Document Detail


Abnormal blood lactate accumulation after exercise in patients with multiple mitochondrial DNA deletions and minor muscular symptoms.
MedLine Citation:
PMID:  15056184     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
STUDY OBJECTIVES: Muscle is one of the most commonly affected organs in mitochondrial disorders, and the symptoms are often exercise related. The cardiopulmonary exercise test with the determination of lactic acid formation could give supplementary information about the exercise-induced metabolic stress and compensatory mechanisms used in these disorders. The aim of this study was to evaluate the exercise capacity and lactate kinetics related to exercise in subjects with two genetically characterized mitochondrial disorders (multiple mitochondrial DNA deletions with PEO, MELAS) compared with lactate kinetics in subjects with metabolic myopathy (McArdle's disease) and in the healthy controls. DESIGN: The subjects were consecutive, co-operative patients of Department of Neurology of Helsinki University Hospital. Molecular genetic analyses were used for group classification of the mitochondrial myopathy. Study subjects: The study groups consisted of 11 patients with multiple deletions (PEO) and five patients with a point mutation in the mitochondrial DNA (MELAS), four patients with a muscle phosphorylase enzyme deficiency (McArdle's disease) and 13 healthy controls. The clinical disease of the patients was relatively mild. MEASUREMENTS AND RESULTS: A graded exercise test with ventilatory gas analyses and venous blood lactic acid analyses was performed. The main finding was the prolonged accumulation of blood lactate after the exercise in the PEO and MELAS groups compared with the controls. An overcompensation in ventilation was found in the MELAS and PEO group. CONCLUSIONS: The blood lactate accumulation after exercise occurs in patients with multiple mitochondrial DNA deletions or MELAS even in patients with only mild exercise intolerance. Cardiopulmonary exercise can be used in the diagnostic process of patients with mitochondrial myopathies.
Authors:
Harri Lindholm; Mervi Löfberg; Hannu Somer; Hannu Näveri; Anssi Sovijärvi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical physiology and functional imaging     Volume:  24     ISSN:  1475-0961     ISO Abbreviation:  Clin Physiol Funct Imaging     Publication Date:  2004 Mar 
Date Detail:
Created Date:  2004-04-01     Completed Date:  2004-06-29     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  101137604     Medline TA:  Clin Physiol Funct Imaging     Country:  England    
Other Details:
Languages:  eng     Pagination:  109-15     Citation Subset:  IM    
Affiliation:
Laboratory Department, Division of Clinical Physiology, Helsinki University Hospital, Helsinki, Finland. harri.lindholm@ttl.fi
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MeSH Terms
Descriptor/Qualifier:
Adult
Case-Control Studies
DNA, Mitochondrial / genetics*
Exercise*
Female
Gene Deletion*
Glycogen Storage Disease Type V / blood,  genetics,  physiopathology*
Humans
Lactic Acid / blood*
MELAS Syndrome / blood,  genetics,  physiopathology
Male
Middle Aged
Mitochondrial Myopathies / blood,  genetics,  physiopathology*
Ophthalmoplegia / blood,  genetics,  physiopathology
Point Mutation
Chemical
Reg. No./Substance:
0/DNA, Mitochondrial; 50-21-5/Lactic Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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