What Are The Side Effects Of Metandienone?

Muscle hypertrophy is principally governed by the interaction of mechanical tension, muscle damage and metabolic stress, which together elicit anabolic signaling cascades (Schoenfeld 2010; Phillips 2017). High‑intensity resistance training (>70 % 1RM) generates substantial mechanical load that activates mechanosensitive pathways such as mTORC1 through phosphorylation of ribosomal protein S6 kinase and the downstream increase in translational capacity (Fukuda 2020). Muscle fiber injury, typically observed with eccentric contractions, further amplifies growth factor release—particularly IGF‑1—and recruits satellite cells for fusion into existing myofibers (Sundberg 2014; Bencik 2016). The resulting transcriptional program is augmented by metabolic stress; prolonged sets and short rest intervals elevate intracellular calcium, lactate, and AMP levels, thereby stimulating AMP‑activated protein kinase (AMPK) and hypoxia‑inducible factor 1α (HIF‑1α), which modulate genes involved in hypertrophy and mitochondrial biogenesis (Wang 2019). Collectively, these intertwined signaling cascades dictate the magnitude of muscle fiber enlargement observed with progressive resistance training.



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