Athlete fatalities at multisport events are actually not common when you take into account overall participation numbers. When they do occur, they receive considerable media attention. The open water swim has gained reputation as the most deadly leg of the triathlon.
An independent review of triathlon fatalities in the United States for the period 2006-2008 identified 14 victims (1 per 67,000 participants) in the age range of 28-65 years, with 13 of the deaths occurring during the swim leg (1). A larger review undertaken by USA Triathlon (USAT) for the period 2003-2011 identified 42 race-related fatalities (1 per 76,000 participants) in the age range of 24-76 years, with 30 of the deaths in the swim (2). Fatalities were not confined to inexperienced triathletes but included athletes from a broad range of triathlon experience.
Media reports imply that cardiac problems are wholly responsible for swimming deaths. Yet, scientific reports on the autopsy findings of triathlon victims are limited. Those that have been done show mild cardiac abnormalities were present in the majority of victims. Dr Larry Creswell, a cardiac surgeon in the University of Mississippi with an interest in athletes and heart disease, emphasises that the mechanisms of sudden fatal arrhythmia and cardiac arrest in these athletes remain unknown (3).
At any rate, even if cardiac abnormalities are found to be present in affected athletes, the bugbear question is:
Why are athletes more vulnerable in the swim leg compared with the bike or run legs of triathlon?
There are a number of factors that might cause even healthy and experienced athletes to suffer shortness of breath and cardiovascular problems during an open water swim. Race panic, excessive hydration, sudden physical exertion and constricting wetsuits have all been documented in the literature, and, from my discussions with fellow athletes, nearly every triathlete and coach has an opinion and/or training strategy for dealing with them.
There is one unusual medical problem that stands out from the others: Swimming Induced Pulmonary Edema (SIPE). I first became aware of this condition last year when I came across a blog posted by Dr Creswell on his website, Athlete's Heart. Experts are now pondering on the role of SIPE in the sudden deaths of athletes in the swim leg of triathlon.
SIPE is not fully understood. Induced pulmonary edema was first recognised in the mid-1990s when researchers focused on healthy scuba divers who experienced problems with breathlessness. It is thought that when an athlete immerses him/herself into cold water, a reflex response triggers physiological changes in the body. While this is a perfectly natural phenomenon sometimes these changes can be significant enough to cause pulmonary edema where blood leaks into the airspace of the lungs.
Typical symptoms can include cough, fatigue, shortness of breath, and coughing up of pink frothy sputum or blood.
In a case report published in Pulmonary Medicine, the authors Carter and Cole point out that many athletes may suffer a minor case of SIPE, which will simply resolve on exiting the water. The athlete may simply think he or she had a "bad day", and perhaps swallowed too much water. In serious cases, failure to recognise these symptoms and respond quickly may lead to seizures and loss of consciousness, clearly life threatening in the open water.
Seasoned triathletes who experience breathing difficulties during a race can be caught by surprise.
Creswell highlights the case of a triathlete identified as KAP who recalls her experience in a thread at Slowtwitch, an online forum discussion. I am posting some of her conversation here because I believe it will resonate with most triathletes in the community, elite and recreational:
"The tri where I experienced SIPE was one I had done 8 times before, so I was very comfortable with the swim course, conditions and everything. That is why, when I was halfway way through my swim and my legs felt like I was dragging kettle bells, I was perplexed. I thought I might have gone out too fast, I thought I might have been too "jazzed" up. And I was convinced it was in my head. So I switched to pulling. When my arms started to shut down is when I knew something was wrong. I sighted to see if I could make it to the buoy to just "hang on" and gather my wits. I realized I couldn't make it because I had developed a cough where I couldn't seem to get any air in. At that point I waved my arm to get attention. And even that was difficult."
KAP's take home message should strike a strong chord for athletes who are highly intrinsically motivated and hell bent on completing a race despite adverse events. She highlights the imperative to listen to your body and not simply attribute symptoms to a sign of mental weakness:
"I hope my experience helps to shed light for other athletes out there. I strongly urge you to listen to your body. If something doesn't feel right, it is not right, and remove yourself from the situation. I know first hand how difficult that is to do. This was my first DNF. But I was lucky. I was experienced enough to know my body well - and even then I was questioning if my symptoms were all in my head."
There seems to be no way of predicting the likelihood of SIPE. Athletes like KAP report having a random, one-off event of SIPE and making a complete recovery without experiencing any repeat episodes.
Treatment involves removal of the victim from the water and emergency assistance, if required. Supportive care with rest and oxygen usually see the symptoms completely resolve.
For those of you wanting some background on the physiological mechanisms behind SIPE, here is a simple overview of the relevant processes.
Cold water contacting the face during immersion activates our so-called 'mammalian diving reflex'. This reflex drives physiological changes in our body, to conserve oxygen and help us stay under water longer. Essentially, the reflex slows our heart rate and narrows the blood vessels in the extremities.
A slow heart rate (bradycardia) sets in, which decreases oxygen requirements of the heart muscle and sees less oxygenated blood pushed to the periphery.
A narrowing of blood vessels in our extremities (peripheral vasoconstriction) is triggered so that blood circulation there is shut down and redirected to our oxygen-sensitive organs (i.e., heart and brain).
As the blood shift takes place, blood collects in the torso (thoracic) region of the body. Blood vessels in the lungs become engorged with blood and expand, filling up the lung tissue, which leads to a shrinkage of the air sacs (alveoli) in the lungs. This sees a reduction in lung airspace volume.
If there is significant difference between the blood pressure in the pulmonary capillaries (small blood vessels of the lungs) and the gas pressure in the lungs, then capillary stress failure can occur. This results in leakage of blood and plasma out of the capillaries into the airspace of the lung, a condition called pulmonary edema.If you are interested in reading further, Dr Rudy Dressendorfer writes another really useful article on the causes of acute pulmonary edema in triathletes.
Harris KM, Henry JT, Rohman E, et al. 2010. Sudden death during the triathlon. JAMA,13:1255-1257.
USAT Fatality Incidents Study. http://www.usatriathlon.org/~/media/d0cc25327b574798934fca3366270f12.ashx
Triathlon fatalities aren't going away. April 25 2014, British Journal of SportsMedicine (BJSM) blog. http://blogs.bmj.com/bjsm/2014/04/25/triathlon-fatalities-arent-going-away/
Author: Kara Gilbert @ KMG Communications
The post Open Water Swimming in Triathlon: Even healthy athletes need to be aware of the heart risks appeared first on Heart Health for Athletes.
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