participants.

Fig.1

Figure 1 shows the age distribution of casual divers versus core participants.

  • 1 percent of casual and 57 percent of core participants are between the ages of 25 and 54.
  • 7 percent of casual and 21.2 percent of core participants are younger than age 25.
  • 2 percent of casual and 21.8 percent of core participants are older than 54.

 

The rate of participation (the percentage of population that participate in scuba diving) by age group is shown in Figure 2.

Fig.2

In the 18 – 44 age range, participation for the casual divers is between 1.2 and 1.4 percent and for the core divers between 0.2 and 0.4 percent. Participation rates vary with age. Casual participation rates increase continuously until age group 35-44 and decreases sharply afterwards. The core participation practically does not vary between age 25 and 64 (3-4 percent) but drops at older age (0.1 percent). Interestingly, both casual and core participation rates for children (6-12) are several times greater than for  65+ age groups.

This may be partly because the later includes wider age range.

Fig.3

As shown in previous reports, scuba diving participants are on average wealthier and better educated than the general population.

Data about cross-participation of scuba divers in other activities shows 3 – 22 times higher participation indices in comparison to the general population. This pertains to aerobic activities, participation in individual and team sports as well as in extreme sports. Nearly 46 percent participate in running/jogging and 36 percent swim for fitness. It is not known what is the overlap nor how many divers do not participate in other sports. However, it is encouraging to see that divers participate in sports more than the rest of population because in the past the DAN medical emergency line and Fatality and Injury monitoring program has observed that some divers get injured due to inadequate physical fitness. More precise data are necessary to identify those who need some additional encouragement.