The biological process of muscle cell enlargement, or hypertrophy, primarily driven by the signaling actions of Insulin-like Growth Factor 1 (IGF-1), a potent anabolic peptide hormone. This mechanism is central to the adaptive response of muscle tissue following resistance exercise, promoting both the synthesis of new muscle proteins and the proliferation of satellite cells. Clinically, optimizing IGF-1 signaling is a key target for improving sarcopenia and enhancing body composition.
Origin
The concept emerged from the discovery of IGF-1 as a key mediator of Growth Hormone (GH) action in the 1970s, originally termed “somatomedin.” Subsequent research clarified its direct role in muscle tissue, leading to the identification of both systemic (endocrine) and local (paracrine/autocrine) IGF-1 isoforms that regulate muscle growth. This mechanism underpins the science of exercise-induced muscle adaptation.
Mechanism
Mechanical tension and muscle damage from resistance training trigger the local production of IGF-1, particularly the mechano-growth factor (MGF) splice variant. IGF-1 binds to its receptor on the muscle cell membrane, activating the PI3K/Akt/mTOR signaling pathway, which is the primary cascade for initiating protein synthesis and inhibiting protein degradation. The resulting net positive protein balance leads to an increase in myofibrillar size and muscle cross-sectional area.
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