Rather than increasing TDEE (a function of RMR, NEAT [e.g., fidgeting], EAT [formal exercise], and TEF [thermic effect of feeding, energy consumed by digestion, etc.]), Tren's effects on fat loss are multifactoral. Tren, and androgen (synonym: AAS) generally, increase skeletal muscle and decrease fat mass; and this decrease in fat mass is not explained merely by the increased metabolic cost of skeletal muscle tissue (synthesis and/or maintenance); it is substantially greater.
Tren causes fat loss by:
* antiadipogenic effects (committment of preadipocytes to a myogenic [muscle tissue] rather than an adipogenic [fat cell] lineage)... envision fat synthesis as a constant process of churn, with turnover of fat cells, with the balance between anabolic processes (lipogenesis) vs. catabolic processes (fat oxidation) constantly in flux
* reducing the quantity of fatty acid incorporation into triglyceride in adipocytes (reduced lipid accumulation; storage of fat within fat cells)
* lipolysis (via the catalytic subunit of cAMP or by ↑β-adrenoreceptor number in adipocytes)
These mechanisms reduce fat mass without reliance on increasing energy expenditure.
I know: "there is no fat loss without a negative calorie balance," they said. Well actually, with drugs, there can be (and routinely, is). This is because hormones dictate to a great extent the abundance of anabolic vs catabolic processes (recall, e.g., lipogenesis vs. fat oxidation & the constant flux of various metabolic processes above).
Newton's law of thermodynamics applies to weight or body mass changes; at a constant bodyweight (energy balance), there can be recomp (this is due to effects on the so-called p-ratio; or partitioning) via these processes.