Calcium sensitivity of force production and myofibrillar ATPase activity in muscles from Thoroughbreds with recurrent exertional rhabdomyolysis

Citation
Ja. Mlekoday et al., Calcium sensitivity of force production and myofibrillar ATPase activity in muscles from Thoroughbreds with recurrent exertional rhabdomyolysis, AM J VET RE, 62(10), 2001, pp. 1647-1652
Citations number
38
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
AMERICAN JOURNAL OF VETERINARY RESEARCH
ISSN journal
00029645 → ACNP
Volume
62
Issue
10
Year of publication
2001
Pages
1647 - 1652
Database
ISI
SICI code
0002-9645(200110)62:10<1647:CSOFPA>2.0.ZU;2-S
Abstract
Objective-To determine whether the basis for recurrent exertional rhabdomyo lysis (RER) in Thoroughbreds lies in an alteration in the activation and re gulation of the myofibrillar contractile apparatus by ionized calcium. Animals-4 Thoroughbred mares with RER and 4 clinically normal (control) Tho roughbreds. Procedures-Single chemically-skinned type-1 (slow-twitch) and type-II (fast -twitch) muscle fibers were obtained from punch biopsy specimens, mounted t o a force transducer, and the tensions that developed in response to a seri es of calcium concentrations were measured. In addition, myofibril preparat ions were Isolated from muscle biopsy specimens and the maximal myofibrilla r ATPase activity, as well as Its sensitivity to ionized calcium, were meas ured. Results-Equine type-I muscle fibers were more readily activated by calcium than were type-II muscle fibers. However, there was no difference between t he type-II fibers of RER-affected and control horses in terms of calcium se nsitivity of force production. There was also no difference between muscle myofibril preparations from RER-affected and control horses in calcium sens itivity of myofibrillar ATPase activity. Conclusions and Clinical Relevance-An alteration in myofibrillar calcium se nsitivity is not a basis for pathologic contracture development In muscles from RER-affected horses. Recurrent exertional rhabdomyolysis in Thoroughbr eds may represent a novel heritable defect in the regulation of muscle exci tation-contraction coupling or myoplasmic calcium concentration.