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Exercise intolerance in mitochondrial myopathy is not related to lactic acidosis
Author(s) -
Vissing John,
Gansted Uffe,
Quistorff Bjørn
Publication year - 2001
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.1026
Subject(s) - mitochondrial myopathy , lactic acidosis , exercise intolerance , medicine , acidosis , crossover study , myopathy , lactic acid , oxidative phosphorylation , endocrinology , placebo , oxidative metabolism , chemistry , metabolism , biology , biochemistry , pathology , mitochondrial dna , heart failure , genetics , alternative medicine , bacteria , gene
Abstract In a double‐blinded, placebo‐controlled, crossover study in seven mitochondrial myopathy patients (MM), we investigated whether lowering of lactate with dichloroacetate (DCA) can improve exercise tolerance and oxidative capacity in MM. DCA lowered plasma lactate at rest and during exercise (from 10.5 ± 2.0 to 5.0 ± 1.6 mM; p = 0.005) but did not improve maximal work load or VO 2 in cycle exercise or phosphorous magnetic resonance spectroscopy ( 31 P‐MRS)‐assessed indices of muscle oxidative metabolism. This indicates that lactate acidosis is not the primary cause of exercise intolerance in MM.