The paper explains how testosterone helps build bigger, stronger muscles by acting on many pathways, including boosting IGF‑1, increasing muscle‑building cells, improving blood flow, and enhancing mitochondria. It shows that these effects don’t need conversion to DHT and involve both genetic and non‑genetic actions. While it doesn’t give new dosing tips, it clarifies why testosterone can be a powerful tool for muscle and performance gains.

Testosterone treatment increases muscle mass, maximal voluntary muscle-strength, aerobic capacity, and some measures of physical function. Activational and epigenetic mechanisms by which androgens improve muscle mass and physical performance and how to apply these anabolic effects to treat functional limitations associated with aging and disease remain incompletely understood. Testosterone treatment induces hypertrophy of type 1 and 2 muscle fibers, and increases muscle progenitor cell numbers by promoting differentiation of mesenchymal progenitor cells into myogenic lineage by an androgen receptor (AR)-mediated pathway. Liganded AR binds to β-catenin, translocates into nucleus where it binds TCF4 and upregulates follistatin that blocks signaling through TGFβ-pathway to promote myogenesis and inhibit adipogenesis. Testosterone increases myoblast proliferation by stimulating polyamine biosynthesis. Stimulation of GH and IGF-1 secretion, intramuscular IGF1-receptor, and muscle protein synthesis, and inhibition of muscle atrophy genes further contribute to testosterone's anabolic effects. Testosterone improves muscle bioenergetics by increasing erythrocytes, oxygen availability, tissue blood flow, and mitochondrial mass and quality. Testosterone increases blood flow by nongenomic mechanisms involving NO production, and calcium and potassium channels in vascular smooth muscle. The conversion of testosterone to 5α-dihydrotestosterone is not required for mediating its anabolic effects. Mechanisms of testosterone's sexually-dimorphic epigenetic and tissue-specific activational effects; and roles of α-keto reductase and steroid 5α-reductase, one-carbon and polyamine metabolism in testosterone's actions remain poorly understood. Strategies to translate testosterone-induced muscle mass and strength gains into patient-important improvements in functional performance and health outcomes are needed to enable its clinical applications to treat functional limitations associated with aging and disease.