Acute endurance exercise increases the nuclear abundance of PGC-1alpha in trained human skeletal muscle.

@article{Little2010AcuteEE,
  title={Acute endurance exercise increases the nuclear abundance of PGC-1alpha in trained human skeletal muscle.},
  author={Jonathan Peter Little and Adeel Safdar and Naomi M. Cermak and Mark Andrew Tarnopolsky and Martin J. Gibala},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2010},
  volume={298 4},
  pages={
          R912-7
        }
}
  • J. LittleA. Safdar M. Gibala
  • Published 27 January 2010
  • Biology
  • American journal of physiology. Regulatory, integrative and comparative physiology
Peroxisome proliferator-activated receptor gamma coactivator (PGC-1alpha) is a transcriptional coactivator that plays a key role in coordinating mitochondrial biogenesis. Recent evidence has linked p38 MAPK and AMPK with activation of PGC-1alpha. It was recently shown in rodent skeletal muscle that acute endurance exercise causes a shift in the subcellular localization of PGC-1alpha from the cytosol to the nucleus, allowing PGC-1alpha to coactivate transcription factors and increase… 
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Exercise increases mitochondrial PGC-1 α content and promotes nuclear-mitochondrial cross-talk to coordinate mitochondrial biogenesis.

It is suggested that in response to acute altered energy demands, PGC-1α re-localizes into nuclear and mitochondrial compartments where it functions as a transcriptional co-activator for both nuclear and mitochondria DNA transcription factors.

Change in PGC-1α expression in rat skeletal muscle after low-intensity prolonged swimming exercise.

The present investigation demonstrated that the time-course of P GC-1α content in nuclear fractions in the EPI muscle was the same as the ALAS mRNA, suggesting that PGC-1 α in the nucleus may have a physiological function as a transcriptional coactivator for enhancing mitochondrial protein expression after exercise.

An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle.

Findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α.

A systematic upregulation of nuclear and mitochondrial genes is not present in the initial postexercise recovery period in human skeletal muscle.

The lack of observed systematic upregulation of nuclear- and mitochondrial-encoded genes suggests that exercise-induced up regulation of PGC-1α targets are differentially regulated during the initial hours following acute exercise in humans.

Acute Endurance Exercise Induces Nuclear p53 Abundance in Human Skeletal Muscle

The selective increase in nuclear p53 abundance following endurance exercise suggests a potential pro-autophagy response to remove damaged proteins and organelles prior to initiating mitochondrial biogenesis and remodeling responses in untrained individuals.

Rapidly elevated levels of PGC-1α-b protein in human skeletal muscle after exercise: exploring regulatory factors in a randomized controlled trial.

The present study contributes new insights into the initial signaling events following a single bout of exercise and emphasizes PGC-1α-ex1b as the most exercise-responsive P GC-1 α isoform.

Glycogen Content Regulates Peroxisome Proliferator Activated Receptor-∂ (PPAR-∂) Activity in Rat Skeletal Muscle

The data would suggest that a factor associated with muscle contraction and/or glycogen depletion activates PPAR-∂ and initiates AMPK translocation in skeletal muscle in response to exercise.

Overexpression of PGC-1α Increases Fatty Acid Oxidative Capacity of Human Skeletal Muscle Cells

PGC-1α overexpression increased oxidative capacity of cultured myotubes by improving lipid metabolism, increasing expression of genes involved in regulation of mitochondrial function and biogenesis, and decreasing expression of MHCIIa.

Sirtuin 1 (SIRT1) Deacetylase Activity Is Not Required for Mitochondrial Biogenesis or Peroxisome Proliferator-activated Receptor-γ Coactivator-1α (PGC-1α) Deacetylation following Endurance Exercise*

It is demonstrated that SIRT1 deacetylase activity is not required for exercise-induced de acetylation of PGC-1α or mitochondrial biogenesis in skeletal muscle and suggested that changes in GCN5 acetyltransferase activity may be an important regulator of P GC-1 α activity after exercise.

Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters

The results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise.
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