ArticleThe Journal of physiology2015
5'-AMP activated protein kinase α2 controls substrate metabolism during post-exercise recovery via regulation of pyruvate dehydrogenase kinase 4.
Article in The Journal of physiology, 2015. 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, 43 citations in OpenAlex.
- Exercise-induced hypertrophic preconditioning alleviates myocardial ischemic injury through trained immunity of macrophages.Journal of translational medicine · 2025Article
- Cellular Feimin enhances exercise performance by suppressing muscle thermogenesis.Nature metabolism · 2025Article
- Decreased AMPK/SIRT1/PDK4 induced by androgen excess inhibits human endometrial stromal cell decidualization in PCOS.Cellular and molecular life sciences : CMLS · 2024Article
- Article
- Exercise metabolism and adaptation in skeletal muscle.Nature reviews. Molecular cell biology · 2023Review
- Skeletal muscle proteins involved in fatty acid transport influence fatty acid oxidation rates observed during exercise.Pflugers Archiv : European journal of physiology · 2023Article
- Signaling pathways regulated by natural active ingredients in the fight against exercise fatigue-a review.Frontiers in pharmacology · 2023Review
- Acute exercise dynamically modulates the hepatic mitochondrial proteome.Molecular omics · 2022Article
- Comparison between low, moderate, and high intensity aerobic training with equalized loads on biomarkers and performance in rats.Scientific reports · 2022Article
- AMPK and the Adaptation to Exercise.Annual review of physiology · 2022Review
- A Multi-Ingredient Formula Ameliorates Exercise-Induced Fatigue by Changing Metabolic Pathways and Increasing Antioxidant Capacity in Mice.Foods (Basel, Switzerland) · 2021Article
- Tuning fatty acid oxidation in skeletal muscle with dietary fat and exercise.Nature reviews. Endocrinology · 2020Review
- Inducible deletion of skeletal muscle AMPKα reveals that AMPK is required for nucleotide balance but dispensable for muscle glucose uptake and fat oxidation during exercise.Molecular metabolism · 2020Article
- Aldosterone from endometrial glands is benefit for human decidualization.Cell death & disease · 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
- Review
- Changes in Northern Elephant Seal Skeletal Muscle Following Thirty Days of Fasting and Reduced Activity.Frontiers in physiology · 2020Article
- Postnatal induction of muscle fatty acid oxidation in mice differing in propensity to obesity: a role of pyruvate dehydrogenase.International journal of obesity (2005) · 2020Article
- Interactive Roles for AMPK and Glycogen from Cellular Energy Sensing to Exercise Metabolism.International journal of molecular sciences · 2018Review
- Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle.Molecular metabolism · 2018Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well known that exercise has a major impact on substrate metabolism for many hours after exercise. However, the regulatory mechanisms increasing lipid oxidation and facilitating glycogen resynthesis in the post-exercise period are unknown. To address this, substrate oxidation was measured after prolonged exercise and during the following 6 h post-exercise in 5´-AMP activated protein kinase (AMPK) α2 and α1 knock-out (KO) and wild-type (WT) mice with free access to food. Substrate oxidation was similar during exercise at the same relative intensity between genotypes. During post-exercise recovery, a lower lipid oxidation (P < 0.05) and higher glucose oxidation were observed in AMPKα2 KO (respiratory exchange ratio (RER) = 0.84 ± 0.02) than in WT and AMPKα1 KO (average RER = 0.80 ± 0.01) without genotype differences in muscle malonyl-CoA or free-carnitine concentrations. A similar increase in muscle pyruvate dehydrogenase kinase 4 (PDK4) mRNA expression in WT and AMPKα2 KO was observed following exercise, which is consistent with AMPKα2 deficiency not affecting the exercise-induced activation of the PDK4 transcriptional regulators HDAC4 and SIRT1. Interestingly, PDK4 protein content increased (63%, P < 0.001) in WT but remained unchanged in AMPKα2 KO. In accordance with the lack of increase in PDK4 protein content, lower (P < 0.01) inhibitory pyruvate dehydrogenase (PDH)-E1α Ser(293) phosphorylation was observed in AMPKα2 KO muscle compared to WT. These findings indicate that AMPKα2 regulates muscle metabolism post-exercise through inhibition of the PDH complex and hence glucose oxidation, subsequently creating conditions for increased fatty acid oxidation.
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