DNP causes proton leak preventing protons from being pumped into the mitochondrial matrix during oxidative phosphorylation, and thus dramatically reduces (essentially obviates) ATP synthesis, increasing RMR (dissipating energy as heat; thermogenesis). Anabolic processes (muscle growth) use ATP (energy-consuming; anabolic) to build macromolecules (proteins) in a state of positive energy balance. Since DNP so effectively increases RMR (inducing negative energy balance) & prevents ATP synthesis, attempting to grow on DNP is laughably illogical. Further, ATP is involved in muscular contraction (recocking of the globular head), and so there's even a direct effect on performing repetitions under load.
DNP, by uncoupling of oxidative phosphorylation ⇒ ↑↑O₂ consumption (reflects ↑RMR) & ADP:ATP ratio, ↑lactate synthesis (the latter due to a compensatory ↑glycolysis due to low ATP, thereby ↑pyruvate [glycolysis end-product]) & ↓glucose (due to the ↑glycolysis). Practically, DNP is less insulin sensitizing than aspirin.
DNP certainly is a poison. Fatal dose in adults is about 1 to 3 g by mouth; 3 g has also proved fatal in divided doses over a period of 5 days. Its practical risks are compounded by wide variation in pharmacokinetics between individuals (e.g., in 2 groups of inpatients suffering from DNP poisoning, one group [intensive HP] being essentially doomed to die and the other [routine HP] being relatively unlikely to die, the elimination half-life [t1/2] of 2,4-DNP was 88.78 ± 14.66 h in the routine HP group, while the t1/2 was only 54.58 ± 12.92) h in the intensive HP group).
I doubt any effect by DNP, either indirect or direct, on thyroid function. The absence of any authoritative evidentiary support (bolstered by conciliator's analysis) is a strong indication of this.