Structured evidence table for Niacin Exercise Performance Randomized Trial, generated from 2 reusable source documents in the Migaku knowledge base.
| topic | claim | evidence level | citation | source |
|---|---|---|---|---|
| Niacin Exercise Performance Randomized Trial | Risk of bias was assessed using Revised Cochrane Risk-of-Bias Tool for Randomized Trials (RoB 2) and Risk of Bias in Non-randomized Studies of Interventions (ROBINS-I V2), and methodological quality was appraised with the Mixed Methods Appraisal Tool (MMAT). | 1 | Wan Q (2026) | Effects of exercise training on skeletal muscle function in patients with mitochondrial myopathy: a systematic review. |
| Niacin Exercise Performance Randomized Trial | Moderate-intensity aerobic and resistance exercise consistently improved maximal oxygen uptake (VO 2 max), maximal workload (W max), muscle strength, and mitochondrial enzyme activity, with no consistent group-level increases observed in creatine kinase (CK) levels or mtDNA mutation burden. | 1 | Wan Q (2026) | Effects of exercise training on skeletal muscle function in patients with mitochondrial myopathy: a systematic review. |
| Niacin Exercise Performance Randomized Trial | Aerobic training enhanced oxidative capacity, phosphocreatine (PCr) recovery, and antioxidant defense, while resistance training improved muscle strength, satellite cell activation, and reduced cytochrome c oxidase (COX)-deficient fibers. | 1 | Wan Q (2026) | Effects of exercise training on skeletal muscle function in patients with mitochondrial myopathy: a systematic review. |
| Niacin Exercise Performance Randomized Trial | Background Mitochondrial myopathy (MM) is a group of rare, progressive muscle disorders characterized by impaired oxidative phosphorylation due to mitochondrial DNA (mtDNA) or nuclear DNA (nDNA) mutations, leading to exercise intolerance, muscle weakness, and metabolic dysfunction. | 1 | Wan Q (2026) | Effects of exercise training on skeletal muscle function in patients with mitochondrial myopathy: a systematic review. |
| Niacin Exercise Performance Randomized Trial | Biomarkers may be useful to overcome intrinsic challenges associated with clinical trial designs in small populations that are both genetically and clinically heterogenous and may facilitate early drug development by guiding dose selection and trial enrichment. | 3 | Stern Sydney (2026) | From Pharmacodynamic Biomarker to Evaluating Treatment Response: Biomarkers in Primary Mitochondrial Diseases |
| Niacin Exercise Performance Randomized Trial | Disease manifestations occur as a result of variant mitochondrial DNA (mtDNA) exceeding a critical threshold (heteroplasmy). | 3 | Stern Sydney (2026) | From Pharmacodynamic Biomarker to Evaluating Treatment Response: Biomarkers in Primary Mitochondrial Diseases |
| Niacin Exercise Performance Randomized Trial | One study found serum FGF‐21 concentrations had a strong positive correlation with age, critical illness, and multisystem involvement, but no correlation with the type of PMM (e.g., MELAS and Leigh syndrome did not differ in magnitude of elevation), mitochondrial defect involved, pathogenic variants, or organ system involvement []. | 3 | Stern Sydney (2026) | From Pharmacodynamic Biomarker to Evaluating Treatment Response: Biomarkers in Primary Mitochondrial Diseases |
| Niacin Exercise Performance Randomized Trial | 1 2 3 Primary mitochondrial diseases (PMDs) are genetic disorders characterized by defects in metabolic pathways contained in the mitochondrion, most commonly in oxidative phosphorylation, with downstream impairment of adenosine triphosphate (ATP) production in muscle tissue []. | 3 | Stern Sydney (2026) | From Pharmacodynamic Biomarker to Evaluating Treatment Response: Biomarkers in Primary Mitochondrial Diseases |
Source documents