Hormonal
Resistance training activates the Akt-mTOR pathway to promote muscle hypertrophy, while endurance training activates the AMPK-PGC-1 pathway to promote mitochondrial biogenesis, and these pathways can interfere with each other when activated concurrently.
Understanding that strength and endurance use different molecular 'switches' helps explain why doing them back-to-back can blunt gains. Separating sessions allows these distinct pathways to operate without cross-talk interference.
Resistance-based exercise induces an increase in the activity of the phosphatidylinositol 3-kinase (PI3-k)–Akt–mammalian target of rapamycin (mTOR) signalling cascade... Endurance-based exercise activates signalling pathways involved in metabolic homeostasis, comprising the adenosine-monophosphate-activated protein kinase (AMPK)–p38 mitogen-activated protein kinase (MAPK)–peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1 axis. Activation of AMPK by endurance exercise may inhibit mTOR signaling via tuberous sclerosis complex (TSC) and suppress resistance-exercise-induced muscle-protein synthesis.
Why this rating
Well-established molecular biology reviewed in the paper.
Source
Molecular responses to strength and endurance training: Are they incompatible?This paper article is one of a selection of papers published in this Special Issue, entitled 14th International Biochemistry of Exercise Conference – Muscles as Molecular and Metabolic Machines, and has undergone the Journal’s usual peer review process.
John A. Hawley · Applied Physiology Nutrition and Metabolism · 2009
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