ReviewFrontiers in physiology2020
Aerobic Exercise Training in Patients With mtDNA-Related Mitochondrial Myopathy.
Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Quantitative assessment of efficacy and evaluation of feasibility of exercise training protocols in adult and pediatric primary mitochondrial disease.BMC medicine · 2026Pooled it
- Reply to Comment on: "Based on a Single Case, Cardiopulmonary Training Cannot Be Recommended as Therapy for Hemiparesis in MELAS With Ischemic Stroke".The Kaohsiung journal of medical sciences · 2026Article
- Cardiopulmonary Exercise Testing (CPET) Guided Sub-Anaerobic Threshold Rehabilitation in MELAS Syndrome: A Case Report.The Kaohsiung journal of medical sciences · 2026Article
- Exercise-mediated regulation of mitochondrial dynamics in aging muscle: implications for mitochondrial diseases.Molecular and cellular biochemistry · 2026Review
- Diabetes management in maternally inherited diabetes and deafness (MIDD): A review and a proposed treatment algorithm.Diabetes, obesity & metabolism · 2026Review
- Mitochondria: the central hub linking exercise to enhanced cardiac function.Frontiers in physiology · 2026Review
- Exercise attenuates the hallmarks of aging: Novel perspectives.Journal of sport and health science · 2025Review
- Focusing on mitochondria in the brain: from biology to therapeutics.Translational neurodegeneration · 2024Review
- Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases.Current issues in molecular biology · 2024Review
- Mitochondrial Chronic Progressive External Ophthalmoplegia.Brain sciences · 2024Review
- Personalized Medicine in Mitochondrial Health and Disease: Molecular Basis of Therapeutic Approaches Based on Nutritional Supplements and Their Analogs.Molecules (Basel, Switzerland) · 2022Review
- Exercise Testing, Physical Training and Fatigue in Patients with Mitochondrial Myopathy Related to mtDNA Mutations.Journal of clinical medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In patients with mitochondrial DNA (mtDNA) mutation, a pathogenic mtDNA mutation is heteroplasmically distributed among tissues. The ratio between wild-type and mutated mtDNA copies determines the mtDNA mutation load of the tissue, which correlates inversively with oxidative capacity of the tissue. In patients with mtDNA mutation, the mutation load is often very high in skeletal muscle compared to other tissues. Additionally, skeletal muscle can increase its oxygen demand up to 100-fold from rest to exercise, which is unmatched by any other tissue. Thus, exercise intolerance is the most common symptom in patients with mtDNA mutation. The impaired oxidative capacity in skeletal muscle in patients with mtDNA mutation results in limitation in physical capacity that interferes with daily activities and impairs quality of life. Additionally, patients with mitochondrial disease due to mtDNA mutation often live a sedentary lifestyle, which further impair oxidative capacity and exercise tolerance. Since aerobic exercise training increase mitochondrial function and volume density in healthy individuals, studies have investigated if aerobic training could be used to counteract the progressive exercise intolerance in patients with mtDNA mutation. Overall studies investigating the effect of aerobic training in patients with mtDNA mutation have shown that aerobic training is an efficient way to improve oxidative capacity in this condition, and aerobic training seems to be safe even for patients with high mtDNA mutation in skeletal muscle.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.