Equine exertional rhabdomyolysis syndrome (ERS) commonly affects the athletic breeds of horses. The intermittent syndrome is characterised by stiffness, muscle cramping and pain and is accompanied by mild to markedly elevated plasma activities of the muscle-derived enzymes, creatine kinase (CK) and aspartate aminotransferase (AST). Although specific causes have been identified there is one sub-condition that appears to be due to malfunction of glycogen storage and release. This is polysaccharide storage myopathy (PSSM). There is a genetic element to PSSM Type 1; The glycogen synthase-1 gene has mutated enabling rapid conversion of glucose to amylase resistant glycogen, resulting in locking up of energy reserves. Type II has a similar effect but tends not give rise to elevated CK; the cause is not known.

Accompanying this induced myopathy are symptoms of fatigue, muscular atrophy and pain. Differing from ERS is the role of muscle atrophy which is believed to be due to the interaction of glycogen synthesis and insulin sensitivity. Increased sensitivity correlates with reduced production, which lessens the support of amino acid uptake from the blood into muscle. This leads to muscle atrophy as exertional breakdown is less likely to be matched by muscle synthesis, as characterised by an increase in creatine kinase.

Muscle atrophy, where protein breakdown is faster than synthesis, as previously described (Knowledge Base – Muscle Maintenance), releases inflammatory and oxidative factors, such as creatine kinase, phagocytes and free amino acids, some of which are not immediately recycled. Additionally, as the energic base for synthesis is reduced, collagen synthesis may be compromised. Incidentally, this helps explains why PSSM tends to be more prevalent in thoroughbreds and other “athletic” breeds.

There are several types of muscle fibres, defined by the speed of “twitch”. Fast twitch, those muscle fibres that give short phase, hard contractions are more numerous in these breeds. Slow twitch fibres that give sustained and continuous contractions have a greater vascular delivery and so are better oxygenated. Short bursts of intense activity rely on glucose breakdown to lactic acid to power the contractions, and this takes place in the absence of oxygen. For more sustained exercise, oxygenated generation of energy can use many nutrients – volatile fatty acids (VFA) from fibre fermentation, amino acids and fat, as well as glucose – and the supply of glucose and release of glycogen is less critical. Therefore, for PSSM induced glycogen dysfunction, moving to VFA driven muscle contraction may be a valid alternative. As it has been shown that training can increase the proportion of Type 2A muscle fibres, from the fast twitch 2X, there is the ability to support more aerobic energy streams.

There are two nutritive routes to help support the PSSM horse; muscle support and energy support. A targeted approach to support muscle build-up, and so achieve stasis with muscle breakdown, is the philosophy behind Muscle Maintenance (MM). MM contains good levels of branch chain and sulphur amino acids that are base units for muscle protein synthesis, especially replacing those components that are metabolised before being reincorporated into muscle. MM components also supports the anti-inflammatory and antioxidative processes, helping reduce muscle protein breakdown, whilst the presence of ω-fatty acids, vitamins and trace elements help support the vascular system and muscle membranes.

In terms of providing energy; there are a number of reasons why glycogen metabolism is disrupted. There may be amylase resistant forms; there is also build-up of two other glycogen forms – proglycogen and macrogen – and it is thought that these forms interact with normal glycogen release. At the same time glucose conversion to glycogen has been reported as being faster in PSSM horse, so there is possibility of inadequate energy provision from glucose/starch. Production of ATP in PSSM horses is compromised with increasing levels of IMP which can also disrupt glycogen metabolism. It is thought that this, along with a rise in lactic acid from anaerobic glycolosis, leads to the horse’s lack of enthusiasm for exercise.

Exercise has been shown to be critical in aiding horses subject to PSSM, both types 1 & 2. It has been theorised that PSSM is a fairly recent condition and is due to developing reliance on fast twitch muscles – and so anaerobic energy usage – in athletic breeds such as the thoroughbred, half & quarter- bred. Training as mentioned, can help increase the proportion of slow twitch muscle fibres, and so have the ability to make a higher use of non-starch/sugar sources. Research work does recommend that less than 10% of digestible energy should be supplied by non-structural carbohydrates, with up 15% being supplied as fat. The rest then is from fibre. However, there is a caveat on nutritional fat. Short chain non-esterified fatty acids have been shown to increase insulin stimulation of glycogen synthesis, and also interfere with lipid oxidation. Long chain fatty acids, however, are recommended.

Support for the PSSM horse is therefore dependant on a number of factors. Firstly, exercise should be gentle and sustained, promoting aerobic energy metabolism, through the tricarboxylic acid (TCA) cycle. Diet should support both the muscle turnover derived from exercise, but also support normal metabolic function, spare glucose for essential metabolic function (as in brain biochemistry, active transport systems) and reduce insulin sensitivity by both sparing action and reducing glucose load. To this end, practical recommendations can be made.

As with most glucose dysfunction disorders (EMS, IR, ERS), fibre, and more specifically forage, should supply the majority of the diet. There are forage sources that are quite high in sugars and NSC, but soaked hay is a trusted source of low sugars. Where it is difficult to source low NSC forage, diluting inherent sugars with a dedicated fibre source is a good alternative.

GWF Nutrition have a range of fibre sources from Alfalfa Soya Oil at 11.0 Mj/kg DE to No Starch Fibregest at 13.5. This gives versatility of supporting forage intake with low starch, fibre products with mid to high energy levels. Fibregest is based on beet pulp, and research has shown the presence of beet fibre improves the overall digestibility of other fibre sources. It is therefore possible to match energy intake with level of activity in the majority of situations.

Depending on the fibre/forage combination it may or may not not be necessary to give additional protein as in the addition of Equilibra. Fed in low quantities, its starch level will not significantly impact on glucose absorption, especially if split between feeds, but it does donate good levels of vitamins and trace elements, as well as omega fatty acids, and prebiotics to further improve fibre digestion. And if extra protein is not necessary, One Cup supplies essential amino acids, vitamins and trace elements.

GWF Nutrition can supply solutions to meet the general recommendations on feeding the PSSM (1 & 2) horse; but there is the added benefit of Muscle Maintenance that specifically targets supporting muscle recovery and regeneration, which in turn reduces insulin dependency. Feeding Muscle Maintenance after exercise will help support a PSSM-type diet.

References

• Annandale EJ, Valberg SJ, Essén-Gustavsson B. Effects of submaximal exercise on adenine nucleotide concentrations in skeletal muscle fibers of horses with polysaccharide storage myopathy. AJVR, Vol 66, No. 5, May 2005.
• Borgia LA, Valberg SJ, McCue ME, Pagan JD, Roe CR. Effect of dietary fats with odd or even numbers of carbon atoms on metabolic response and muscle damage with exercise in Quarter Horse–type horses with type 1 polysaccharide storage myopathy. AJVR, Vol 71, No. 3, March 2010. 326-337.
• Borgia L, Valberg S, McCue M, Watts K, Pagan J. Glycaemic and insulinaemic responses to feeding hay with different non-structural carbohydrate content in control and polysaccharide storage myopathy-affected horses. Journal of Animal Physiology and Animal Nutrition 95 (2011) 798–807.
• Bröjer JT, Essén-Gustavsson B, Annandale EJ, Valber SJ. Proglycogen, macroglycogen, glucose, and glucose-6-phosphate concentrations in skeletal muscles of horses with polysaccharide storage myopathy performing light exercise. AJVR, Vol 67, No. 9, September 2006. 1589-1595.
• Firshman AM, Valberg SJ, Baird JD, Hunt L, DiMauro S. Insulin sensitivity in Belgian horses with polysaccharide storage myopathy. Am J Vet Res 2008;69:818–823.
• Geor RJ. Role of dietary energy source in the expression of chronic exertional myopathies in horses. J ANIM SCI 2005, 83:E32-E36.
• Isgren CM, Upjohn MM, Fernandez-Fuente M, Massey C, Pollott G, et al. (2010) Epidemiology of Exertional Rhabdomyolysis Susceptibility in Standardbred Horses Reveals Associated Risk Factors and Underlying Enhanced Performance. PLoS ONE 5(7): e11594. doi:10.1371/journal.pone.0011594
• Moore-Colyer, M.J.S., Longland, A.C., 2001. The effect of plain sugar-beet pulp on the in vitro gas production and in vivo apparent digestibility of grass hay when offered to ponies. In: The Proceedings of the Seventeenth Equine Nutrition and Physiology Symposium, pp. 145–147.
• Murray, J.M.D., Longland, A.C., Moore-Colyer, M.J.S., 2005a. In vitro fermentation of different ratios of hightemperature dried lucerne and sugar beet pulp incubated with an equine faecal inoculum. Anim. Feed Sci. Technol. 129, 89–98.
• Murray JMD, Longland A, Hastie PM, Moore-Colyer M, Dunnett C. The nutritive value of sugar beet pulp-substituted lucerne for equids. Animal Feed Science and Technology 140 (2008) 110–124.
• Schröder U, Licka TF, Zsoldos R, Hahn CN, MacIntyre, Schwendenwein I, Schwarz B, Van Den Hoven R. Effect of Diet on Haflinger Horses With GYS1 Mutation (Polysaccharide Storage Myopathy Type 1). Journal of Equine Veterinary Science 35 (2015) 598–605.
• Valberg SJ. Muscle Conditions Affecting Sport Horses. Vet Clin Equine 34 (2018) 253–276.
• Valberg SJ, McCue ME, Mickelson JR. The Interplay of Genetics, Exercise, and Nutrition in Polysaccharide Storage Myopathy. Journal of Equine Veterinary Science 31 (2011) 205-210.