Mixed
Acute endurance exercise stimulates skeletal muscle mitochondrial biogenesis through integrated retrograde signaling from mitochondria to the nucleus, involving the activation of kinases (AMPK, CaMK, MAPK, PKA) and the translocation of transcriptional coactivators like PGC-1α to regulate nuclear gene expression.
To boost your muscle's energy production capacity (mitochondrial biogenesis), engage in endurance exercise. This can be moderate intensity continuous exercise (MICE), high-intensity interval exercise (HIIE), or sprint interval exercise (SIE). The specific intensity determines which fuel sources are used and which signaling pathways are prioritized, but all forms of endurance exercise trigger the necessary retrograde signaling from mitochondria to the nucleus to increase mitochondrial content and function.
This review provides an overview of recent advances in our understanding of the molecular events associated with acute endurance exercise-regulated signalling pathways and kinases in skeletal muscle with a focus on phosphorylation. We critically appraise recent evidence highlighting the involvement of mitochondrial and nuclear protein phosphorylation and/or translocation in skeletal muscle adaptive responses to an acute bout of endurance exercise that ultimately stimulate mitochondrial biogenesis and contribute to exercise’s wider health and fitness benefits.
Why this rating
This is a comprehensive review article synthesizing global mass spectrometry-based phosphoproteomic approaches and extensive literature, indicating high-quality evidence synthesis.
Source
Exercise-Regulated Mitochondrial and Nuclear Signalling Networks in Skeletal Muscle
Elizabeth G. Reisman et al. · Sports Medicine · 2024
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