Muscle disorders or myopathies are a common cause of poor performance and health complications in horses. Muscle conditions that historically were classified as “Monday Morning Disease” are now better defined by a broad spectrum of disorders that result in rhabdomyolysis or ‘tying-up’ and clinically manifest with muscle pain or cramping, exercise intolerance, muscle weakness and stiffness. Many muscle disorders present with similar clinical signs, but the causes are varied. Some muscle diseases are present from birth as genetic disorders, others are acquired disorders that develop spontaneously during adulthood. Other horses may suffer from exercise-related episodes, which have been documented in approximately 3 percent of exercising horses.
Many advances have been made over the last few decades in identifying the causes of muscle disease in horses. Specific genetic mutations have been discovered that affect equine muscle function and have a breed-specific prevalence. Diagnosis using DNA-based tests can identify several specific equine muscle disorders, including type 1 polysaccharide storage myopathy (PSSM1), hyperkalemic periodic paralysis (HYPP), glycogen branching enzyme deficiency (GBED) and malignant hyperthermia (MH). There are likely many heritable muscle disorders that have yet to be identified, and this field of study remains an active and exciting area of ongoing research. Appropriate management procedures and specific dietary interventions can help reduce the severity of clinical symptoms and the frequency of myopathic episodes in horses with certain types of myopathies, including recurrent exertional rhabdomyolysis (RER), PSSM and HYPP.
DVM, PhD, DACVIM, ACVSMR
Michigan State University
Sharon Spier, DVM, PhD, DACVIM
University of California, Davis
Rhabdomyolysis, commonly referred to as tying-up, is the breakdown of skeletal muscle tissue causing painful contractures, typically in the large muscle masses of the horse, around the croup, loins and thigh area. “What has been most helpful in looking at this condition is recognizing that when horses have muscle breakdown, it is the same thing as saying an animal has colic or an animal has a cough, it is a symptom, not one specific disease in itself,” explains Dr. Stephanie Valberg, DVM, PhD, DACVIM, ACVSMR, Professor and Mary Anne McPhail Dressage Chair in Equine Sports Medicine at Michigan State University. A past recipient of the prestigious AAEP (American Association of Equine Practitioners) Milne State of the Art Award, Dr. Valberg is widely recognized as one of the world’s leading experts in myopathies in the horse, including rhabdomyolysis and its various forms. Non-exercise induced rhabdomyolysis includes inflammatory, nutritional or toxic myopathies and can also be caused by traumatic injury. In contrast, exertional rhabdomyolysis (ER) is a type of myopathy that is induced by activity or exercise. It can be sporadic, or chronic, such as in the cases of recurrent exertional rhabdomyolysis (RER) and PSSM. “The thing that is confusing about these two conditions (rhabdomyolysis and ER) is similar to what we see with colic horses, even though they all have different causes they all look painful with cramping and pawing. Horses with rhabdomyolysis all have the same clinical signs,” says Dr. Valberg. “When these horses cramp and develop muscle damage, the muscles contract and don’t relax and they’re severely painful. They start to sweat because of the activation of their sympathetic nervous system — a stress-induced response — they have a very short stride because they have severe cramping in all of their muscle groups and they may look like they are colicking because of the pain, so they can paw or lay down. Often times, that severity of muscle cramping and pain can last for a couple of hours and, in severe cases, over 24 hours when they have that kind of muscle pain.” The causes of non-exercise induced and exercise induced rhabdomyolysis differ even though, acutely, they look very similar.
“What has been most helpful in looking at this condition is recognizing that when horses have muscle breakdown, it is the same thing as saying an animal has colic or an animal has a cough, it is a symptom, not one specific disease in itself.”
— Stephanie Valberg, DVM, PhD, DACVIM, ACVSMR
Professor and Mary Anne McPhail Dressage Chair in Equine Sports Medicine at Michigan State University
Exertional rhabdomyolysis is a common muscle disorder related to exercising horses and equine athletes and involves painful constriction or cramping of the muscles during and after activity or exercise. The condition can present as a one-time acute onset of symptoms or can reoccur chronically. “You can have a horse that just sporadically develops one episode of ER, then you rest it and you get its diet balanced and the horse then goes on to be just fine, never having another episode. However, there are some unfortunate horses that will chronically have that particular condition,” says Dr. Valberg. Horses with ER may develop a short stride or refuse to move, sweat excessively and may develop firm, tight muscles especially in the gluteal muscles and hind limbs. In severe cases, a horse with ER may produce urine that is red or dark brown due to myoglobin, a muscle protein that is excreted when there is severe muscle damage. In susceptible horses, ER may be influenced by the horse’s gender, temperament, level of stress, diet, degree of fitness along with the duration and intensity of exercise.
Sporadic episodes of ER are often attributed to exercising a horse excessively or exercising beyond a horse’s fitness level and have also been associated with inclement weather events. “Sometimes it’s a horse exerting themselves in really hot, humid weather without having enough electrolytes,” says Dr. Valberg. “Under those conditions, they’ll develop a case of tying up. You can then get everything straightened around, make sure they are fed properly and have a good base of training, and they’ll never have another episode.” Nutritional factors associated with sporadic ER may include excessive starch or sugar in the diet or a deficiency or imbalance of electrolytes, minerals and dehydration. All horses should consume 70 percent or more of their diet as hay or pasture every day, with essential omega- 3 fatty acids, antioxidants, vitamins and trace minerals supplemented to provide ideal levels that are most often lacking in hay. All feed changes, including hays, should be made gradually over 7 to 10 days. The availability and importance of plain, white salt cannot be underestimated for working horses as it can be a simple way to prevent some cases of ER that can develop from inadequate electrolytes. Salt should be consistently available to all horses, and a horse should consume one to two ounces of salt daily. Higher amounts of salt will be required if the horse is sweating heavily from hot weather or intense exercise. If a horse does not seem to be consuming a salt block, one teaspoon to two tablespoons of salt can be mixed in with the regular feed daily. Consuming salt will encourage most horses to drink, which can help to prevent dehydration, and clean, fresh water should be available at all times. Caution should be used with salt supplementation if a horse will not have access to water for a period of time, such as when they are being trailered. Magnesium, calcium and phosphorus should also be included in the diet in adequate concentrations to support proper muscle function. Muscle spasms can occur if there is a deficiency or borderline deficiency of magnesium. Calcium, as well, plays an important role in normal muscle contraction and relaxation. Selenium and vitamin E are antioxidants that the horse relies on while exercising to neutralize free radicals and help prevent oxidative damage to the muscles and other tissues. Natural vitamin E (d-alpha-tocopherol) is the preferred form due to its superior bioavailability and systemic retention. It is often supplemented to exercising horses because of its relatively safe toxicity threshold and antioxidant benefits. The dietary requirements for selenium may be increased in horses working at an intense level. However, selenium has a low toxicity threshold, and all sources of selenium in the diet should first be analyzed before supplemental selenium is added.
While ER can be a one-time occurrence, those horses that experience repeated episodes of the condition become reclassified as chronic cases. Currently, the four defined causes of chronic ER include: recurrent exertional rhabdomyolysis (RER), polysaccharide storage myopathy type 1 (PSSM1) and type 2 (PSSM2) and malignant hyperthermia (MH). There are likely more underlying causes that have yet to be identified.
PHOTO BY CUTTING HORSE CENTRAL
Recurrent exertional rhabdomyolysis is thought to have genetic and environmental components that together act to interfere with the regulation of muscle contraction. A specific genetic defect has not yet been identified, however, research suggests it lies within the process of muscle contraction and relaxation. Some research suggests that RER can be caused by an abnormal regulation of calcium within the muscle cell. Horses affected with RER show an abnormal movement of calcium inside the cell, which results in contracture when the muscle cells are exposed to agents that trigger calcium release from storage sites inside the muscle cells. “With RER, the thing that causes confusion is that it actually has nothing to do with how much calcium the horse is eating or even how much calcium is in the bloodstream. Rather, it has everything to do with the management of normal amounts of calcium that are inside muscle cells and abnormalities with the way they are shuttling that calcium from the storage sites inside the cell out into the myoplasm to react with contractile proteins,” says Dr. Valberg.
Clinical symptoms are typically seen after 15 to 30 minutes of aerobic exercise and may include a loss of impulsion and the development of a stiff gait. Affected horses will have muscle cramps and will be reluctant to move with sweating and pain developing in affected muscle groups. Following an episode of RER, muscle enzymes including creatine kinase (CK) and aspartate aminotransferase (AST) will be increased in the blood and can be used to monitor the severity of the ER episode. Although rare, death is possible in severe cases. Found mainly in Thoroughbred, Standardbred and some Arabian and Warmblood breeds, RER is reported most frequently in young fillies in race training who seem to be more prone to a nervous or an easily-stressed disposition. “The thing that is really common with horses that have RER is that it is a stress-induced disorder,” explains Dr. Valberg. “Usually these horses are fit and often times they have great promise and can show great speed. They typically start to develop signs of ER when they are in a high stress environment, such as a race training center or at a racetrack. When they arrive at this new area and they aren’t getting a lot of turn-out, they’ll start showing signs of ER when they are exercising, wound-up and tight. It’s not necessarily when they are racing, but more when they are galloping on the track and being held back to a certain speed for example,” she illustrates. During a racing season, about 5 to 10 percent of Thoroughbred racehorses develop some form of ER, with 75 percent of those horses having more than four episodes in four months. In most cases, the horse will be able to return to athletic function after an episode of ER, although recovery is dependent on the individual horse and the severity of the episode.
Management of horses with RER requires keeping dietary and exercise routines consistent while promoting calm behavior and minimizing stress as much as possible. Regular, gentle exercise such as turnout and avoiding stall confinement is encouraged. “These horses are more reactive and more likely to be high-stress and nervous when they are on a high non-structural carbohydrate (NSC) diet, so one of the ways we try to manage this condition is to replace some of the starch and sugar in their diet with fat supplementation, so that they maintain their weight and have enough energy and calories but also have less of a hot feed in their system to decrease their stress level,” says Dr. Valberg of the important role diet can play in managing this condition. Grass hay is a good forage foundation for the diet, and a hay analysis may be advised to determine sugar and starch levels in the forage. Although the tolerance of NSC for each horse is different, general recommendations are to keep starch and sugar levels in concentrates at 20 percent or less of the daily digestible energy (DE) requirement for horses with RER. This diet goal requires a change in management for most racing Thoroughbreds, shifting a widely held belief that performance could be compromised if horses racing at a top level are fed lower amounts of starch and sugar. In fact, dietary calories from fat and oils, up to 25 percent of daily DE, can be utilized as an excellent alternate energy source to sugars and starches in performance horses that have a high daily DE requirement when forage alone cannot provide all necessary calories to maintain weight or activity level. With greater knowledge, horse owners, trainers and veterinarians are shifting away from using vegetable-based fats like corn oil as a dietary fat source because these types of fats have an elevated concentration of omega-6 fatty acids that can lead to a more potent inflammatory response in the horse. As a healthier option, flax oil can be used as a replacement for vegetable oil because the high omega- 3 content in flax oil helps to lessen the inflammatory response. Flax oil can be fed up to 1 cup daily for horses that weigh on average 1,000 pounds and that require additional calories from fat in their diet. Fat is an important source of calories that athletic horses use during exercise, and adding fat to the diet of a performance horse can help to limit glycogen used by muscle cells. Replacing sugar and starch calories with fat calories may also help to reduce excitable behavior, promoting a calming effect in horses prone to RER. Adequate levels of vitamin E and selenium are necessary to protect against damage from cellular oxidation. As a general guideline, it is advisable to add 1,000 to 2,000 IU of natural vitamin E (d-alpha- tocopherol) for every cup of oil that is added to the ration. Supplemental electrolytes (sodium, chloride, potassium) may also be warranted for RER horses if they sweat above maintenance levels in hot and humid conditions.
“The genetic mutation causes the muscle to constantly think it needs to make more glycogen, so it’s consistently putting up to twice as much sugar into the muscle than is normal and not releasing readily when horses begin to exercise. When it is focused on doing that, then the horse starts to exercise and it doesn’t release that sugar for energy metabolism.”
— Stephanie Valberg, DVM, PhD, DACVIM, ACVSMR
Professor and Mary Anne McPhail Dressage Chair in Equine Sports Medicine at Michigan State University
Polysaccharide storage myopathy is a glycogen storage disease of the muscle. There are currently two known forms of PSSM: type 1 PSSM (PSSM1) and type 2 PSSM (PSSM2). PSSM1, the more common form, is known to affect more than 20 breeds. “We now know that because it’s an inherited disorder, it impacts a large number of breeds, including horses that have been derived from the original Belgian draft horse in Europe. Our North American Belgians and Percherons are examples of this lineage, and have a high frequency of genetic defect that causes type one PSSM,” says Dr. Valberg. “Interestingly, when you have draft breeds derived from the United Kingdom, like Clydesdales and Shires, those horses are not impacted by this disease. We see it in Quarter Horses and Quarter Horse-related breeds like Paints and Appaloosas, as well as to a certain extent in Tennessee Walkers, Rocky Mountain Horses, Morgans and occasionally in Warmbloods.” A recent survey suggested that the prevalence of PSSM among overtly healthy Quarter Horses in the U.S. was likely between 6 and 12 percent. In contrast to the nervous behavior observed in horses with RER, many horses with PSSM have been described as having a very calm, almost sedate demeanor. Horses are typically in good body condition (and sometimes are overweight) at the time of diagnosis.
PSSM1 is caused by a genetic mutation of the glycogen synthase (GYS1) gene. This mutation causes the glycogen synthase enzyme to be abnormally active resulting in the excessive conversion of glucose into glycogen within the muscle cell. While glycogen is being formed, it cannot be broken down resulting in the loss of glycogen as an energy source to the cell. A muscle biopsy from a horse with PSSM1 shows an abnormal accumulation of glycogen in cells and also an abnormal form of glycogen. PSSM2 has recently been described in horses that also have abnormal glycogen accumulation in their muscle cells but do not carry the GYS1 mutation. Both types of PSSM can be diagnosed based on a microscopic evaluation of a muscle biopsy. “Type 2 PSSM is a descriptive term to apply to horses that don’t have the genetic defect from type PSSM1. They have clinical signs and their muscle biopsies have shown that they have some abnormalities in the appearance of glycogen under the microscope, causing them to be classified as PSSM2,” says Dr. Valberg. “Our current research is focused on what causes PSSM2. We think there are probably a number of different disorders grouped in that category. There is a second group of horses that we categorize as PSSM2 that we’re now calling Myofibrillar Myopathy and it turns out that they seem to have PSSM2 because they have abnormal looking sugar in their muscle caused by pooling of glycogen in areas that represent damage to the contractile filaments in their muscle. We are focusing on those horses now and seeing that they potentially have a need for higher essential amino acids and better antioxidant strategies in their diet to manage that condition.”
Type 1 of polysaccharide storage myopathy (PSSM1), historically known as Equine Polysaccharide Storage Myopathy (EPSM), is a genetic mutation characterized by abnormal glycogen accumulations in muscle tissue. Glycogen, a long-branched chain of glucose molecules linked together, serves as the primary storage form of glucose in the liver and skeletal muscle. After a meal, a normal horse will slowly absorb glucose from the gastrointestinal tract and excess glucose will be stored as glycogen in muscle and liver cells until the glucose is needed to provide a source of energy to muscle cells and other cells throughout the body. Under normal circumstances, when the muscles need energy, glycogen is broken down from cellular stores, and glucose is used as needed for fuel. In the case of horses affected by PSSM1, most of the cellular glucose remains in the form of glycogen and cannot be easily utilized by the cell. “The genetic mutation causes the muscle to constantly think it needs to make more glycogen, so it’s consistently putting up to twice as much sugar into the muscle than is normal and not releasing readily when horses begin to exercise. When it is focused on doing that, then the horse starts to exercise and it doesn’t release that sugar for energy metabolism,” says Dr. Valberg. When the muscle cells of a horse with PSSM are deprived of energy from glucose, a variety of clinical signs develop that are related to poor performance.
Because horses with PSSM cannot break down the glucose stored in their muscle cells appropriately, their muscles can be effectively starved during exercise, which results in damage to the muscle cells. Clinical signs observed in a horse with PSSM include pain, sweating, stiffness and a reluctance to move. Horses may become exercise intolerant or may demonstrate poor performance. A serum biochemistry panel from a horse that has experienced an episode of tying up from PSSM shows elevations in their CK and AST enzymes, which can both leak from damaged muscle cells. Although horses with PSSM can exhibit clinical signs without exercise, symptoms tend to occur in relation to the amount and intensity of exercise and can be worsened if the horse consumes a diet that is high in non-structural carbohydrates. Trigger factors that induce a myopathic episode typically include a change in the exercise routine of the horse, including unaccustomed stall confinement, and being rested for a few days prior to exercise. Infection or illness seems to also predispose affected horses to myopathic episodes. Treatment for a horse diagnosed with either PSSM1 or PSSM2 should include a forage-based, low-starch and low-sugar diet that is supplemented with fat to provide calories. Daily exercise is also an important part of the management protocol for horses with PSSM. “I think the most important thing with these horses is that we reduce the non-structural carbohydrates in the diet because insulin causes even more dysfunction of the glycogen storage enzyme. We restrict the non-structural carbohydrates and then circumvent the whole issue by giving additional fatty acids, so they have that particular energy source,” says Dr. Valberg.
Many horses with PSSM are easy keepers, so understanding the horse’s caloric requirements and ideal body condition are the first steps in their disease management. Because horses with PSSM cannot mobilize adequate amounts of glucose from the stored glycogen in their cells to meet their cellular energy needs during exercise, dietary management is focused on reducing the intake of sugar and starch, which provide excessive glucose and insulin stimulation. Sweet feed, corn, wheat, oats, barley and molasses should be avoided as these types of feeds can magnify symptoms of PSSM. To encourage weight loss in overweight horses with PSSM, grains or concentrate feeds may need to be reduced or eliminated. If additional calorie restriction is still needed, the volume of forage can be reduced, down to a minimum of 1.5 percent of their body weight. Slow feeder devices can be used to provide consistent access to forage throughout the day. A forage analysis may be helpful for both pasture grass and hay with the goal of feeding forage that has a total NSC content that is 12 percent or lower.
Fats and oils can serve as alternative energy sources to sugar and starch in horses that need to gain weight or in equine athletes that have a high energy requirement. When the ration of a PSSM-affected horse includes fat instead of sugar or starch, their muscle cells will efficiently utilize the components of fat (free fatty acids) for energy during aerobic (with oxygen) exercise, which limits the need for glucose as an energy source. In horses that are not overweight, 10 percent of the digestible energy can be supplied as fat. Flax oil is recommended due to its high omega-3 fatty acid content at a volume up to one cup daily. Other oils, such as soy oil or canola oil, can be used as well. Excess fat supplementation that results in unwanted weight gain should be avoided. Adequate levels of vitamin E should be provided to protect against oxidative damage that can be a byproduct of fat metabolism. Natural vitamin E (d-alpha-tocopherol) can be supplemented in the diet at a dose of 1,000 to 2,000 IU for every cup of oil. A comprehensive supplement that includes omega-3 fatty acids, antioxidants, vitamins, minerals and amino acids is recommended to help balance a forage-based diet*. Consistent access to forage and small, frequent meals provided throughout the day rather than single, large meals may help to moderate blood glucose surges. Hay should have a nonstructural carbohydrate content of less than 12 percent.
Daily turnout and exercise are equally as important as dietary changes for successful PSSM management. Regular, gentle exercise from pasture turnout is essential, and it is recommended to resist the urge to keep a PSSM horse confined to a stall or small paddock. Horses are more likely to experience muscle enzyme elevations when confined, whereas horses turned out to exercise at will and that can walk around to forage do not experience elevations in their muscle enzymes. As little as ten minutes of exercise has been shown to be extremely beneficial in reducing muscle damage. Exercise should be applied though careful conditioning programs that steadily increase demand and allow the horse to adapt to the intensity of work with adequate warm up and cool down time. While consistent, low-impact exercise from turnout can be crucial for muscle health, the pasture itself may need evaluation to determine sugar and starch levels. Using a grazing muzzle or restricting the horse to a dry lot might be necessary when the pasture is rich from new growth or to encourage weight loss. Keeping the horse fit and in consistent exercise enhances glucose utilization and improves energy metabolism in the skeletal muscle.
“I think the most important thing with (horses that have PSSM) is that we reduce the non-structural carbohydrates in the diet because insulin causes even more dysfunction of the glycogen storage enzyme. We restrict the non-structural carbohydrates and then circumvent the whole issue by giving additional fatty acids, so they have that particular energy source.”
— Stephanie Valberg, DVM, PhD, DACVIM, ACVSMR
Professor and Mary Anne McPhail Dressage Chair in Equine Sports Medicine at Michigan State University
Hyperkalemic periodic paralysis is an inherited disease of the muscle that is caused by a point mutation in the sodium channel gene in the muscle of affected horses. This genetic defect originated from the American Quarter Horse stallion, Impressive. Confirmed cases of HYPP have been limited to descendants of this sire. Spread of the gene that causes HYPP is a byproduct of wildly popular breeding from Impressive in the 1980s and early 1990s for his standout conformation and coveted heavy muscling. An estimated 4 percent of Quarter Horses are currently affected, as well as other breeds that allowed outcrossing such as the Appaloosa and Paint Horse. In 1996, the American Quarter Horse Association (AQHA) officially declared HYPP as an undesirable genetic defect and established mandatory genetic testing for all foals born after 1988 with bloodlines descending from Impressive.
“HYPP is due to a point mutation that results in an amino acid substitution in a key part of the voltage- dependent skeletal muscle sodium channel alpha subunit,” explains Dr. Sharon Spier, DVM, PhD, Dipl. ACVIM, Professor Emeritus of Medicine and Epidemiology at the University of California at Davis, who is widely regarded for her expertise in HYPP. “In horses with HYPP, the resting membrane potential is closer to firing than normal horses, making their muscles overly excitable in response to changes in serum potassium concentrations. The mutation causes a subpopulation of sodium channels to fail to inactivate, resulting in persistent depolarization of muscle cells and temporary weakness.” Horses with HYPP have a defect in a channel that transports sodium in skeletal muscle. Sodium channels are “pores” in the muscle cell membrane that control contraction of the muscle fibers. In affected horses, high potassium levels cause sodium to leak in to muscle tissue through the defective channels. When cellular sodium levels rise, cells push out potassium in an attempt to maintain the correct concentration and electrical gradient between the outside and the inside of the cell. Unfortunately, this causes the potassium concentration outside the cell to rise further, resulting in a vicious cycle, which causes the muscle to be overly excitable resulting involuntary contractions.
Hyperkalemia, which is an excessive amount of potassium in the blood, causes the muscles in the horse to contract more easily than normal. “Clinical signs among horses carrying the same mutation range from asymptomatic to daily muscle fasciculations and weakness or collapse. In the majority of horses, intermittent clinical signs begin by 2 to 3 years of age, with no apparent abnormalities between episodes,” says Dr. Spier. These intermittent attacks of weakness and muscle tremors can progress to paralysis or involuntary recumbency that can last from minutes to hours. Other clinical signs during an HYPP attack include an elevated heart rate, prolapse of the third eyelid, abnormal respiratory noises and sweating. HYPP can be fatal if the horse develops respiratory paralysis or cardiac arrest during the hyperkalemic episode. An attack does not necessarily have a single predisposing factor such as exercise, however, there are common risk factors that come together to potentially trigger an HYPP episode. “Ingestion of diets high in potassium (greater than 1.1 percent (dry matter)), such as those containing alfalfa hay, molasses, electrolyte supplements and kelp-based supplements or sudden dietary changes commonly trigger episodes,” explains Dr. Spier. “Fasting, anesthesia or heavy sedation, trailer rides and stress may also precipitate clinical signs, however, the onset of signs may be unpredictable without an obvious cause. Other possible precipitating factors that have been noted in humans and horses are exposure to cold, pregnancy and concurrent disease and rest following exercise. Exercise, per se, does not appear to stimulate clinical signs and serum CK shows no change to very modest increases during episodic fasciculations and weakness.”
Dietary management is the key to preventing HYPP episodes. Management centers around the diet with the goal of keeping a steady blood plasma potassium concentration. The lower the amount of potassium in the blood, the less likely abnormal cells are prone to activation. “Ideally, horses with recurrent episodes of HYPP should be fed a balanced diet containing between 0.6 percent and 1.1 percent to 1.5 percent total potassium concentration and meals containing less than 33 grams of potassium,” says Dr. Spier. While potassium is abundant in the equine diet, it is possible to limit a horse’s intake of this mineral. Pasture and hay should constitute the basis for all equine diets, and forages (pasture and/or hay) should be analyzed to determine the potassium content of these feeds as the concentration of potassium can vary between different types of forages depending on maturity and soils. For horses with HYPP, forage choices narrow considerably as many hays and pasture grasses contain elevated concentrations of potassium. Pasture grass can work well in an HYPP diet as the high-water content makes it unlikely that horses will consume large amounts of potassium in a short period of time. However, it is important to know the plants in the pasture to prevent consumption of higher potassium plants, such as legumes and clover. In general, alfalfa and brome hays typically contain higher levels of potassium than what an HYPP-affected horse would be able to handle and should be fed sparingly, if at all. Horses with HYPP should be allowed consistent access to hay that has low or moderate potassium levels such as Timothy or Bermuda grass hays. Fasting for any prolonged period of time should be avoided. A comprehensive omega-3 fatty acid, antioxidant, vitamin and mineral supplement* can be helpful to balance a forage-based diet.
If concentrates or grain are fed, small meals should be fed multiple times throughout the day so that only small amounts of potassium are available for absorption into the bloodstream at any given time. Lower potassium feeds such as unmolassed beet pulp, oats, wheat, barley and soybean hulls (not soybean meal) are ideal. Fats and pure oils can also be used as energy sources for horses that need calories above what forage provides. Sweet feeds or commercial feeds that contain high amounts of molasses should be limited. Other high-potassium feeds to be aware of include soybean meal, electrolyte supplements and kelp. Horses with HYPP should be provided with adequate vitamin E, selenium and balanced minerals, as well as plain white salt (sodium chloride) to satisfy sodium requirements along with clean, fresh water. Commercial complete feeds with a guaranteed potassium content may be a convenient option to feed HYPP horses. It is very important to make all feed changes gradually as sudden changes in the diet may cause severe symptoms if a new portion of the diet contains a higher potassium content.
While it would be logical to assume that exercise may exacerbate HYPP symptoms because blood potassium concentrations increase as a result of exercise, the opposite is actually true. Light, regular exercise or frequent access to a large paddock is encouraged for horses with HYPP. Stall confinement is often contraindicated for horses with HYPP. Stress can also be a factor in triggering an attack. Keeping a consistent daily routine and taking care to avoid stressful situations can be helpful for horses prone to HYPP episodes.
“Horse owners should be grateful for the breed association’s commitment to education and research on heritable diseases of muscle,” says Dr. Spier with appreciation. “We have enjoyed tremendous progress in my career as far as understanding genetic diseases and the role nutrition plays in our performance horses. I am excited for the future health of our horses as researchers such as Dr. Stephanie Valberg and Dr. Carrie Finno continue to make headway in documenting the various disorders of muscle.”
PHOTO BY ELIZABETH HAY PHOTOGRAPHY
Muscle disorders can present a challenge to equine athletes, but with individualized management, many horses are able to maintain their level of performance, remain comfortable when they are not working and lead normal lives. Emerging research in the field of equine myopathy is showing great potential, paving the way for improved treatments for horses suffering from various muscle disorders. “We are seeing, in some cases, that when there is strong environmental interaction with a horse that has some underlying genetic susceptibility there are a lot of things that can happen in the environment to influence whether that disease is going to manifest itself or not,” says Dr. Valberg. “With new genome sequencing and mapping of the reference genome we are seeing new technologies that can be used to better understand what is happening in the muscle. We are currently using technologies like proteomics where you can look and see what all the proteins are doing before you try a treatment, then compare them after the treatment has been given to gauge their response. This gives you an amazing unbiased view of how disease conditions impact the muscle and how they can be changed. We have improved technology available to us, so we can better define these conditions, then find the most targeted and effective treatment.” Dr. Spier echoes the importance of this specialized field of study. “The research is very rewarding,” she says. For HYPP in particular Dr. Spier states, “Now that we have numerous genetic tests offered at licensed laboratories, equine breeders are more prepared for how to use these important tools.” In addition to advanced diagnostic testing, management practices and dietary strategies are better established. Specialized feeding and exercise programs are essential to maintaining the performance and health of horses diagnosed with RER, PSSM and HYPP. With a strong working relationship between riders and veterinarians, horses with genetic muscle diseases can be managed successfully.
* Platinum Performance® Equine, Platinum Performance® GI or Platinum Performance® CJ