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Cited by 211Mitochondrial Function and PathologyCardiovascular and exercise physiologyMuscle Physiology and Disorders

The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.

Aerobic training is safe and improves exercise capacity in patients with mitochondrial myopathy

Jeppesen, T. D., Schwartz, M., Olsen, D. B., Wibrand, F., Krag, T., Duno, M., Hauerslev, S., Vissing, J.·2006·Brain
DOI 10.1093/brain/awl149
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Abstract

Exercise intolerance is a prominent symptom in patients with mitochondrial myopathy (MM), but it is still unsettled whether exercise training is safe and beneficial for patients with MM. To address this, we studied the effect of 12 weeks cycle training on exercise capacity, quality of life and underlying molecular and cellular events in five patients with single large-scale deletions, one with a microdeletion and 14 with point mutations of mitochondrial DNA (mtDNA), and 13 healthy subjects. Each training session lasted 30 min, and was performed at an intensity of 70% of VO2max (maximal oxygen uptake). Each subject performed 50 training sessions in 12 weeks. All subjects were evaluated before and after training, and 13 MM patients were studied after 8 weeks of deconditioning. Evaluation included VO2max and mutation load and mtDNA quantity, mitochondrial enzymatic activity, and number of centrally nucleated, apoptotic, ragged red and cytochrome oxidase (COX)-negative fibres in muscle biopsies from the quadriceps muscle. After 12 weeks of training, VO2max and muscle citrate synthase increased in MM (26 and 67%) and healthy (17 and 65%) subjects, while mtDNA quantity in muscle only increased in the MM patients (81%). In the MM patients, training did not change mtDNA mutation load in muscle, mitochondrial enzyme complex activities, muscle morphology and plasma creatine kinase. After deconditioning, VO2max and citrate synthase activity returned to values before training, while muscle mtDNA mutation load decreased. These findings show that aerobic training efficiently improves oxidative capacity in MM patients. Based on unchanged levels of mutant load in muscle, morphological findings on muscle biopsy and plasma creatine kinase levels during training, the treatment appears to be safe. Regular, supervised aerobic exercise is therefore recommended in MM patients with the studied mutations.

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Metadata

Authors
Jeppesen, T. D., Schwartz, M., Olsen, D. B., Wibrand, F., Krag, T., Duno, M., Hauerslev, S., & Vissing, J.
Affiliations
Rigshospitalet (DK)
ORCID
Venue
Brain
Publisher
Oxford University Press (OUP)
Published
2006-06-09
Volume
129
Issue
12
Pages
3402-3412
ISSN
  • 0006-8950 (ISSN-L)
  • 1460-2156
DOI
10.1093/brain/awl149
OpenAlex
W2111001861
Cited by
211
References
32
Citations by year
2026: 4 · 2025: 10 · 2024: 9 · 2023: 10 · 2022: 5 · 2021: 14 · 2020: 13 · 2019: 20 · 2018: 6 · 2017: 8 · 2016: 7 · 2015: 12 · 2014: 10 · 2013: 13 · 2012: 19
FWCI
4.21
Type
journal article
Language
en
Open access
closed
Locations
  • Brain (publishedVersion)
  • PubMed (publishedVersion)
  • HighWire Press Open Archive (submittedVersion)
Funders
  • Sundhed og Sygdom, Det Frie Forskningsråd
  • Fondation pour la Recherche Médicale
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
mitochondrial myopathy, aerobic exercise training, exercise capacity, exercise intolerance, mitochondrial DNA mutations, mitochondrial DNA deletions, VO2max, citrate synthase, mitochondrial enzyme activity, deconditioning, creatine kinase, muscle biopsy, exercise safety, quality of life
MeSH terms
Adult, Aerobiosis, Creatine Kinase, DNA, Mitochondrial, Exercise Therapy, Female, Heart Rate, Humans, Lactates, Male, Middle Aged, Mitochondria, Oxygen Consumption, Quality of Life, Treatment Outcome, Mitochondrial Myopathies, Gene Deletion, Point Mutation, Muscle, Skeletal

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