FREE SHIPPING over $40
OVER 9000 FIVE-STAR REVIEWS
5% OFF ALL SUBSCRIPTIONS
100% HAPPINESS GUARANTEE
Analyze Diet
0
Home / Equine Research Bank / Equine Vet J / Characterisation of phenotypic patterns in equine exercise-a...
Equine veterinary journal2024; doi: 10.1111/evj.14128

Characterisation of phenotypic patterns in equine exercise-associated myopathies.

Abstract: Equine exercise-associated myopathies are prevalent, clinically heterogeneous, generally idiopathic disorders characterised by episodes of myofibre damage that occur in association with exercise. Episodes are intermittent and vary within and between affected horses and across breeds. The aetiopathogenesis is often unclear; there might be multiple causes. Poor phenotypic characterisation hinders genetic and other disease analyses. Objective: The aim of this study was to characterise phenotypic patterns across exercise-associated myopathies in horses. Methods: Historical cross-sectional study, with subsequent masked case-control validation study. Methods: Historical clinical and histological features from muscle samples (n = 109) were used for k-means clustering and validated using principal components analysis and hierarchical clustering. For further validation, a blinded histological study (69 horses) was conducted comparing two phenotypic groups with selected controls and horses with histopathological features characterised by myofibrillar disruption. Results: We identified two distinct broad phenotypes: a non-classic exercise-associated myopathy syndrome (EAMS) subtype was associated with practitioner-described signs of apparent muscle pain (p < 0.001), reluctance to move (10.85, p = 0.001), abnormal gait (p < 0.001), ataxia (p = 0.001) and paresis (p = 0.001); while a non-specific classic RER subtype was not uniquely associated with any particular variables. No histological differences were identified between subtypes in the validation study, and no identifying histopathological features for other equine myopathies identified in either subtype. Conclusions: Lack of an independent validation population; small sample size of smaller identified subtypes; lack of positive control myofibrillar myopathy cases; case descriptions derived from multiple independent and unblinded practitioners. Conclusions: This is the first study using computational clustering methods to identify phenotypic patterns in equine exercise-associated myopathies, and suggests that differences in patterns of presenting clinical signs support multiple disease subtypes, with EAMS a novel subtype not previously described. Routine muscle histopathology was not helpful in sub-categorising the phenotypes in our population. Background: Les myopathies induites à l'exercice demeurent fréquentes, hétérogènes cliniquement et représentent des désordres idiopathiques caractérisés par des épisodes de dommages myofibrillaires en lien avec l'exercice. Les épisodes sont intermittents et varient à la fois chez le même cheval, entre chevaux et entre les différentes races. L'étiopathogénie demeure obscure et pourrait être multifactorielle. La pauvre caractérisation phénotypique des myopathies ne simplifie pas les analyses génétiques ni celles d'autres maladies. Objective: Le but de cette étude est de caractériser les patrons phénotypiques en lien avec les myopathies induites à l'exercice chez le cheval. TYPE D'ÉTUDE: Étude transversale historique et étude subséquente de validation de cas témoins aveugle. MÉTHODES: Les facteurs clés cliniques et histologiques provenant d'échantillons de muscles (n = 109) ont été utilisés pour l'algorithme de K‐moyennes et validés par le biais d'analyse des composantes principales et de classification hiérarchique. Pour validation additionnelle, une étude histologique à l'aveugle (69 chevaux) a été faite comparant les deux groupes phénotypiques avec des contrôles sélectionnés et des chevaux avec éléments histopathologiques caractérisés par de la discontinuité myofibrillaire. RÉSULTATS: Deux phénotypes distincts ont été identifiés: un premier sous‐type de syndrome de myopathie induite à l'exercice non‐classique (EAMS) associé à de la douleur musculaire telle que décrite par le praticien suivant le cheval (χ  = 19.33, p < 0.001), difficulté à se déplacer (χ  = 10.85, p = 0.001), démarche anormale (χ  = 34.61, p < 0.001), ataxie (χ  = 10.88, p = 0.001) et parésie (χ  = 10.88, p = 0.001); alors qu'un sous‐type RER classique non‐spécifique n'était associé à aucune variable en particulier. Aucune différente histologique n'a été identifié entre les sous‐types dans l'étude de validation et aucune caractéristique histopathologique d'autres myopathies équines n'a été identifiées dans les différents sous‐types. Unassigned: Aucune population indépendante pour validation; petite taille d'échantillon pour les sous‐types peu nombreux identifiés; aucun cas contrôles positifs de myopathie fibrillaire; description des cas provenant de multiples praticiens indépendants et non‐aveugles. Conclusions: Cette étude est la première utilisant des méthodes de regroupement informatique pour identifier des patrons phénotypiques de myopathies équines induites à l'exercice et suggère que des différences existent dans les patrons de signes cliniques en faveur de multiples sous‐types de maladie, incluant EAMS qui représente un nouveau sous‐type non décrit jusqu'à maintenant. L'histopathologie musculaire de routine n'a pas permis de sous‐catégoriser les phénotypes dans cette population.
© 2024 The Author(s). Equine Veterinary Journal published by John Wiley & Sons Ltd on behalf of EVJ Ltd.
Get Full Text
Publication Date: 2024-07-05 PubMed ID: 38965932DOI: 10.1111/evj.14128Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
LinkedInCopy
  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research article explores the different patterns and characteristics found in horses suffering from equine exercise-associated myopathies, a collection of muscle disorders linked with exercise. The article uses computational methods to better identify and understand these disorders, and to reveal that there are potentially multiple different disease subtypes.

Objective and Method of Study

  • The main goal of this research was to identify phenotypic patterns in equine exercise-associated myopathies, a prevalent and varying collection of muscle disorders in horses associated with exercise.
  • The researchers performed a historical cross-sectional study using historical clinical and histological features from muscle samples of 109 horses.
  • These data were used in an algorithm for k-means clustering, this was then validated through a technique called principal components analysis and hierarchical clustering.
  • To further validate the study’s findings, a blind histological study was conducted using 69 more horses, comparing two identified phenotypic groups with selected controls and horses with characterized myofibrillar disruption.

Key Findings

  • The study found two distinct phenotypes associated with the myopathies. These are known as the non-classic exercise-associated myopathy syndrome (EAMS) and non-specific classic RER subtype.
  • Notably, EAMS is associated with muscle pain, reluctance to move, unusual gait, ataxia and paresis. None of these abnormalities were unique to the non-specific classic RER subtype.
  • No significant histological differences were found between these subtypes in the validation phase of this study.
  • Furthermore, no identifying histopathological features for other equine myopathies was identified in either suffering groups.

Conclusions

  • The research, for the first time, applied computational methods to understand phenotypic patterns in equine exercise-associated myopathies. This highlighted the possibility of multiple disease subtypes, with EAMS representing a new subtype that was previously undescribed.
  • However, the authors noted certain limitations to their study, including the lack of an independent validation population, small sample sizes, the absence of positive control myofibrillar myopathy cases and the fact that their case descriptions derived from multiple independent and unblinded practitioners.

Cite This Article

APA
Lindsay-McGee V, Massey C, Li YT, Clark EL, Psifidi A, Piercy RJ. (2024). Characterisation of phenotypic patterns in equine exercise-associated myopathies. Equine Vet J. https://doi.org/10.1111/evj.14128

Publication

Equine veterinary journal
ISSN: 2042-3306
NlmUniqueID: 0173320
Country: United States
Language: English

Researcher Affiliations

Lindsay-McGee, Victoria
  • Department of Clinical Sciences and Services, Royal Veterinary College, London, UK.
Massey, Claire
  • Department of Clinical Sciences and Services, Royal Veterinary College, London, UK.
Li, Ying Ting
  • Department of Clinical Sciences and Services, Royal Veterinary College, London, UK.
Clark, Emily L
  • The Roslin Institute, University of Edinburgh, Edinburgh, UK.
Psifidi, Androniki
  • Department of Clinical Sciences and Services, Royal Veterinary College, London, UK.
  • The Roslin Institute, University of Edinburgh, Edinburgh, UK.
Piercy, Richard J
  • Department of Clinical Sciences and Services, Royal Veterinary College, London, UK.

References

This article includes 79 references
  1. Tietjen DP, Guzzi LM. Exertional rhabdomyolysis and acute renal failure following the Army Physical Fitness Test.. Mil Med 1989;154:23–25.
  2. Brown JA, Elliott MJ, Sray WA. Exercise‐induced upper extremity rhabdomyolysis and myoglobinuria in shipboard military personnel.. Mil Med 1994;159:473–475.
  3. Aizawa H, Morita K, Minami H, Sasaki N, Tobise K. Exertional rhabdomyolysis as a result of strenuous military training.. J Neurol Sci 1995;132:239–240.
  4. Armed Forces Health Surveillance Branch. Update: exertional rhabdomyolysis, active component, U.S. Armed Forces, 2011.. MSMR 2012;19:17–19.
  5. Clarkson PM. Exertional rhabdomyolysis and acute renal failure in marathon runners.. Sports Med 2007;37:361–363.
  6. Kruse DH. “Tyson Squats” as a cause of rhabdomyolysis.. J Emerg Nurs 1998;2:116–117.
  7. Mahakkanukrauh A, Sangchan A, Mootsikapun P. Exertional rhabdomyolysis following excessive exercise of university freshman cheer‐training.. J Med Assoc Thail 2003;86:789–792.
  8. Springer BL, Clarkson PM. Two cases of exertional rhabdomyolysis precipitated by personal trainers.. Med Sci Sports Exerc 2003;35:1499–1502.
  9. Oh JY, Laidler M, Fiala SC, Hedberg K. Acute exertional rhabdomyolysis and triceps compartment syndrome during a high school football camp.. Sports Health 2012;4:57–62.
  10. MacLeay JM, Sorum SA, Valberg SJ, Marsh WE, Sorum MD. Epidemiologic analysis of factors influencing exertional rhabdomyolysis in thoroughbreds.. Am J Vet Res 1999;60:1562–1566.
  11. McGowan CM, Fordham T, Christley R. Incidence and risk factors for exertional rhabdomyolysis in thoroughbred racehorses in the United Kingdom.. Vet Rec 2002;151:623–626.
  12. Upjohn M, Archer R, Christley R, McGowan C. Incidence and risk factors associated with exertional rhabdomyolysis syndrome in National Hunt racehorses in Great Britain.. Vet Rec 2005;156:763–766.
  13. Isgren CM, Upjohn MM, Fernandez‐Fuente M, Massey C, Pollott G, Verheyen KLP. Epidemiology of exertional rhabdomyolysis susceptibility in standardbred horses reveals associated risk factors and underlying enhanced performance.. PLoS One 2010;5(7):e11594.
  14. McGowan CM, Posner RE, Christley RM. Incidence of exertional rhabdomyolysis in polo horses in the USA and the United Kingdom in the 1999/2000 season.. Vet Rec 2002;150:535–537.
  15. Singer ER, Barnes J, Saxby F, Murray JK. Injuries in the event horse: training versus competition.. Vet J 2008;175:76–81.
  16. Wilberger MS, Mckenzie EC, Payton ME, Rigas J, Valberg SJ. Prevalence of exertional rhabdomyolysis in endurance horses in the Pacific northwestern United States.. Equine Vet J 2015;47:165–170.
  17. Norton EM, Mickelson JR, Binns MM, Blott SC, Caputo P, Isgren CM. Heritability of recurrent exertional rhabdomyolysis in standardbred and thoroughbred racehorses derived from SNP genotyping data.. J Hered 2016;107(6):537–543.
  18. Tozaki T, Hirota K, Sugita S, Ishida N, Miyake T, Oki H. A genome‐wide scan for tying‐up syndrome in Japanese thoroughbreds.. Anim Genet 2010;41:80–86.
  19. Fritz KL, McCue ME, Valberg SJ, Rendahl AK, Mickelson JR. Genetic mapping of recurrent exertional rhabdomyolysis in a population of North American thoroughbreds.. Anim Genet 2012;43:730–738.
    doi: 10.1111/j.1365-2052.2012.02351.xgoogle scholar: lookup
  20. Keen J. Diagnosis and management of equine rhabdomyolysis.. In Pract 2011;33:68–77.
  21. Scalco RS, Snoeck M, Quinlivan R, Treves S, Laforét P, Jungbluth H. Exertional rhabdomyolysis: physiological response or manifestation of an underlying myopathy?. BMJ Open Sport Exerc Med 2016;2:e000151.
    doi: 10.1136/bmjsem-2016-000151google scholar: lookup
  22. Valberg SJ, Cardinet GH III, Carlson GP, DiMauro S. Polysaccharide storage myopathy associated with recurrent exertional rhabdomyolysis in horses.. Neuromuscul Disord 1992;2:351–359.
  23. Valentine B, Credille KM, Lavoie JP, Fatone S, Guard C, Cummings JF. Severe polysaccharide storage myopathy in Belgian and Percheron draught horses.. Equine Vet J 1997;29:220–225.
  24. Sprayberry KA, Madigan J, LeCouteur RA, Valentine BA. Renal failure, laminitis, and colitis following severe rhabdomyolysis in a draft horse‐cross with polysaccharide storage myopathy.. Can Vet J 1998;39:500–503.
  25. Bloom B, Valentine B, Gleed R, Cable C. Postanaesthetic recumbency in a Belgian filly with polysaccharide storage myopathy.. Vet Rec 1999;144:73–75.
  26. Valberg SJ, Mickelson JR, Gallant EM, MacLeay JM, Lentz L, de laCorte F. Exertional rhabdomyolysis in quarter horses and thoroughbreds: one syndrome, multiple aetiologies.. Equine Vet J 1999;31:533–538.
  27. Valentine B, De Lahunta A, Divers T, Ducharme N, Orcutt R. Clinical and pathologic findings in two draft horses with progressive muscle atrophy, neuromuscular weakness, and abnormal gait characteristic of shivers syndrome.. J Am Vet Med Assoc 1999;215:1621–1665.
  28. Valentine BA, McDonough S, Chang Y‐F, Vonderchek A. Polysaccharide storage myopathy in Morgan, Arabian, and Standardbred related horses and welsh‐cross ponies.. Vet Pathol 2000;37:193–196.
  29. Valentine BA, Habecker PL, Patterson JS, Njaa BL, Shapiro J, Holshuh HJ. Incidence of polysaccharide storage myopathy in draft horse‐related breeds: a necropsy study of 37 horses and a mule.. J Vet Diagn Invest 2001;13:63–68.
  30. Valentine B, Cooper B. Incidence of polysaccharide storage myopathy: necropsy study of 225 horses.. Vet Pathol 2005;42:823–827.
  31. Valentine BA, Cooper BJ. Development of polyglucosan inclusions in skeletal muscle.. Neuromuscul Disord 2006;16:603–607.
  32. McCue ME, Valberg SJ, Miller MB, Wade C, DiMauro S, Akman HO. Glycogen synthase (GYS1) mutation causes a novel skeletal muscle glycogenosis.. Genomics 2008;91:458–466.
  33. Maile CA, Hingst JR, Mahalingan KK, O'Reilly AO, Cleasby ME, Mickelson JR. A highly prevalent equine glycogen storage disease is explained by constitutive activation of a mutant glycogen synthase.. BBA‐Gen Subjects 2017;1861:3388–3398.
    doi: 10.1016/j.bbagen.2016.08.021google scholar: lookup
  34. Stanley RL, McCue ME, Valberg SJ, Mickelson JR, Mayhew IG, McGowan C. A glycogen synthase 1 mutation associated with equine polysaccharide storage myopathy and exertional rhabdomyolysis occurs in a variety of UK breeds.. Equine Vet J 2009;41:597–601.
  35. McCue ME, Armién AG, Lucio M, Mickelson JR, Valberg SJ. Comparative skeletal muscle histopathologic and ultrastructural features in two forms of polysaccharide storage myopathy in horses.. Vet Pathol 2009;46:1281–1291.
    doi: 10.1354/vp.08-vp-0177-m-flgoogle scholar: lookup
  36. Valberg SJ, Nicholson AM, Lewis SS, Reardon RA, Finno CJ. Clinical and histopathological features of myofibrillar myopathy in warmblood horses.. Equine Vet J 2017;49:739–745.
    doi: 10.1111/evj.12702google scholar: lookup
  37. Valberg SJ, McKenzie EC, Eyrich LV, Shivers J, Barnes NE, Finno CJ. Suspected myofibrillar myopathy in Arabian horses with a history of exertional rhabdomyolysis.. Equine Vet J 2016;48:548–556.
    doi: 10.1111/evj.12493google scholar: lookup
  38. Selcen D, Engel AG. Myofibrillar myopathy caused by novel dominant negative αB‐crystallin mutations.. Ann Neurol 2003;54:804–810.
  39. Selcen D, Ohno K, Engel AG. Myofibrillar myopathy: clinical, morphological and genetic studies in 63 patients.. Brain 2004;127:439–451.
  40. Vattemi G, Neri M, Piffer S, Vicart P, Gualandi F, Marini M. Clinical, morphological and genetic studies in a cohort of 21 patients with myofibrillar myopathy.. Acta Myologica 2011;30:121–126.
  41. Fichna JP, Maruszak A, Żekanowski C. Myofibrillar myopathy in the genomic context.. J Appl Genet 2018;59:431–439.
  42. Valberg SJ, Finno CJ, Henry ML, Schott M, Velez‐Irizarry D, Peng S. Commercial genetic testing for type 2 polysaccharide storage myopathy and myofibrillar myopathy does not correspond to a histopathological diagnosis.. Equine Vet J 2021;53:690–700.
  43. Valberg SJ, Henry ML, Herrick KL, Velez‐Irizarry D, Finno CJ, Petersen JL. Absence of myofibrillar myopathy in quarter horses with a histopathological diagnosis of type 2 polysaccharide storage myopathy and lack of association with commercial genetic tests.. Equine Vet J 2022;55(2):230–238.
  44. Miro. 2021. [cited 2024 Mar 20]. Available from: https://www.miro.com
  45. Pedregosa F, Varoquaux G, Gramfort A, Michel V, Thirion B, Grisel O. Scikit‐learn: machine learning in Python.. J Mach Learn Res 2011;12:2825–2830.
  46. McKinney W. Proceedings of the 9th Python in Science Conference (Austin, TX).
  47. Waskom ML. seaborn: statistical data visualization.. J Open Source Softw 2021;6:3021.
    doi: 10.21105/joss.03021google scholar: lookup
  48. Hunter JD. Matplotlib: a 2D graphics environment.. Comput Sci Eng 2007;9:90–95.
  49. Ward JH. Hierarchical grouping to optimize an objective function.. J Am Stat Assoc 1963;58:236–244.
  50. Dubowitz V, Sewry CA, Oldfors A. Muscle biopsy: a practical approach. Amsterdam: Elsevier Health Sciences; 2021.
  51. Draper A, Bender JB, Firshman AM, Baird JD, Reed S, Mayhew IG. Epidemiology of shivering (shivers) in horses.. Equine Vet J 2015;47:182–187.
  52. Valberg SJ, Williams ZJ, Henry ML, Finno CJ. The equine movement disorder “Shivers” is associated with selective cerebellar purkinje cell axonal degeneration.. Vet Pathol 2015;52:1087–1098.
  53. Tuomi T, Santoro N, Caprio S, Cai M, Weng J. The many faces of diabetes: a disease with increasing heterogeneity.. Lancet 2014;383:1084–1094.
  54. Li L, Cheng W‐Y, Glicksberg BS, Gottesman O, Tamler R, Chen R. Identification of type 2 diabetes subgroups through topological analysis of patient similarity.. Sci Transl Med 2015;7(311):311ra174.
  55. Skyler JS, Bakris GL, Bonifacio E, Darsow T, Eckel RH, Groop L. Differentiation of diabetes by pathophysiology, natural history, and prognosis.. Diabetes 2017;66:241–255.
  56. Ahlqvist E, Storm P, Käräjämäki A, Martinell M, Dorkhan M, Carlsson A. Novel subgroups of adult‐onset diabetes and their association with outcomes: a data‐driven cluster analysis of six variables.. Lancet Diabetes Endocrinol 2018;6:361–369.
  57. Udler MS, Kim J, vonGrotthuss M, Bonàs‐Guarch S, Cole JB, Chiou J. Type 2 diabetes genetic loci informed by multi‐trait associations point to disease mechanisms and subtypes: a soft clustering analysis.. PLoS Med 2018;15:e1002654.
  58. Dapas M, Lin FTJ, Nadkarni GN, Sisk R, Legro RS, Urbanek M. Distinct subtypes of polycystic ovary syndrome with novel genetic associations: an unsupervised, phenotypic clustering analysis.. PLoS Med 2020;17:e1003132.
  59. Barros FC, Papagorghiou AT, Victora CG, Noble JA, Pang R, Iams J. The distribution of clinical phenotypes of preterm birth syndrome: implications for prevention.. JAMA Pediatr 2015;169:220–229.
  60. Bos L, Schouten LR, vanVught LA, Wiewel MA, Ong DSY, Cremer O. Identification and validation of distinct biological phenotypes in patients with acute respiratory distress syndrome by cluster analysis.. Thorax 2017;72:876–883.
  61. Calfee CS, Delucchi KL, Sinha P, Matthay MA, Hackett J, Shankar‐Hari M. Acute respiratory distress syndrome subphenotypes and differential response to simvastatin: secondary analysis of a randomised controlled trial.. Lancet Respir Med 2018;6:691–698.
  62. Millar JE, Wildi K, Barnikowski N, Bouquet M, Hyslop K, Passmore MR. Characterizing preclinical sub‐phenotypic models of acute respiratory distress syndrome: an experimental ovine study.. Physiol Rep 2021;9:e15048.
  63. Ahmad T, Lund LH, Rao P, Ghosh R, Warier P, Vaccaro B. Machine learning methods improve prognostication, identify clinically distinct phenotypes, and detect heterogeneity in response to therapy in a large cohort of heart failure patients.. J Am Heart Assoc 2018;7:e008081.
  64. Lewis SL, Holl HM, Long MT, Mallicote MF, Brooks SA. Use of principle component analysis to quantitatively score the equine metabolic syndrome phenotype in an Arabian horse population.. PLoS One 2018;13:e0200583.
  65. Selcen D. Myofibrillar myopathies.. Neuromuscul Disord 2011;21:161–171.
    doi: 10.1016/j.nmd.2010.12.007google scholar: lookup
  66. Rudolph JA, Spier SJ, Byrns G, Rojas CV, Bernoco D, Hoffman EP. Periodic paralysis in quarter horses: a sodium channel mutation disseminated by selective breeding.. Nat Genet 1992;2:144–147.
  67. Spier S, Carlson G, Holliday T, Cardinet G 3rd, Pickar J. Hyperkalemic periodic paralysis in horses.. J Am Vet Med Assoc 1990;197:1009–1017.
  68. Scalco RS, Gardiner AR, Pitceathly RDS, Zanoteli E, Becker J, Holton JL. Rhabdomyolysis: a genetic perspective.. Orphanet J Rare Dis 2015;10:1–15.
  69. Olsen E, Dunkel B, Barker WHJ, Finding EJT, Perkins JD, Witte TH. Rater agreement on gait assessment during neurologic examination of horses.. J Vet Intern Med 2014;28:630–638.
  70. Williams ZJ, Velez‐Irizarry D, Gardner K, Valberg SJ. Integrated proteomic and transcriptomic profiling identifies aberrant gene and protein expression in the sarcomere, mitochondrial complex I, and the extracellular matrix in warmblood horses with myofibrillar myopathy.. BMC Genomics 2021;22:438.
    doi: 10.1186/s12864-021-07758-0google scholar: lookup
  71. Güttsches AK, Brady S, Krause K, Maerkens A, Uszkoreit J, Eisenacher M. Proteomics of rimmed vacuoles define new risk allele in inclusion body myositis.. Ann Neurol 2017;81:227–239.
  72. De Bleecker JL, Ertl BB, Engel AG. Patterns of abnormal protein expression in target formations and unstructured cores.. Neuromuscul Disord 1996;6:339–349.
  73. Bönnemann C, Thompson TG, van derVen PFM, Goebel HH, Warlo I, Vollmers B. Filamin C accumulation is a strong but nonspecific immunohistochemical marker of core formation in muscle.. J Neurol Sci 2003;206:71–78.
  74. Bornemann A, Schmalbruch H. Desmin and vimentin in regenerating muscles.. Muscle Nerve 1992;15:14–20.
  75. Rivero JLL. A scientific background for skeletal muscle conditioning in equine practice.. J Vet Med Ser A 2007;54:321–332.
  76. Rivero JLL, Piercy RJ. Chapter 6. Equine sports medicine and surgery.. In: Hinchcliff KW, Kaneps A, Geor R, editors. Philadelphia: Saunders; 2014. p. 69–108.
  77. Snow D, Guy P. Muscle fibre type composition of a number of limb muscles in different types of horse.. Res Vet Sci 1980;28:137–144.
  78. Valentine BA. In: Zachary JF, editor. Pathologic basis of veterinary disease. 6th ed. Missouri: Mosby; 2017. p. 908–953.e901.
  79. Kruijt N, van denBersselaar LR, Kamsteeg EJ, Verbeeck W, Snoeck MMJ, Everaerd DS. The etiology of rhabdomyolysis: an interaction between genetic susceptibility and external triggers.. Eur J Neurol 2021;28:647–659.

Citations

This article has been cited 0 times.
Subscribe to our newsletter
Join 99,034 horse owners like you who receive our email updates on horse health and nutrition.