Skeletal muscle metabolic response to exercise in horses with ‘tying-up’ due to polysaccharide storage myopathy.
Abstract: Polysaccharide storage myopathy (PSSM) is a distinct cause of exertional rhabdomyolysis in Quarter Horses that results in glycogen and abnormal polysaccharide accumulation. The purpose of this study was to determine if excessive glycogen storage in PSSM is due to a glycolytic defect that impairs utilisation of this substrate during exercise. Muscle biopsies, blood lactates and serum CK were obtained 1) at rest from 5 PSSM Quarter Horses, 4 normal Quarter Horses (QH controls) and 6 Thoroughbreds with recurrent exertional rhabdomyolysis (TB RER) and 2) after a maximal treadmill exercise test in PSSM and QH controls. In addition, 3 PSSM horses performed a submaximal exercise test. At rest, muscle glycogen concentrations were 2.4x and 1.9x higher in PSSM vs. QH controls or TB RER, respectively. Muscle lactates at rest were similar between PSSM and QH controls but significantly higher in PSSM vs. TB RER. Muscle glucose-6-phosphate concentrations were also higher in PSSM horses than controls combined. During maximal exercise, mean muscle glycogen concentrations declined 2.7x more and mean lactate increased 2x more in PSSM vs. QH controls; however, differences were not statistically significant. Blood lactate concentrations after maximal exercise did not reflect generally higher muscle lactate in PSSM vs. QH controls. No change in blood lactate concentrations occurred in PSSM horses with submaximal exercise. Serum CK activity increased significantly 4 h after maximal and submaximal exercise and was significantly higher in PSSM vs. QH controls. These results show that during maximal exercise, PSSM horses utilised muscle glycogen and produce lactic acid via a functional glycolytic pathway and that during submaximal exercise oxidative metabolism was unimpaired. The excessive glycogen storage and formation of abnormal polysaccharide in PSSM horses therefore appear to reflect increased glycogen synthesis rather than decreased utilisation. The specific subset of horses with exertional rhabdomyolysis due to PSSM would likely benefit clinically from a diet low in soluble carbohydrates like grain with fat added as well as gradually increasing daily exercise to reduce excessive glycogen accumulation and enhance utilisation.
Publication Date: 1999-02-10 PubMed ID: 9952328DOI: 10.1111/j.2042-3306.1999.tb03789.xGoogle Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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The research studies the metabolic response of horses’ muscles to exercise, particularly in horses with ‘tying-up’ due to Polysaccharide storage myopathy (PSSM). It finds that the storage of excessive glycogen in PSSM horses is due to an increase in glycogen synthesis, not a decrease in usage, and that horses with this condition could benefit from a specific diet and exercise regimen.
Objective and Methodology
- This research aimed to understand whether the excessive accumulation of glycogen in horses with Polysaccharide Storage Myopathy (PSSM), a condition causing muscle cramping and stiffness, is due to a metabolic defect obstructing the proper use of glycogen during exercise.
- The study analyzed muscle biopsies, blood lactate levels, and serum CK values taken from resting and exercising Quarter Horses (both normal and those with PSSM) and Thoroughbreds with recurrent exertional rhabdomyolysis (a muscle disorder).
Results of the Study
- At rest, muscle glycogen concentrations in PSSM horses were found to be significantly higher than in normal Quarter Horses or Thoroughbreds with recurrent exertional rhabdomyolysis.
- Muscle lactate levels were similar between PSSM and normal Quarter Horses, but significantly higher in PSSM horses compared to Thoroughbreds.
- During a maximal exercise test, muscle glycogen concentrations in PSSM horses declined significantly more, and lactate levels increased more than in normal Quarter Horses, indicating that the glycolytic pathway (a metabolic pathway that coverts glucose to lactate) was functional in these horses.
- Unlike normal Quarter Horses, PSSM horses did not show a significant change in blood lactate levels after exercise, indicating that their oxidative metabolism was unimpeded during submaximal exercise.
- Additionally, serum CK activity, an indicator of muscle damage, showed a significant increase post-exercise in PSSM horses as compared to normal Quarter Horses.
Conclusions and Implications
- Despite the common belief that impaired utilization of glycogen could be a reason for its excessive accumulation in PSSM horses, this study found rather that this was due to increased synthesis of glycogen. As such, the PSSM horses were not found to be incapable of effectively utilizing glycogen during exercise.
- Given these findings, it was suggested that PSSM horses might benefit from a diet low in soluble carbohydrates with added fat and gradually increased daily exercise. This could help in reducing excessive glycogen accumulation and improving its utilization, thereby managing the symptoms of PSSM better.
Cite This Article
APA
Valberg SJ, Macleay JM, Billstrom JA, Hower-Moritz MA, Mickelson JR.
(1999).
Skeletal muscle metabolic response to exercise in horses with ‘tying-up’ due to polysaccharide storage myopathy.
Equine Vet J, 31(1), 43-47.
https://doi.org/10.1111/j.2042-3306.1999.tb03789.x Publication
Researcher Affiliations
- Department of Clinical and Population Sciences, University of Minnesota, St Paul 55108, USA.
MeSH Terms
- Adenosine Triphosphate / metabolism
- Animals
- Female
- Glucose-6-Phosphate / metabolism
- Glycogen / metabolism
- Glycogen Storage Disease / complications
- Glycogen Storage Disease / metabolism
- Glycogen Storage Disease / veterinary
- Heart Rate
- Horse Diseases / etiology
- Horse Diseases / metabolism
- Horses
- Lactates / blood
- Lactates / metabolism
- Male
- Muscle, Skeletal / metabolism
- Physical Conditioning, Animal / physiology
- Polysaccharides / metabolism
- Pyruvic Acid / metabolism
- Rhabdomyolysis / etiology
- Rhabdomyolysis / metabolism
- Rhabdomyolysis / veterinary
Citations
This article has been cited 8 times.- Meng S, Zhang Y, Lv S, Zhang Z, Liu X, Jiang L. Comparison of muscle metabolomics between two Chinese horse breeds. Front Vet Sci 2023;10:1162953.
- Raspa F, Dinardo FR, Vervuert I, Bergero D, Bottero MT, Pattono D, Dalmasso A, Vinassa M, Valvassori E, Bruno E, De Palo P, Valle E. A Fibre- vs. cereal grain-based diet: Which is better for horse welfare? Effects on intestinal permeability, muscle characteristics and oxidative status in horses reared for meat production. J Anim Physiol Anim Nutr (Berl) 2022 Mar;106(2):313-326.
- Tosi I, Art T, Cassart D, Farnir F, Ceusters J, Serteyn D, Lemieux H, Votion DM. Altered mitochondrial oxidative phosphorylation capacity in horses suffering from polysaccharide storage myopathy. J Bioenerg Biomembr 2018 Oct;50(5):379-390.
- McCoy AM, Schaefer R, Petersen JL, Morrell PL, Slamka MA, Mickelson JR, Valberg SJ, McCue ME. Evidence of positive selection for a glycogen synthase (GYS1) mutation in domestic horse populations. J Hered 2014 Mar-Apr;105(2):163-72.
- Naylor RJ, Livesey L, Schumacher J, Henke N, Massey C, Brock KV, Fernandez-Fuente M, Piercy RJ. Allele copy number and underlying pathology are associated with subclinical severity in equine type 1 polysaccharide storage myopathy (PSSM1). PLoS One 2012;7(7):e42317.
- Barrey E, Mucher E, Jeansoule N, Larcher T, Guigand L, Herszberg B, Chaffaux S, Guérin G, Mata X, Benech P, Canale M, Alibert O, Maltere P, Gidrol X. Gene expression profiling in equine polysaccharide storage myopathy revealed inflammation, glycogenesis inhibition, hypoxia and mitochondrial dysfunctions. BMC Vet Res 2009 Aug 7;5:29.
- McCue ME, Valberg SJ, Miller MB, Wade C, DiMauro S, Akman HO, Mickelson JR. Glycogen synthase (GYS1) mutation causes a novel skeletal muscle glycogenosis. Genomics 2008 May;91(5):458-66.
- Pösö AR. Monocarboxylate transporters and lactate metabolism in equine athletes: a review. Acta Vet Scand 2002;43(2):63-74.
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