Lancaster
Member
- Joined
- Jun 13, 2021
- Messages
- 29
This study provides for the first time the structural and functional evidence of a time-dependent induction of cardiac hypertrophy toward pathological state after treatment with every supra-physiological dose of testosterone. Short-term testosterone treatment induced physiological cardiac hypertrophy with contractile maintenance and MHC isoform switching toward α-MHC. Upon the long-term treatment of high testosterone, cardiac hypertrophy was apparent with myocardial deposition of collagen and contractile reduction in active tension without affecting MHC isoforms (Table 1 and Figs 1, 3, 4, 5). Reductions in ERK1/2 and mTOR activation may serve as possible underlying mechanism of this long-term testosterone-induced cardiac transition toward pathological hypertrophy. Our data suggest that physiological cardiac hypertrophy occurs during the early phase of high testosterone administration; however, the pathological outcome of cardiac hypertrophy will be resulted upon the prolonged treatment.
In rats, with serum concentrations equivalent to 3770 ng/dl in T10 and 4300 ng/dl in T20 — levels that nobody advocates for, nor claims are safe.