Hi Everybody! I have been enjoying the discussions from the wings for a while now but since Truman Prevatt hinted that I am shy regarding the work I have been doing, I decided to prove him wrong and offer some of what I have been studying with the rest of you.
My background is that I have a Ph.D. in Pharmacology, specializing in renal and cardiovascular,and have been teaching Medical school for 8 years now. My husband, Carlos, and I got involved with endurance 2 years ago; He rides and I crew. We have 2 boys Daniel, 9, who also rides with his father, and Scott, 5 who helps Mom. Our most recent accomplishment where we "field tested" some of my knowledge was the Old Dominion, where Carlos and Cody were 1 of the 10 to finish the race. Cody`s recovery rates at all the vet checks were 2 minutes or less, with no need to sponge him for cooling, even though the temperatures were in the 90`s and humidity was the same. Much of the success is due to the fact that Cody is a remarkable horse, and we like to think that our planning and program helped with the rest.
Just a little background on electrolytes to begin with. The major electrolytes that are of importance in the endurance situation are sodium (Na+), potassium (K+), calcium (Ca2+), chloride (Cl-) and magnesium (Mg2+). Of all of these, K+ is the most crucial to maintain in order to avoid most of the metabolic problems, such as "thumps" and cramping and "tying-up".
Without going in to a complete lecture, the body is extremely efficient at reabsorbing Na+ in the kidneys in order to reabsorb water during periods of dehydration. This Na+ reabsorption and water reabsorption is done at the expense of K+ losses. In other words, when the horse starts to become dehydrated his kidneys will filter the blood and reabsorb almost 99% of the Na+ in it. Whenever Na+ is reabsorbed back into the bloodstream water will follow so that the urine output is decreased and the animal conserves water. The downfall is that as the kidneys reabsorb this Na+ back into the blood, they are eliminating K+. Therefore the urine contains a lot of K+ and little Na+.
This K+ loss in the urine is compounded by extreme K+ losses in the sweat. K+ may be concentrated in horse sweat 10-20x greater than in the blood.
Other factors causing K+ depletion in these horses are alkalosis, which results from the horses breathing rapidly, epinephrine (adrenaline - which is really flowing at the beginning of the race!) and insulin release, which occurs most when the animals are fed sugary concoctions.
So what`s the big deal about K+? K+ is the electrolyte in the body that is responsible for setting the "resting membrane potential" of all electrically active tissues; which includes the heart, the entire nervous system, and the response of muscle tissue to contract. The "resting membrane potential" is going to determine
1) How sensitive the tissue is to electrical stimulation.
2) Whether that tissue will react, or whether it will relax.
3) How fast the tissue will react.
4) Whether the tissue can react a second time, or does it becomes refractory.
For those who don`t care about all the background, the bottom line is that K+ depletion will lead to:
1) Vasoconstriction and reduced blood flow to the muscles. This will result in cramping, tying-up and the breakdown of muscle tissue. When muscle tissue breaks down (known as rhabdomyolysis) it releases a protein called myoblobin. Myoglobin is toxic to the kidney - resulting in damage and reduced ability of the kidneys to compensate for further dehydration and reduced ability to rehydrate after the race.
2) Increased sensitivity of the nerve that controls the diaphragm and therefore respiration rate. When this nerve (the phrenic nerve) becomes sensitive it begins to respond to the electrical impulses coming from the pacemaker of the heart and will fire and cause the diaphragm to contract in synchrony with every heartbeat. This is "thumps" - or medically known as synchronized diaphragmatic flutter.
Treatment of thumps usually entails the administration of electrolyte solutions containing extra calcium. The calcium itself will suppress electrical activity, therefore it will decrease the sensitivity of the nerve to the diaphragm so that it does not respond to the heartbeat. However, calcium alone does not treat the underlying cause of the problem, which is potassium depletion (compounded by alkalosis). Thumps can be avoided by maintaining K+ to begin with.
So the question of the day is "How much K+ is needed to avoid these problems?" Obviously there is much research aimed at just this question. The point is, that a 2 oz. dose of standard electrolytes is nowhere near sufficient to make up for what the horses are losing. In addition, some calcium is essential to balance what is happening electrically in the animals.
The electrolyte formula that I used for our horse at the Old Dominion was 4 oz of the powdered Equilytes (which would be 1420 mg of K+) plus an additional teaspoon of KCl (which is an additional 2240 mg of K+) mixed in unsweetened applesauce. We administer this every 10-15 miles, which often means between vetchecks. In addition, early in the race I add 600 mg of Ca2+ with Vitamin D to the electrolyte mixture.
A few words about calcium. No matter what form it is in, the absorption of calcium out of the gut into the bloodstream is absolutely dependent on vitamin D. In horses fed routine diets of alfalfa which contains high amounts of calcium and phosphorous, these animals have shut down the production of the hormone that is responsible for signalling the manufacture of vitamin D. Therefore they do not absorb calcium when it is presented to them orally in electrolyte solutions. The calcium then remains in the gut and will suppress electrical and muscle activity in the gut and can lead to suppression of gut motility, colic and impactions. Even if the horses do not receive alfalfa in their diets, too much orally administered calcium may reduce gut motility. If gut sounds are not normal, I do not add extra calcium to the electrolyte solution. However, I always give calcium with VITAMIN D.
Now as you can all see, I am never short of words so I would like to dispel the myth that I am "shy". I hope this will help some of you understand the overall importance and "why" we give electrolytes. Let me finish by saying that I have not had the opportunity to do the necessary blood tests on a large number of horses to absolutely document our results. I do know that under the most extreme conditions our horse had unbelievable recoveries (1-2 minutes) and never showed any indications of cramping or metabolic problems. His pulse after trotting him out for the CRI was many times lower than the initial reading. This is a young 6 year old gelding who has less than 500 total miles.
I would love to hear anybody else`s opinions or answer any questions you might have. You know where to find me!
(continuation of electrolyte discussion with emphasis on thumps)
I am pleased to know that some of you found my first article on electrolytes helpful. Stephanie Teeter let me know that in can be found on the endurance homepage along with other articles by Dane Frazier, Mike Tomlinson and Greg Meyer.
With regards to the article by Dane Frazier and the importance of Calcium in the development of "thumps"-SDF, I would like to express my agreement with his review of the role of calcium as a second messenger in many cell physiological processes. Calcium is an absolutely essential electrolyte and the number of roles that it plays can not be completely listed to this date. However, even the cellular concentration of calcium is linked to potassium. For any of you biochemists out there:
1) The intracellular concentrations of Na+ and K+ are main- tained by an energy requiring pump known as the Na+/K+ ATPase.
2) The Na+/K+ ATPase pumps Na+ out of cells and K+ into cells. Therefore, intracellular Na+ concentrations are low and K+ concentrations are high, with respect to outside the cells.
3) The rate at which the Na+/K+ ATPase works is dependent on how much K+ is available on the outside of the cell. When extra- cellular K+ is low the pump slows down, leading to an increase in the amount of Na+ that is inside the cell. The cells must somehow get rid of this Na+,
4) Na+ is then eliminated through 2 alternate routes. The first is through Na+/Ca2+ exchange. So that intracellular Ca2+ may actually increase, as intracellular Na+ is returned to normal. The second alternate pathway for Na+ is in exchange for protons (H+). This results in a movement of H+ into the cells, making them acidic, but leaving a deficit of H+ outside the cells, possibly(?) adding to the alkalosis of the plasma.
5) The extra calcium that is brought in through Na/Ca2+ exchange must be stored inside the cells, because if it is free, "floating" around it starts to turn on many biochemical processes as it works as a second messenger. This could be spontaneous muscle contractions (from tremors to cramping), or contraction of the smooth muscle of blood vessels, reducing blood flow and leading to further muscle cramping. In the heart it can lead to many different forms of arrhythmias and can be life threatening.
I do not want to be misinterpreted as down playing the role of calcium in the development of thumps - SDF. Normal extracellular calcium is essential for maintaining the integrity of cell membranes, for stabilizing the electrical charges across membranes, and also extracellular calcium helps modulate how much Na+ enters cells during action potentials (when the nerve fires and tells the muscles to contract). When extracellular Ca2+ is low the nerve cells become "irritable" and fire more easily. But because K+ is low, they are also more "irritable", since K+ determines where those cells are at rest. It is really a combination of many factors that leads to thumps.
I haven`t even addressed what part alkalosis (low plasma H+ concentration) plays. To make a very long story short, during alkalosis the connections between the nerve cells all down the length of the nerve fiber are called gap junctions. In order for a signal to be transmitted down the entire length of a nerve fiber the electrical impulse must pass from one cell to the next through gap junctions. When these gap junctions are narrowed, it is difficult for the signal to continue - it is meeting a high degree of resistance. When they are opened, electrical impulses can travel easily since resistance is low. Alkalosis opens gap junctions and lowers the resistance to electrical activity. Therefore, even a very small impulse can travel farther, recruit more channels and activity and lead to firing of the nerve. This is most likely also involved in thumps. By the way, alkalosis will also cause the kidneys to eliminate more potassium - complicating everything starting from ground zero. Conversely, potassium depletion (like from dehydration) will cause alkalosis, leading to decreased resistance to electrical activity. A double whammy!
I think that`s enough for tonight. There is no simple explanation of what is occuring in the endurance horses. Although I do not ride, I always crew. Electrophysiology and cardiovascular pharmacology are my obsessions. If you are interested I can supply references regarding the basics of what I have been discussing. My personal opinion regarding thumps in the endurance horse, is that it is an extremely unpredictable condition and the thumping horse should not continue. There is absolutely no way at a vet check for a veterinarian to know what plasma K+ levels, Ca2+ levels and pH of blood are. Electrolyte supplements may temporarily suppress the situation, but what is going to happen over the next 10 miles. Calcium alone may suppress the problem, but the underlying causes are very involved. I do not feel it is worth risking the horse. I would be interested in others opinions.
Lynn Crespo
Associate Professor and Chair
Department of Pharmacology
Nova-Southeastern University
My home is in Davie, FL!
lynn@alpha.acast.nova.edu
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