ArticleThe Journal of physiology2013
AMP-activated protein kinase is required for exercise-induced peroxisome proliferator-activated receptor co-activator 1 translocation to subsarcolemmal mitochondria in skeletal muscle.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 43 citations in OpenAlex.
- Exercise training improves exercise capacity independent of AMPKα2 T172-mediated adaptations in skeletal muscle.bioRxiv : the preprint server for biology · 2026Article
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- The Molecular Signature of High-intensity Training in the Human Body.International journal of sports medicine · 2022Review
- Transcription Factor Movement and Exercise-Induced Mitochondrial Biogenesis in Human Skeletal Muscle: Current Knowledge and Future Perspectives.International journal of molecular sciences · 2022Review
- Article
- Article
- Impaired Mitochondrial Function Results from Oxidative Stress in the Full-Term Placenta of Sows with Excessive Back-Fat.Animals : an open access journal from MDPI · 2020Article
- PGC-1α as a Pivotal Factor in Lipid and Metabolic Regulation.International journal of molecular sciences · 2018Review
- The Janus Head of Oxidative Stress in Metabolic Diseases and During Physical Exercise.Current diabetes reports · 2017Review
- Black Tea High-Molecular-Weight Polyphenol-Rich Fraction Promotes Hypertrophy during Functional Overload in Mice.Molecules (Basel, Switzerland) · 2017Article
- The Implication of PGC-1α on Fatty Acid Transport across Plasma and Mitochondrial Membranes in the Insulin Sensitive Tissues.Frontiers in physiology · 2017Review
- Skeletal muscle Heat shock protein 60 increases after endurance training and induces peroxisome proliferator-activated receptor gamma coactivator 1 α1 expression.Scientific reports · 2016Article
- Molecular mechanisms for mitochondrial adaptation to exercise training in skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Review
- How the Body Talks to the Brain; Peripheral Mediators of Physical Activity-Induced Proliferation in the Adult Hippocampus.Brain plasticity (Amsterdam, Netherlands) · 2015Review
- Transcriptional modulation of mitochondria biogenesis pathway at and above critical speed in mice.Molecular and cellular biochemistry · 2015Article
- Sodium butyrate epigenetically modulates high-fat diet-induced skeletal muscle mitochondrial adaptation, obesity and insulin resistance through nucleosome positioning.British journal of pharmacology · 2015Article
- Muscle over mind.Cell metabolism · 2014Article
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In skeletal muscle, mitochondria exist as two subcellular populations known as subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria. SS mitochondria preferentially respond to exercise training, suggesting divergent transcriptional control of the mitochondrial genomes. The transcriptional co-activator peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) and mitochondrial transcription factor A (Tfam) have been implicated in the direct regulation of the mitochondrial genome in mice, although SS and IMF differences may exist, and the potential signalling events regulating the mitochondrial content of these proteins have not been elucidated. Therefore, we examined the potential for PGC-1α and Tfam to translocate to SS and IMF mitochondria in human subjects, and performed experiments in rodents to identify signalling mechanisms regulating these translocation events. Acute exercise in humans and rats increased PGC-1α content in SS but not IMF mitochondria. Acute exposure to 5-aminoimidazole-4-carboxamide-1-β-ribofuranoside in rats recapitulated the exercise effect of increased PGC-1α protein within SS mitochondria only, suggesting that AMP-activated protein kinase (AMPK) signalling is involved. In addition, rendering AMPK inactive (AMPK kinase dead mice) prevented exercise-induced PGC-1α translocation to SS mitochondria, further suggesting that AMPK plays an integral role in these translocation events. In contrast to the conserved PGC-1α translocation to SS mitochondria across species (humans, rats and mice), acute exercise only increased mitochondrial Tfam in rats. Nevertheless, in rat resting muscle PGC-1α and Tfam co-immunoprecipate with α-tubulin, suggesting a common cytosolic localization. These data suggest that exercise causes translocation of PGC-1α preferentially to SS mitochondria in an AMPK-dependent manner.
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