ArticleThe Journal of clinical endocrinology and metabolism2013
Slow-twitch fiber proportion in skeletal muscle correlates with insulin responsiveness.
Article in The Journal of clinical endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00727779 (Mechanisms by Which Strength Training Ameliorates the Metabolic Syndrome), which is not on this map. Cited by 106 papers, 3 of them syntheses that pooled it.
What it found
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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.
Mechanisms by Which Strength Training Ameliorates the Metabolic Syndrome
Who cites it
106 citing papers in PubMed, 3 syntheses or guidelines pooled it, 217 citations in OpenAlex.
- A Systematic Review and Meta-analysis of the Association Between ACTN3 R577X Genotypes and Performance in Endurance Versus Power Athletes and Non-athletes.Sports medicine - open · 2024Pooled it
- PROKR1-CREB-NR4A2 axis for oxidative muscle fiber specification and improvement of metabolic function.Proceedings of the National Academy of Sciences of the United States of America · 2024Pooled it
- Exercise is associated with younger methylome and transcriptome profiles in human skeletal muscle.Aging cell · 2024Pooled it
- The Effect of Lower Limb Combined Neuromuscular Electrical Stimulation on Skeletal Muscle Signaling for Glucose Utilization, Myofiber Distribution, and Metabolic Function after Spinal Cord Injury.International journal of environmental research and public health · 2023Trial
- Trial
- Trial
- Pre-Training Muscle Characteristics of Subjects Who Are Obese Determine How Well Exercise Training Will Improve Their Insulin Responsiveness.Journal of strength and conditioning research · 2017Trial
- The effects of resistance exercise training on arterial stiffness in metabolic syndrome.European journal of applied physiology · 2016Trial
- Article
- Local Suppression ofJournal of microbiology and biotechnology · 2026Article
- The impact of metabolic syndrome on changes in trunk muscle CSA: a 10-year longitudinal study.Journal of bone and mineral metabolism · 2026Article
- Effects of empagliflozin alone and in combination with exercise on the soleus muscle in obese type 2 diabetic rats.The journal of physiological sciences : JPS · 2026Article
- Sarcopenia in cognitive disorders: Toward a shared pathophysiological framework.Osteoporosis and sarcopenia · 2026Review
- Fiber type-specific expression of LACTB leverages a function in oxidative metabolism.Histochemistry and cell biology · 2026Article
- Distinct HIF1α and HIF2α functions control skeletal muscle metabolism and erythropoiesis.The Journal of clinical investigation · 2026Article
- BRD4 directs myofiber identity and metabolic adaptation through CHD4 cooperation.Nature communications · 2026Article
- Skeletal muscle atrophy and dysfunction in obesity and type-2 diabetes mellitus: Myocellular mechanisms involved.Reviews in endocrine & metabolic disorders · 2025Review
- Skeletal muscle alterations in type 2 diabetes mellitus with and without dyslipidemia.Lipids in health and disease · 2025Article
- The impact of exercise on skeletal muscle proteome of prediabetic subjects analyzed with data independent mass spectrometry.Scientific reports · 2025Article
- Dysregulated skeletal muscle myosin super-relaxation and energetics in male participants with type 2 diabetes mellitus.Diabetologia · 2025Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
contextThe metabolic syndrome, characterized by central obesity with dyslipidemia, hypertension, and hyperglycemia, identifies people at high risk for type 2 diabetes.
objectiveOur objective was to determine how the insulin resistance of the metabolic syndrome is related to muscle fiber composition.
designThirty-nine sedentary men and women (including 22 with the metabolic syndrome) had insulin responsiveness quantified using euglycemic clamps and underwent biopsies of the vastus lateralis muscle. Expression of insulin receptors, insulin receptor substrate-1, glucose transporter 4, and ATP synthase were quantified with immunoblots and immunohistochemistry. PARTICIPANTS AND
settingParticipants were nondiabetic, metabolic syndrome volunteers and sedentary control subjects studied at an outpatient clinic.
main outcome measuresInsulin responsiveness during an insulin clamp and the fiber composition of a muscle biopsy specimen were evaluated.
resultsThere were fewer type I fibers and more mixed (type IIa) fibers in metabolic syndrome subjects. Insulin responsiveness and maximal oxygen uptake correlated with the proportion of type I fibers. Insulin receptor, insulin receptor substrate-1, and glucose transporter 4 expression were not different in whole muscle but all were significantly less in the type I fibers of metabolic syndrome subjects when adjusted for fiber proportion and fiber size. Fat oxidation and muscle mitochondrial expression were not different in the metabolic syndrome subjects.
conclusionLower proportion of type I fibers in metabolic syndrome muscle correlated with the severity of insulin resistance. Even though whole muscle content was normal, key elements of insulin action were consistently less in type I muscle fibers, suggesting their distribution was important in mediating insulin effects.
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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.