Research
Hormonal
AMPK activation inhibits ribosome biogenesis by blocking mTORC1 signaling, while mTORC1 signaling may negatively affect mitochondrial biogenesis, creating a molecular competition.
This is a molecular detail. For training, it means high-energy demand (endurance) signals the body to build mitochondria, potentially suppressing the signal to build protein (muscle) if not managed.
GoodSupportsHIGH confidence
First, AMPK mechanistically blocks mTORC1 signaling through direct phosphorylation of the complex... Given the proposed role mTORC1 signaling has on skeletal muscle ribosome biogenesis, it seems plausible that this process is impaired during situations of heightened AMPK signaling.
Why this rating
The paper cites multiple studies across cell lines, rodents, and humans supporting this mechanism, though direct human biogenesis data is sparse.
Source
Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities
Paulo H. C. Mesquita et al. · Frontiers in Physiology · 2021
DOI 10.3389/fphys.2021.725866
narrative_reviewCited 60×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Endurance training prioritizes mitochondrial biogenesis over ribosome biogenesis, potentially interfering with resistance training adaptations through AMPK-mTORC1 signaling competition.Moderate
- Low-load resistance training to failure (30% 1RM) can simultaneously increase both ribosome and mitochondrial biogenesis, challenging the strict competition paradigm.Moderate
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