J. Anim. Sci. 2005. 83:E32-E36
© 2005 American Society of Animal Science
Role of dietary energy source in the expression of chronic exertional myopathies in horses1
R. J. Geor2
Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2W1, Canada
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Abstract
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Muscle disorders characterized by the development of pain and stiffness during and after exercise (exertional rhabdomyolysis, ER) are common in horses. Two heritable forms of chronic ER have been identified: 1) polysaccharide storage myopathy (PSSM), a condition characterized in quarter horses and related breeds, but also reported to occur in other breeds; and 2) recurrent exertional rhabdomyolysis (RER) in Thoroughbreds. Although the pathophysiology of PSSM and RER are different, there is epidemiological and experimental evidence that feeding diets rich in hydrolyzable carbohydrates (starch and simple sugars) enhances the phenotypic expression of both disorders. The PSSM is characterized by increased insulin sensitivity, excessive muscle glycogen storage, and the accumulation of amylase-resistant polysaccharide in muscle. The feeding of concentrates rich in hydrolyzable carbohydrates may enhance disease expression by increasing the quantity of glucose available for muscle glycogen synthesis. On the other hand, diets rich in starches and simples sugars may increase clinical expression of RER via enhancement of stress and anxiety, factors known to increase the risk of ER in horses with RER. A decrease in the frequency and severity of ER has been observed when horses with PSSM and RER are fed diets with reduced DE from hydrolyzable carbohydrates (<10 to 15% of total diet) and increased DE from fat (15 to 20%) and other energy sources, such as beet pulp and soybean hulls.
Key Words: Exertional Rhabdomyolysis • Horse • Hydrolyzable Carbohydrates • Polysaccharide Storage Myopathy • Recurrent Exertional Rhabdomyolysis
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Introduction
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Muscle disorders characterized by development of pain and stiffness during and after exercise (exertional rhabdomyolysis, ER) are common in many breeds of horses. Some horses experience repeated episodes of ER that can severely limit athletic potential. Research over the past 10 to 15 yr has identified two specific forms of chronic ER, namely polysaccharide storage myopathy (PSSM) in quarter horses and recurrent exertional rhabdomyolysis (RER) in Thoroughbreds (Valberg et al., 1999b
). Polysaccharide storage myopathy was first described in quarter horses and quarter horse-related breeds such as Appaloosas and Paints (Valberg et al., 1992). Subsequently, a comparable condition has been recognized in other horse breeds, including Morgans, warmblood-related breeds, draft horses, and Welsh ponies (Valentine et al., 1997, 2000, 2001a; Quiroz-Rothe et al., 2002). Features of PSSM include repeated development of muscle stiffness and pain during mild exertion; persistent elevation in serum creatine kinase (CK) activity, even when horses are rested for a few weeks; excessive muscle glycogen storage; and the accumulation of amylase-resistant polysaccharide in skeletal muscle (Valberg et al., 1999b).
The term recurrent exertional rhabdomyolysis (RER) has been used to define a myopathic condition of Thoroughbreds, for which there is in vitro evidence of abnormal regulation of intracellular Ca cycling (Valberg et al., 1999b). A similar, if not identical, condition also may occur in Standardbred and Arabian horses (McKenzie et al., 2003b). Both RER and PSSM seem to have a genetic basis, with varying severity of phenotype potentially explained by the influence of environmental factors such as diet and exercise regimens. Indeed, there is accumulating epidemiological and experimental evidence that diet composition, specifically the amount of hydrolyzable (or soluble) carbohydrate and fat, is one factor that alters the phenotypic expression of RER and PSSM. The purpose of this article is to review current understanding of the pathophysiology of PSSM and RER, with an emphasis on the role of dietary energy source in the expression of these disorders.
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Polysaccharide Storage Myopathy
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Much of the work on the pathophysiology of PSSM has been done on quarter horses and it is currently not known if similar pathophysiological mechanisms are important in non-quarter horse breeds with clinical evidence of chronic, intermittent rhabdomyolysis and skeletal muscle polysaccharide accumulation. For example, in some draft horses with histopathological evidence of amylase-resistant polysaccharide, the clinical signs are more consistent with the neuromuscular disorder "shivers" (weakness and muscle atrophy) than with true exertional myopathy (Valentine et al., 1997), and it is possible that the abnormal muscle polysaccharide observed in skeletal muscle from these horses is an incidental finding or that clinical signs reflect the coexistence of "shivers" and PSSM (Valentine et al., 2000, 2001a). The remainder of this discussion concerns the pathogenesis of PSSM in quarter horses.
High muscle glycogen concentrations and the accumulation of amylase-resistant polysaccharide complexes in 1 to 40% of skeletal muscle fibers are characteristic findings in affected horses (Valberg et al., 1999b). Muscle glycogen concentrations may be two- to threefold higher than in unaffected horses. In one report, mean (±SD) muscle glycogen concentration (micromoles of glucosyl units per kilogram of dry muscle) in five quarter horses with PSSM was 1,131 (96), compared with 476 (30) in five Thoroughbred horses (Valberg et al., 1999b). Detection of amylase-resistant polysaccharide in muscle of horses with a history of recurrent ER is considered diagnostic for PSSM. However, the accumulation of polysaccharide may be a gradual process; in a small group of quarter horse foals with clinical and laboratory evidence of chronic intermittent ER, polysaccharide accumulation in skeletal muscle was not apparent until 2 yr of age (De La Corte et al., 2002).
The mechanisms underlying enhanced glycogen storage in quarter horses with PSSM have been partially elucidated. Unlike skeletal muscle glycogenoses in humans and other species (DiMauro and Lamperti 2001), excessive glycogen storage is not due to decreased capacity for glycogen utilization. During controlled exercise protocols, net glycogen breakdown and accumulation of lactate in skeletal muscle (middle gluteus medius) were similar in affected quarter horses and controls (Valberg et al., 1999a,b). Similarly, the activities of key glycolytic enzymes, measured in homogenates of muscle biopsies, did not differ between affected and control horses (Valberg et al., 1998). Instead, excessive muscle glycogen storage may be related to enhanced insulin sensitivity and uptake of glucose into skeletal muscle. There are several lines of evidence in support of the hypothesis that quarter horses with PSSM have enhanced whole-body insulin sensitivity. Glucose clearance following bolus i.v. administration (0.5 g/kg of BW) was 1.5 times faster in affected quarter horses compared with healthy control horses (Figure 1A), whereas glucose concentrations after oral glucose administration were significantly lower (De La Corte, 1999a). Furthermore, affected horses had lower resting insulin concentrations and lower insulin concentrations than controls after i.v. (Figure 1B) or oral administration of glucose, and i.v. insulin resulted in more profound hypoglycemia when compared with controls (De La Corte, 1999a). Blood glucose and insulin concentrations were also lower in affected horses than in healthy controls after consumption of a meal of sweet feed (De La Corte et al., 1999c), findings consistent with enhanced glucose clearance and insulin sensitivity. The strongest evidence of enhanced insulin sensitivity in PSSM was provided by a more recent study that demonstrated a twofold higher rate of glucose clearance in affected vs. control horses during a euglycemic-hyperinsulinemic clamp (Annandale et al., 2004).
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Figure 1. Mean (±SEM) plasma glucose (A) and serum insulin (B) concentrations in six quarter horses with polysaccharide storage myopathy (PSSM; closed symbols) and 10 healthy control horses (open symbols) before (time 0) and after an i.v. injection of glucose at 300 mg/kg BW. Glucose (P < 0.001) and insulin (P < 0.01) concentrations were lower in horses with PSSM than in controls at all time points after glucose administration (data redrawn from De La Corte et al., 1999a).
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There are no published data on glucose uptake into skeletal muscle of quarter horses with PSSM. However, skeletal muscle, which comprises approximately 50% of BW in light-breed horses, is the largest mass of insulin-responsive tissue in the body, and it is reasonable to speculate that horses with PSSM have increased capacity for skeletal muscle glucose uptake. The skeletal muscle contents of insulin receptor and the insulin-sensitive glucose transporter, GLUT4, did not differ between affected quarter horses and healthy controls (Annandale et al., 2004). Thus, enhanced glycogen storage in quarter horses with PSSM is not associated with enhanced expression of insulin receptor or GLUT4 proteins in skeletal muscle. It is possible that excessive glycogen storage is related to enhanced recruitment (and/or activity) of GLUT4 transporters at the sarcolemma or dysregulation of glycogen synthase. Further research is needed to examine these issues.
Dietary Energy Source and Clinical Expression of Polysaccharide Storage Myopathy
There is clinical and research evidence that dietary energy source modifies clinical expression of PSSM. Clinical signs of ER are more frequent and severe in horses with PSSM that receive little exercise and are fed moderate to large amounts of concentrates or grain with high hydrolyzable (nonstructural) carbohydrate content (Valberg et al., 1997; Valentine et al., 2001b). Conversely, feeding a diet with restricted hydrolyzable carbohydrate content (on a total dietary basis, <10% of DE as nonstructural carbohydrate) and added fat (up to 15 to 25% of DE from fat) has resulted in clinical improvement of affected horses, with a gradual decrease in the frequency and severity of episodes of muscle pain and necrosis (Valentine et al., 2001b; Firshman et al., 2003; McKenzie et al., 2003b; Ribeiro et al., 2004). General dietary recommendations for long-term management of horses with confirmed PSSM include: 1) feeding a minimum of 1% of BW as forage daily, ideally a grass or oat hay because these forages have lower nonstructural carbohydrate content compared with legumes; 2) removal of all concentrates containing grain and molasses from the diet; and 3) use of alternative energy sources, such as corn oil, rice bran, and/or beet pulp, when supplemental energy is required (Firshman et al., 2003; McKenzie et al., 2003b).
Whether it is the decrease in dietary hydrolyzable carbohydrate or the increase in dietary fat that underlies clinical improvement in horses with PSSM is controversial. In light of the putative mechanisms of enhanced glycogen storage in horses with PSSM, it can be hypothesized that diets with high hydrolyzable carbohydrate content (e.g., concentrates rich in starch and sugar) enhance expression of disease via increased availability of glucose for skeletal muscle glycogen synthesis. Thus, restriction of dietary hydrolyzable carbohydrate would be expected to minimize postprandial increases in glucose and insulin, and thereby limit glucose availability in skeletal muscle. However, the dose-response relationship between dietary hydrolyzable carbohydrate content and muscle glycogen concentration in horses with PSSM has not been established. Alternatively, clinical improvement of horses with PSSM may depend on the addition of fat to the diet. It has been reported that signs of muscle dysfunction can persist when affected horses are fed an all-forage diet with low hydrolyzable carbohydrate content, whereas clinical signs of muscle dysfunction abate when even a small amount of vegetable-source fat is added to the diet (McKenzie et al., 2003b). In a crossover study, the feeding of 0.5 kg/d of stabilized rice bran to quarter horses with PSSM resulted in a 20 to 25% decrease in muscle glycogen content compared with the control ration of grass hay (De La Corte et al., 1999b).
The mechanism by which dietary fat improves muscle function in horses with PSSM is unknown. One hypothesis is that a higher fat ration results in decreased skeletal muscle insulin sensitivity, glucose uptake, and glycogen synthesis (Valentine et al., 2001b; McKenzie et al., 2003b). However, whereas the consumption of diets with increased saturated fat is strongly linked to development of insulin resistance, diets enriched with polyunsaturated fats are without effect on insulin-mediated glucose metabolism (Storlien et al., 2000). Because fat sources used in horse diets are highly unsaturated, these comparative data cast some doubt on the proposed mechanism for clinical improvement in PSSM horses fed higher-fat diets. Alternatively, the clinical benefit of a high-fat, low-starch diet in PSSM horses may be related to enhanced fat metabolism in skeletal muscle (Ribeiro et al., 2004).
There are conflicting views on the quantity of dietary fat required for clinical improvement of horses with confirmed PSSM. Valentine et al. (2001b) reported that horses with PSSM show the greatest improvement when fed a diet that provides, on a total dietary basis, at least 20 to 25% of DE from fat. Other researchers have reported clinical improvement when affected horses are fed diets with only 5 to 15% of DE provided by fat (Firshman et al., 2003; Ribeiro et al., 2004). Further research is needed to determine whether the quantity of dietary fat alters clinical response and long-term outcome in horses with PSSM. On balance, however, it seems that a decrease in the hydrolyzable carbohydrate (starches and simple sugar) content of the ration (< 5% DE) is the most important dietary recommendation for horses with PSSM. When forage alone does not meet daily DE needs, a source of fat, such as vegetable oil (as much as 600 mL/d for a 500-kg horse) or rice bran (0.5 to 2.0 kg/d), should be added to the diet. For horses in heavy training, other feedstuffs, such as beet pulp, may be needed to meet DE requirements and ensure palatability of the diet.
It is important to emphasize that the implementation of a daily exercise regimen is also important for the successful management of horses with PSSM. Firshman et al. (2003) reported that PSSM horses of owners who followed recommendations for alterations in both diet and physical activity were significantly (P = 0.04) more likely to show improvement in the severity and frequency of ER compared with horses of owners that followed dietary recommendations only. Regular exercise may prevent development of excessive muscle glycogen storage in horses with PSSM (Firshman et al., 2003).
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Recurrent Exertional Rhabdomyolysis in Thoroughbreds
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Recurrent exertional rhabdomyolysis is a heritable defect in myocellular Ca regulation that, under conditions of stress and excitement, can result in excessive muscle contraction and muscle necrosis (Lentz et al., 1999; MacLeay, 1999b; Valberg, 1999b; McKenzie et al., 2003b). In vitro testing has demonstrated that skeletal muscle from Thoroughbreds with clinical evidence of RER is hypersensitive to agents that induce release of calcium from the sarcoplasmic reticulum (e.g., caffeine, halothane). Thus, lower concentrations of caffeine are needed to induce muscle contraction compared with muscle from healthy control horses (Lentz et al., 1999). Excitement and stress may act as a trigger factors for initiation of excessive muscle contraction in horses with the RER trait. This hypothesis is based on clinical observations and epidemiological data that have identified nervous temperament as a key factor in the clinical expression of RER (MacLeay et al., 1999a; McKenzie et al., 2003b). The highest prevalence and greatest severity of episodes was observed in 2- and 3-yr-old fillies with a nervous temperament (MacLeay et al., 1999a).
Dietary Energy Source and Clinical Expression of Recurrent Exertional Rhabdomyolysis
A limited number of controlled trials have provided evidence that dietary energy source modulates temperament and expression of muscle damage in Thoroughbred horses with RER (MacLeay et al., 2000; McKenzie et al., 2003a). However, the effect of energy source seems to depend on daily DE intake. Specifically, when RER-affected Thoroughbred horses were fed diets that provided 21.4 Mcal/d with much of the energy as either fat (2.3 kg/d of stabilized rice bran; 20% DE from fat and 34% DE from nonstructural carbohydrate) or hydrolyzable carbohydrate (2.5 kg/d of sweet feed; 8% DE from fat and 47% DE from nonstructural carbohydrate), there was no difference in postexercise muscle necrosis as indicated by serum CK activity. On the other hand, when RER horses were fed a larger amount of sweet feed (4.5 kg/d; 8% DE from fat and 53% DE from non-structural carbohydrate), with daily DE intake (28.8 Mcal) similar to that of racehorses in training, there was a significant increase in postexercise serum CK activity (MacLeay et al., 2000). In a subsequent crossover study from the same laboratory, RER horses were fed diets with either high (4.5 kg of sweet feed/d [<5% DE from fat and 45% DE from nonstructural carbohydrate], 5.7 kg forage) or low (4.3 kg fat and fiber concentrate [20% DE from fat, and 9% DE from nonstructural carbohydrate], 5.7 kg forage) hydrolyzable carbohydrate content, with both diets providing approximately 28.8 Mcal/d (McKenzie et al., 2003a). Postexercise serum CK activity was increased (>3,000 U/L) when horses were fed the high hydrolyzable carbohydrate diet but not the lower hydrolyzable carbohydrate, higher fat concentrate diet. Based on these observations, it has been recommended that horses with RER in race training receive a diet that provides no more than 20% of DE from nonstructural carbohydrate and at least 20% of DE from fat (McKenzie et al., 2003b).
The mechanism by which high-calorie rations containing a substantial amount of hydrolyzable carbohydrate (approximately 45 to 50% or more of DE from nonstructural carbohydrate) enhance exercise-induced muscle damage in horses with RER is unclear, but may be related to the effect of dietary energy source on behavior. In the study by McKenzie et al. (2003a), RER horses fed the high-fat concentrate had lower resting heart rate and exhibited a calmer demeanor than when fed the high hydrolyzable carbohydrate diet. Given the strong link between nervousness, excitement, and episodes of rhabdomyolysis in RER-affected horses (MacLeay et al., 1999a), it is possible that a reduction in dietary hydrolyzable carbohydrate decreases risk of ER via modulation of nervousness and excitement. Studies of healthy horses have also shown an effect of dietary energy source on behavior. Holland et al. (1996) demonstrated decreased spontaneous activity and reactivity of horses fed concentrates with added corn oil and lecithin. The authors attributed this change in behavior to the added dietary fat; however, corn oil or lecithin was substituted for corn and oat starch in the test diets, and it can be argued that the observed behavioral modifications were due to the decrease in dietary starch rather than the addition of fat. Interestingly, studies in rats have demonstrated that high-sucrose diets enhance corticotrophin releasing hormone expression in the hypothalamus, augment sympathetic nervous system activation, and increase stress and anxiety (Levine et al., 2003).
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Implications
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The clinical expression of polysaccharide storage myopathy in quarter horses and related breeds and recurrent exertional rhabdomyolysis in Thoroughbreds is enhanced by feeding concentrates with high hydrolyzable carbohydrate (starch and simple sugars) content. Conversely, feeding diets with decreased digestible energy from hydrolyzable carbohydrate and substitution with alternative energy sources, such as vegetable oils and fats, beet pulp, and soybean hulls, decreases the frequency and severity of episodes of exertional rhabdomyolysis.
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Footnotes
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1 Presented at the ASAS Symposium: Equine Carbohydrate-Associated Disorders, St. Louis, MO, July 26, 2004. 
2 Correspondence—phone: 519-824-4120, ext. 54324; fax: 519-767-1450; e-mail: rgeor{at}uoguelph.ca.
Received for publication August 12, 2004.
Accepted for publication November 18, 2004.
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Abstract
Introduction
