Excessive training does not induce mitochondrial dysfunction or impair insulin signalling within skeletal muscle - PubMed
4 hours ago
- #overtraining
- #mitochondrial biogenesis
- #insulin signaling
- Excessive training does not cause mitochondrial dysfunction or impair insulin signaling in skeletal muscle, challenging the notion that it inherently harms metabolic health.
- A 3-week overtraining protocol in highly trained endurance athletes increased mitochondrial content and respiratory capacity, with preserved intrinsic oxidative phosphorylation.
- Insulin signaling improved after excessive training, as shown by enhanced Akt phosphorylation during a glucose challenge, indicating no induction of insulin resistance.
- Mitochondrial H2O2 emission and oxidative stress increased with overtraining, but mitochondrial biogenesis was evident without functional impairment.
- Proteomics identified upregulated proteins related to fatty acid metabolism and mitochondrial content, while overreached athletes showed blunted increases in cytoskeleton, glycogen metabolism, and protein translation proteins.
- Despite individual variations leading to overreaching, no reductions in mitochondrial bioenergetics or insulin signaling were observed in the skeletal muscle.