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Skeletal muscle mitochondrial myopathy as a cause of exercise intolerance in a horse
Author(s) -
Valberg Stephanie J.,
Carlson Gary P.,
Cardinet George H.,
Birks Eric K.,
Jones James H.,
Chomyn Anne,
DiMauro Salvatore
Publication year - 1994
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880170308
Subject(s) - exercise intolerance , myopathy , mitochondrial myopathy , horse , medicine , skeletal muscle , physical medicine and rehabilitation , mitochondrial dna , biology , genetics , heart failure , paleontology , gene
Although exertional myopathies are commonly recognized in horses, specific etiologies have not been identified. This is the first report in the horse of a deficiency of Complex I respiratory chain enzyme associated with profound exercise intolerance. Physical examination, routine blood tests, endoscopy, and ultrasonograms of the heart and iliac arteries were unremarkable. With slow, incremental exercise (speeds 1.5–7 m/s), the Arabian mare showed a marked lactic acidosis, increased mixed venous PVO 2 , and little change in oxygen consumption. Muscle biopsies contained large accumulations of mitochondria with bizarre cristae formations. Biochemical analyses revealed a very low activity of the first enzyme complex in the mitochondrial respiratory chain (NADH CoQ reductase). The exercise intolerance and muscle stiffness in this horse were attributed to a profound lactic acidosis resulting from impaired oxidative energy metabolism during exercise. © 1994 John Wiley & Sons, Inc.