We've written about what hyponatremia is and how it can pose a risk to athletes competing in endurance events (and individuals working in extreme conditions) before in some detail. But, to bring you up to speed, hyponatremia is a medical term describing low (hypo) blood sodium levels (natremia – 'Na' being the chemical symbol for sodium).
The common cause of the condition for athletes is excessive drinking, which leads to a dilution of sodium levels in the blood. This can be made worse by the loss of sodium in sweat during prolonged exercise.
When blood sodium levels drop below this ideal range initial symptoms can include nausea, lethargy, muscle cramps, weakness/fatigue, headaches and/or restlessness. If these symptoms sound familiar and you've experienced them towards the end of prolonged periods of exercise, then hyponatremia is something you're going to want to read up on.
Hyponatremia is a hot topic in the world of sports medicine research, mainly because, although the numbers of serious cases are relatively small, some athletes still get pretty sick - or even die - needlessly from the condition every year. Arguably this is due to a lack of widespread understanding of what causes it and how to treat it.
In 2015 there was a large conference organised in Carlsbad, California where world leading experts on hyponatremia were invited to present their latest research findings and opinions. The main output from this conference was a revised ‘position statement’ on Exercise Associated Hyponatremia (EAH). The report is an impressively comprehensive, 9,000 word body of work.
Sadly, we were not able to attend the conference in person - a real shame as the surf in Carlsbad is also amazing - but I did sit and watch all of the presentations on YouTube afterwards and learned a lot from that. I also reached out to many of the experts who attended in order to try to connect with them around what we’re doing with Precision Hydration as it's very much related.
One of the speakers who was kind enough to agree to a chat with me after the event was Dr Doug Lewis from Wichita, Kansas. Dr Lewis has an interesting background; he's a Cystic Fibrosis doctor by day (individuals with CF often have very high sweat sodium losses) and at the weekends he's an avid triathlete, having completed Ironman Arizona a staggering 10 times in the last 10 years!
As Dr Lewis and I exchanged many calls and emails, it became clear that we had some similar unanswered questions floating around in our heads about athletes, sweat sodium loss/replacement and hydration. Doug has a very high sweat rate - as do I - and had discovered (via some organised trial and error) that taking in higher levels of salt with his drinks in long, hot races had had a positive impact on his performances.
He also has a professional interest in the topic due to his work with Cystic Fibrosis patients. So we started bouncing ideas around for research projects that might help produce some more concrete information (known in the research world as ‘evidence based guidelines’) to help athletes and CF sufferers get their own hydration replacement levels dialled in more accurately.
As conversations evolved Doug introduced me to Dr Tamara Hew-Butler. Tamara is an Associate Professor of Exercise Science at Oakland University in Detroit and one of the world’s leading authorities on Exercise Associated Hyponatremia. She was in fact the lead author of that hyponatremia position statement back in 2015, so it was pretty exciting to connect with her.
Now, one of the areas of controversy in the study of exercise associated hyponatremia is what the various causes of it actually are. Quite a few studies have been done seemingly demonstrating that drinking more that you can sweat or pee out is the key factor leading to the condition developing and "over-drinking" remains the number one "bad guy" in the room.
But, if you also do a lot of sweating and/or lose a lot of salt in your sweat - as CF patients or athletes with higher sweat sodium losses do - logic suggests that this could also make the condition worse, or more likely to occur in the first place.
This is probably why some people who don’t get diagnosed with CF until well into adulthood do so when they've developed hyponatremia in hot weather (as in this example). Not all researchers agree on this point, but Drs Hew-Butler and Lewis were keen to investigate this theory and saw a collaboration with Precision Hydration as a way to dip into this area.
To get the process underway, Dr Lewis highlighted 2 very interesting hyponatremia case studies he had become aware of in recent years. One was of an adult CF patient who'd developed EAH after a week working as an aid volunteer in hot and humid Haiti and the other was of an triathlete who doesn't have CF, but who got hyponatremia following an Ironman event back in 2014.
Both of the individuals highlighted were ill enough with hyponatremia that they had to be admitted to hospital and in fact could easily have died if they did not receive proper medical attention.
Luckily, their hospital records were very detailed, so Dr Lewis and Dr Hew-Butler had access to enough information to compare and contrast precisely had what happened to them both and could speculate on whether over-consuming dilute drinks - and possibly salt loss through their sweat - was implicated in their development hyponatremia.
The interesting part for us at PH was that we were asked by the good doctors to Sweat Test the two individuals and comment on the cases. As expected, the chap with CF loses a very high amount of sodium in his sweat; ~2,900mg of sodium per litre of sweat. That's compared to an average of ~950mg/l for healthy individuals from the thousands of tests we've done over the years.
But, the triathlete also had sweat sodium losses that were approximately double the average, coming in at ~1,880mg/l. Whilst this level is high, it's not off the charts (my own losses are very similar) and, in fact, a significant percentage of athletes we've tested in the past have shown similar levels of loss (or even more as in this case from one test a few years ago).
Having reviewed the evidence, Dr Lewis and Dr Hew-Butler wrote the two examples up into a ‘case report’ to submit to a peer-reviewed medical journal in order to share them with the wider scientific community to forward knowledge in this area and stimulate more discussion on the role that sodium loss in sweat could be playing in development of exercise associated hyponatremia.
Now, there are a lot of peer-reviewed medical journals in the world (‘Hepatitis Monthly’ having the most catchy title of all the ones I've come across in my time) but one of the most influential and credible is The BMJ (formally known as the British Medical Journal) and we waited for quite a while to see if this highly prestigious journal would consider our work useful, correct and worthy of publication.
After a few months of deliberation and clarification (thanks to Dr Lewis for doing the heavy lifting when it came to the re-drafts!), our paper, "Considering exercise-associated hyponatraemia as a continuum" was finally accepted and published.
Essentially, the big take home message from the paper is that there's evidence that high sweat sodium losses can be influential in the development of exercise associated hyponatremia (along with a relative overconsumption of fluids) and this is neatly summarised in the learning points highlighted at the end of the paper itself (with it broken down in layman's terms in my italics)...
1) Exercise-associated hyponatremia (EAH) probably exists along a continuum.
i.e. EAH can be caused purely by over-drinking, but also by a combination of heavy salt losses through sweating and only moderate fluid consumption. The traditional view is that hyponatremia is caused solely by over-drinking and that salt loss in sweat is irrelevant and we'd challenge this.
2) EAH is always due to a component of over-hydration relative to the available exchangeable sodium reserves.
i.e. for hyponatremia to occur, you have to dilute the available sodium in your body and that available sodium differs from person to person depending on the rate of loss through your sweat.
3) The higher an individual’s sweat sodium concentration, the easier it is to over-consume fluids relative to exchangeable sodium reserves.
i.e. If someone has higher sweat sodium losses, the available sodium stores in their body can be depleted more quickly than other people, making it easier for them to dilute their levels, even if they don't over drink dramatically.
4) As sweat sodium concentration increases on the EAH spectrum, the more likely it is that an individual needs sodium replacement along with drinking to thirst to prevent EAH and maintain performance. This is true even for those with cystic fibrosis.
i.e. People who lose more salt in their sweat (or just sweat more) are increasingly more likely to need to supplement sodium with the fluids they drink during exercise to avoid hyponatremia and maintain their performance level.
5) The development of evidence-based sodium replacement guidelines is essential during prolonged exercise, especially when held in hot and humid climates.
i.e. We need to be able to offer athletes (and people with CF) better guidelines (based on scientific evidence) about roughly how much salt and fluid they need to replace based on their individual sweat and sodium losses. Especially in hot and humid conditions and for long duration exercise.
Needless to say, we’re extremely proud to have put another brick in the wall of knowledge that's currently being built around the personalisation of hydration practices and sodium replacement guidelines for athletes.
This paper comes hot on the heels of our first paper - Normative data on regional sweat-sodium concentrations of professional male team-sport athletes - which was published last year, so we’ll be having a drink (but definitely won't be over-drinking!) this weekend to celebrate.
We also need to say a huge thank you to Dr Doug Lewis and Dr Tamara Hew-Butler for being open to collaborating with us on this piece of work in the first place (and for doing most of the hard work in getting it written up!). We’re still in regular contact both of them and hope to be doing more collaborative research in the not too distant future.
By the way, if you’re keen to learn more you can read the abstract of the paper online. The full article is behind the BMJ paywall, so if you're not a BMJ subscriber but you're keen to read the whole thing, drop us a line at firstname.lastname@example.org and we’ll see what we can do about reading it out over the phone to you or something like that ;-)