Almost-the-Last-part Acid Base Balance: Potassium, Acid/Base, Elyte supplementation
|September 8, 2013||Posted by Melinda under Vet & Sports Medicine|
Moving onto Potassium.
Recall that for most of the sodium discussion we were talking about ECC. This is because the majority of Sodium is outside the cells.
Do you remember where the majority of Potassium is stored? Inside the cells (ICC).
Recall that we can only measure what is in the plasma, which is part of the ECC. Also recall that the divider between the ICC and the ECC does not allow potassium or sodium to freely flow go between the compartments.
When we “measure” potassium, we are measuring the potassium that is in the plasma, which is a relatively small proportion of the body’s potassium. Based on how we know stuff moves between the different body compartments (or doesn’t) allows us to make assumptions of what’s happening in the entire body, even though we only have a plasma measurement.
Important point: Small changes in potassium plasma has HUGE consequences, so the body regulates it within a very narrow range – much more narrow than sodium.
Potassium = electrical signals
Your heart runs off of electrical signals. It’s very important that potassium levels remain in their very small range.
Because control of potassium is so important, it turns out that potassium is rather boring from an exercise physiology perspective, because the body has developed to be really good at maintaining it within it’s range, because the consequences of NOT doing that are catastrophic. (DEATH!!!!!!!).
In fact, you already know one of the mechanisms the body uses to control potassium.
Remember ALDO? At decreased plasma volume ALDO tells the kidney’s to retain sodium (which helped move water into the plasma space to increase plasma volume). At the same time, it increases the elimination of potassium from the plasma.
There are actually two signals that tell ALDO that it needs to increase sodium retention and get rid of more potassium.
1. The first signal is the loss of water and sodium in sweat that reduces the volume of plasma.
The second signal is an increase of potassium in the plasma. As water and sodium leave the plasma as sweat, potassium is left behind. As a result, even though the total number of potassium molecules haven’t changed, the concentration of potassium is increasing because there is less and less water in the plasma.
The body needs to get rid of potassium, and preserve sodium and ALDO fits that description perfectly.
Except for one problem. ALDO is a long term mechanism in the kidney, and because small changes of potassium in the plasma can be deadly, the body needs a short term immediate solution!
Buffering in the intracellular compartment (ICC) is a much much faster way of minimizing changes of potassium concentration in the plasma.
pH = number of hydrogen (H+ or “H”) ions floating around.
Depending on the pH, potassium is either moved in or out of cells.
Acidosis = increased number of H ions in the plasma. In this state potassium is moved out of cells and into the plasma. If you measured potassium levels they would be relatively high (remember when you are “measuring” something – you are measuring plasma).
Alkalosis = decreased number H ions in the plasma. The cells take up potassium from the plasma and the amount of potassium measurable in the plasm decreases.
You aren’t likely to have too little potassium in the body because it turns out that getting enough potassium through the diet is really easy. Most foods have more than enough potassium. So, it’s not an electrolyte I’m necessarily concerned about during an endurance ride – it’s not being lost in huge quantities (minimal loss in sweat), and it’s fairly easy to replace in the normal diet, even if you (or the horse) aren’t eating that much.
Bottom line: potassium levels seem to take care of themselves for the sake of our endurance horse discussion. Potassium levels in the plasma are linked to the pH and acid base status. Acid base status and pH are linked not only to potassium but a HUGE wide range of critical cell functions.
While potassium is rather boring, acid base status during exercise is much more interesting! So my vote is that we move on from potassium, to the broader and more exciting world of acid base.
First, realize I am NOT giving you an entire acid-base discussion – instead I am picking and choosing what aspects and disorders are relevant to our discussion about the endurance horse. There’s a ton of acid-base balance considerations and disorders if your horse has crappy kidneys, or if your horse has some sort of endocrine disorder…….but let’s just focus on the concepts relative to the healthy endurance horse for now.
Acidosis = increased hydrogen ions
Alkalosis = decreased hydrogen ions
Technically there are additional terms I should be using like “acidemia” and “alkalemia” but since the differences between these terms and the ones above I consider subtle and not important for understanding the concepts, just ignore me if I start using them interchangeably…….
We’ve used the term “buffer” so let’s define it.
Buffer = a hydrogen ion sponge.
When hydrogen ions are increased, buffers bind hydrogen.
When hydrogen ions decrease, buffers releases hydrogen that was previously bound to it.
When an hydrogen ion is bound, it no longer contributes to the pH. So, having a buffer present minimizes the changes in pH caused by and increase or decrease in hydrogen ions. The buffer may not be able to totally eliminate the pH change caused by the change in hydrogen ions, but the pH change is less than it would have been other wise.
For example, pretend we dump 20 hydrogen ions into a solution that does not contain any buffers. All 20 H+’s would cause a pH change.
Now pretend our solution contained buffers that were capable of binding to 10 H+’s. When you dump those extra 20 H’s in, 10 of them would be bound, and only 10 H+’s would be acting to cause a pH change – a much smaller pH change than when all 20 H+’s were causing a change.
Now pretend our solution contained enough buffer that it was capable of binding 20 (or even more! 30 or 40!) hydrogen ions. Now when you add 20 hydrogen ions, all of them are bound and the pH doesn’t change at all.
The body can use lots of different things as buffers, but one of the most important involves bicarb and CO2.
Bicarbonate is the “hydrogen” sponge or buffer. When there’s an increase in hydrogen ions, bicarb binds to the hydrogen, and turns into water and CO2.
Binding the hydrogen ion makes it “disappear” from the body’s “pH calculator” and it doesn’t cause pH to go up or down.
Body pH depends on the ratio between bicarb and CO2. I like to remember the equation A = B/C to help me remember what happens to the pH under different circumstances. B = bicarb, C = CO2. A = body pH. The ratio between B and C must remain constant. If one goes up, the other must go down in order to maintain pH at a constant level. If B or C gets out of balance, pH changes.
If the amount of hydrogen ions decreases, less bicarb will bind to hydrogen and turn into CO2. The amount of bicarb increases and the amount of CO2 decreases. Considering the equation A= B/C ==> A (pH) increases in this situation, meaning that you now have ALKALOSIS.
If the amount of hydrogen ions increases, more bicarb will be “used” up binding to it and turn into CO2. Thus you have less bicarb and more CO2. Using the same equation, A now decreases meaning that you now have ACIDOSIS.
In general there are four different scenarios or problems that can occur in the balance between CO2 and bicarb.
In the picture below, the BLUE arrows represent what initially caused the pH change. The red arrows represent how the body tries to compensate to bring the bicarb:CO2 ratio back to normal (and thus pH back to normal).
Fortunately for us, only ONE of these scenarios is likely to occur in our endurance horses in an endurance race.
Metabolic alkalosis (top right hand corner)
In our normal healthy endurance horses with nice normal healthy lungs, CO2 doesn’t build up because the lungs are very efficient at “blowing off” CO2 as fast as the body can produce it (getting rid of increased bicarb takes the kidneys a little bit longer). So, respiratory acidosis is not likely to occur. Respiratory alkalosis is also unlikely to occur in our healthy lung/healthy athlete horse scenario.
At slower speeds and shorter distances, there is no significant acid-base disorders.
However, as the sweat loss of water and elytes occurs at elevated rates, a slowly progressing metabolic alkalosis occurs, especially in dehydrated endurance horses – as a direct result of sweating.
The way of thinking about acid-base that we’ve discussed up to this point is helpful to understand how and why the horse is compensating. Referring to our chart for metabolic alkalosis, I see that bicarb must be rising, which would cause the pH to rise (become alkalotic). The lungs are going to compensate for this by blowing off less CO2 than normal to try to and return the pH to normal. Lungs compensation occurs quickly, kidney compensation occurs more slowly.
What might be less clear is how sweating (loss of water, sodium, and chloride) is making bicarb increase in the first place.
One “fact” I was given in school during clin path discussions is that in “primary metabolic alkalosis” (which is what we have in endurance horses), bicarb is increasing in response to the loss of chloride.
The horse is losing chloride in it’s sweat, decreasing both concentration and total content, and the bicarb is being retained in it’s place.
Increase in bicarb is an increase in the “base” in the blood. pH rises, and “alkalotic”.
As you can imagine….it turns out acid base is not nearly as simple as these equations that I was forced to memorize and dutifully regurgitate on tests, and that I’ve presented here to you.
Hinchcliff tried its best to convince me that instead of this “traditional” view of acid base that “is limiting and simplified”, I should instead use a “physiobiochem” something-or-other-system to evaluate and discuss acid base.
Considering I STILL don’t get this “new fangled” approach and I’ve been over it 3x with a giant white board……I’m not sure I’m the best person to try and explain it. But there’s an interesting phenomenon that occurs during this alkalonizing effect due to Cl/Bicarb.
Instead of looking at Bicarb, CO2, and pH and their ratios and effects on one another, Hinchcliff says I should care about “SID”.
*SID = strong ion difference = anions-cations = (Na+K) – (Cl + lactate)
==> amounts of these free ions (which just like the hydrogen ions in the other method, can contribute to pH because they aren’t bound).
==> remember that this equation refers to the concentrations of these ions in the plasma – which is the only place they can be measured!
*Anions = postitively charged ions like sodium and potassium. Cations = negatively charged ions. The SID equation starts off more complicated and then they went on and on and on about how you could justify ignoring a bunch of the different things (like magnesium and calcium and…) so I just skipped to the end and am giving you their “working” equation ==> which consisted of these 4 ions.
We’ve already established that when endurance horses sweat they are losing a lot of chloride. While Na is being lost in the sweat at roughly equal concentrations to plasma levels, Cl concentration in the sweat is higher than plasma (because Cl is attracted to the Na, has to do with total “charges” being lost in the sweat and electroneutrality). Remember that Na concentrations in plasma, even after lots of sweating is relatively unchanged even though total Na content of the body has decreased. However Cl concentration in the plasma AND total content has decreased.
Horses can lose 30L or more of sweat with minimal changes in plasma sodium concentration. Potassium is mostly stored inside cells, and the body is quick to correct any abnormalities because of K’s tie to electrical activity. So, we can assume that the first part of the SID equation (the anion part) is the same as before the sweat loss. And, turns out that lactate (portion of the second part of the equation) does not accumulate in low-intensity endurance exercise.
Thus we are left with Cl as the ion that has the biggest influence on the SID equation after sweat loss.
Turns out that the loss of lots and lots of negatively charge chloride causes alkalosis, because of the retention of bicarb. (I know I already said this, but repetition on these concepts helps!)
BUT, It turns out that the metabolic alkalosis is not as severe (ie the pH doesn’t rise as much) as predicted by the amount of chloride ions (and thus bicarb being retained)
That’s because as water and chloride leave, there’s a counteracting “acid” effect from other things that aren’t included in the SID equation.
As water leaves the plasma as sweat, the plasma proteins and cells (like redblood cells) are left behind. These cells and proteins are some of the very few things that cannot pass between the barrier that separates the ECC into “plasma” and “other space outside of cells”. Here’s a reminder of the compartments.
Because the plasma proteins and cells in the plasma cannot redistribute, as water leaves the ECC they become more and more concentrated in the plasma.
Because of their molecular composition they act as “acids” , and lower the pH slightly from what would be expected from the chloride loss.
To put it another way, the loss of chloride is acting as increasing the “B” in the A= B/C equation. The plasma proteins and cells in the plasma are acting like the “C”. A little increase in C offsets the big increase in B just a bit, with the net result being a pH that is a little closer to normal, than if there was no change in C.
Here’s what I find REALLY interesting.
One of the adaptations of training is to increase plasma proteins. Another training adaptation in sweaty, hot conditions is to sweat more efficiently, with a decrease in chloride lost in sweat (decrease in sodium loss, decrease in overall sweat loss).
Losing less chloride would minimize alkalosis. Increasing plasma protein could theoretically increase the acidotic effect……with the net effect being an even smaller degree of alkalosis.
Hinchcliff mentions that in one study “properly electrolyted endurance horses” did not develop this slowly progressing metabolic alkalosis characteristic of slow-intensity endurance exercise. However, it doesn’t seem to be clear to anyone what “properly electrolyted” actually entails on a practical and useful level, except that the net result was no metabolic alkalosis at the end of the ride in this study.
I wonder whether the effects of conditioning (decreased chloride loss, increased plasma protein) could have a similar effect of making the metabolic alkalosis go away?
Diet or eating could be a factor too.
It turns out that the balance of cations/anions in the horse’s food can impact their acid base balance. For some reason when we are talking about cation/anion balance inside the horse it’s called “SID” and when we are talking about their food it’s called “DCAD”.
DCAD = balance of cations/anions
There can be low and high DCAD diets, meaning that the relative amounts of cations is higher than anions or vice versa. Some of the studies are interesting…..but they aren’t totally in agreement and there is a lot of “inconclusive” data, especially when the diets on a long-term basis – some studies show that by feeding a diet that isn’t balanced DCAD, you can actually cause chronic systemic alkalosis or acidosis in horses.
What was MORE interesting to me was this little factoid:
Feeding a mixed hay forage + grain results in rapid (1-3 hours post consumption) changes in plasma electrolytes and acid base. There is actually a systemic plasma acidosis!!!!!!!
Time for a little recap.
1. Endurance exercise causes a slowly progressing metabolic alkalosis
2. Studies have shown that “properly electrolyting” endurance horses can eliminate metabolic alkalosis
3. Some of the adaptations to training seem to mitigate the alkalosis
4. Eating causes an acid base balance effect that is opposite of what occurs during endurance exercise.
==>I could not find a study that looked at how eating affected the acid base balance of an endurance horse.
==>How training adaptations affect acid base balance in endurance horses has not been well studied.
I think these 2 points are critical to understanding the how best to support endurance horses – specifically in the realm of acid base balance – through endurance rides.
So far on this blog (and in this series) we’ve talked about a lot of physiological parameters – plasma volume, sodium concentrations and total sodium, electrolyte availability, hydrogen, heat training, sweating……But what does this actually mean in the BIG PICTURE of moving down the trail 50 or a 100 miles at a time?
Depending on what sport you are asking your horse to compete in, why horses get tired and fatigued and what limits horse performance differs.
According to Hinchcliff, 3 day eventing horses are limited by their capacity to thermoregulate. Draft horses are limited by the strength of muscles, Standardbred/Thoroughbred racing horses are limited by oxygen transport.
What about endurance horses?
Ummm…..not quite as straightforward. Here is what Hinchcliff (which has chapters written by different authors) managed to say at various points, some of it sorta contradictory.
1. Endurance horses are limited in their performance by their capacity to maintain fluid and elyte homeostasis (balance).
2. There is no marked accumulation of lactate and “acidification” is NOT a major cause of fatigue in endurance horses.
3. Shortage of fuel and glycogen stores might play a role in endurance horse fatigue. Low blood glucose concentrations would limit the amount of glucose available to central nervous system and among other things, contribute to “Central Fatigue” rather than fatigue associated with muscle work overload etc.
4. Factors NOT related to substrate supply (like fuel and glycogen stores….) are more important in fatigue development, such as the loss of elytes in sweat.
So, what I got out of that is that we aren’t sure why endurance horses get tired.
It might be because they get dehydrated, or their elytes levels get screwed up. It’s probably NOT because of lactic acid build up in the muscles, or because of a lack of muscle strength. It might be because they get “low blood sugar” (or it might absolutely NOT be that….).
Good to know. (there was a bit of sarcasm there….)
In the previous post of the series I touched on some of my reservations of electrolyte supplementation, and I won’t repeat that here. What I would like to end with is what information I was able to find on electrolyte supplementation for endurance horses.
Electrolyte loss in training
I think we briefly touched on this during our sodium discussion but let’s expand that a bit.
Known fact: horses lose LARGE amounts of key electrolytes in their sweat (remember – their sweat composition is different from ours)
How much do they lose: Ummmmm………
– Old studies had questionable figures because older methodologies were used that overestimate losses.
– Newer studies still confirm sweat is hypertonic to plasma and “substantial losses” occur during endurance exercise.
– Exact amounts lost “depend on activity and duration”. Nice a specific eh? :). While the older studies seem to delight in conjuring up visions of glasses and piles of salt, the newer ones seem a bit more “hedgy”.
– Primarily Sodium and Chloride are lost
– Chloride loss is what is primarily responsible for the slowly progressing metabolic alkalosis.
Do you need to supplement? How do you supplement?
Hinchcliff, usually eager to provide recommendations at the end of each chapter on training and injury prevention is curiously silent on the subject of electrolyte supplementation except to say that with “effective electrolyte supplementation strategies” the metabolic alkalosis doesnt occur, and “without replacement there are substantial deficits during endurance activities”.
In summary, specific electrolyte supplementation advice is vague.
-Effects of training on electrolytes or acid base balance aren’t understood.
-Electrolytes and sweat between horses and humans are different and make studies not easily interchangeble.
It’s important to consider the individual. According to a lot of the human literature, because I’m not losing potassium in my sweat and as a human my sweat is very hypotonic, I shouldn’t need to supplement with electrolytes as much as I do in order to perform athletically. But I do need them. *shrug*. Like we discussed in the previous posts, biochemistry adapts with training just like the rest of the body systems and there may be those individuals that don’t adapt as well as the rest, or an individual that may need more “support” during a transition to a longer distance.
Keep in mind that on the human side there was a lot that we thought intuitively made sense that would help or support athletic effort that did NOT.
The horse gut is a powerful reserve that we humans don’t have.
Considering having a salt source for the horse at the end of the ride. I saw a comment that horses can potentially rehydrate too fast at the end of an endurance ride – such as a 100 – ahead of replacing the sodium lost during a ride and can end up with sodium levels that are too low (hyponatremic). This is definitely not so good for the horse’s brain. And while the brain of the horse is microscopically tiny, apparently they need it to live because messing with the brain makes the horse rather unhappy (can you tell that it is almost 1am and I’m still writing? I started this thing at 8:30p or so). I have no idea if this is a real concern and has really happened….. or a made up concern by someone in a lab, but throwing everything I have at you guys….
Based on the effects of eating and the post-feeding acidosis, consider your “elecrolyte program” to include more than just the powder you throw in your horses feed dish, or into an oral syringe.
There are 3 situations that were specifically cited as problematic for electrolytes and you may want to consider supplementing:
1. Larger than normal fluid or elyte losses because of exercise in hot or humid conditions. After reading through this concept it looks like they are more concerned with maintianing hydration which is the key to thermoregulation than any actual deficits or imbalances with elytes
2. Competition following long periods of training without water available. I would hope that most endurance people would trailer in the night before. If a horse can rehydrate after a 100 mile ride like Tevis over night (per my professors, who do a bunch of the Tevis research every year), I’m pretty sure it can perform a similar miracle if I show up the afternoon before the ride.
3. Limited recovery time between phases of 3 days competitions or multiple event competitive events. Multi-days came to mind. Perhaps the hydration considerations on multiday rides are different than one day rides or 100’s. Although, I suspect that in general, multiday horses have time to rehydrate overnight.
I got Farley’s blood results from Tevis Robinson’s Flat (36 miles into the ride) and in the next post, I’ll talk about the results in the context of what we have been discussing.
[…] both a decrease in total amount of chloride AND a decrease in chloride concentration in the serum. (Here’s a post that details the mechanisms for those of you that need a refresher. From this point I’m going […]