ArticleAmerican journal of physiology. Endocrinology and metabolism2013
Mitochondrial and performance adaptations to exercise training in mice lacking skeletal muscle LKB1.
Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Exercise training improves exercise capacity independent of AMPKα2 T172-mediated adaptations in skeletal muscle.bioRxiv : the preprint server for biology · 2026Article
- Chondroitin Sulfate A-Selenium Nanoparticles Activate Autophagy Through the AMPK-mTOR Pathway to Alleviate Oxidative Stress and Mitochondrial Dysfunction to Repair Kashin-Beck Disease Chondrocytes.Biological trace element research · 2026Article
- The Role of AMPKα in the Mechanism of Development and Treatment of Heart Failure.Reviews in cardiovascular medicine · 2025Review
- Tissue-Specific Ablation of Liver Fatty Acid-Binding Protein Induces a Metabolically Healthy Obese Phenotype in Female Mice.Nutrients · 2025Article
- Tissue-Specific Ablation of Liver Fatty Acid-Binding Protein Induces a Metabolically Healthy Obese Phenotype in Female Mice.bioRxiv : the preprint server for biology · 2025Article
- LncRNAs are involved in regulating ageing and age-related disease through the adenosine monophosphate-activated protein kinase signalling pathway.Genes & diseases · 2024Review
- Upregulation of CCL5/RANTES Gene Expression in the Diaphragm of Mice with Cholestatic Liver Disease.Advances in experimental medicine and biology · 2023Article
- Effects of Voluntary Running Wheel Exercise-Induced Extracellular Vesicles on Anxiety.Frontiers in molecular neuroscience · 2021Article
- Loss of USF2 promotes proliferation, migration and mitophagy in a redox-dependent manner.Redox biology · 2020Article
- Exercise during pregnancy mitigates the adverse effects of maternal obesity on adult male offspring vascular function and alters one-carbon metabolism.Physiological reports · 2020Article
- Lack of skeletal muscle liver kinase B1 alters gene expression, mitochondrial content, inflammation and oxidative stress without affecting high-fat diet-induced obesity or insulin resistance.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- AMPK, Mitochondrial Function, and Cardiovascular Disease.International journal of molecular sciences · 2020Review
- Ketogenic diet feeding improves aerobic metabolism property in extensor digitorum longus muscle of sedentary male rats.PloS one · 2020Article
- The Role of AMPK in the Regulation of Skeletal Muscle Size, Hypertrophy, and Regeneration.International journal of molecular sciences · 2018Review
- β-Hydroxybutyrate Elicits Favorable Mitochondrial Changes in Skeletal Muscle.International journal of molecular sciences · 2018Article
- AMPK in skeletal muscle function and metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Review
- AMPK: guardian of metabolism and mitochondrial homeostasis.Nature reviews. Molecular cell biology · 2018Review
- Nutrition and Training Influences on the Regulation of Mitochondrial Adenosine Diphosphate Sensitivity and Bioenergetics.Sports medicine (Auckland, N.Z.) · 2017Review
- Impaired exercise tolerance, mitochondrial biogenesis, and muscle fiber maintenance in miR-133a-deficient mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- AMPK activity regulates trafficking of mitochondria to the leading edge during cell migration and matrix invasion.Molecular biology of the cell · 2016Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
LKB1 and its downstream targets of the AMP-activated protein kinase family are important regulators of many aspects of skeletal muscle cell function, including control of mitochondrial content and capillarity. LKB1 deficiency in skeletal and cardiac muscle (mLKB1-KO) greatly impairs exercise capacity. However, cardiac dysfunction in that genetic model prevents a clear assessment of the role of skeletal muscle LKB1 in the observed effects. Our purposes here were to determine whether skeletal muscle-specific knockout of LKB1 (skmLKB1-KO) decreases exercise capacity and mitochondrial protein content, impairs accretion of mitochondrial proteins after exercise training, and attenuates improvement in running performance after exercise training. We found that treadmill and voluntary wheel running capacity was reduced in skmLKB1-KO vs. control (CON) mice. Citrate synthase activity, succinate dehydrogenase activity, and pyruvate dehydrogenase kinase content were lower in KO vs. CON muscles. Three weeks of treadmill training resulted in significantly increased treadmill running performance in both CON and skmLKB1-KO mice. Citrate synthase activity increased significantly with training in both genotypes, but protein content and activity for components of the mitochondrial electron transport chain increased only in CON mice. Capillarity and VEGF protein was lower in skmLKB1-KO vs. CON muscles, but VEGF increased with training only in skmLKB1-KO. Three hours after an acute bout of muscle contractions, PGC-1α, cytochrome c, and VEGF gene expression all increased in CON but not skmLKB1-KO muscles. Our findings indicate that skeletal muscle LKB1 is required for accretion of some mitochondrial proteins but not for early exercise capacity improvements with exercise training.
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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.