O papel das alterações dos receptores androgênicos na hipertrofia muscular induzida pelo treinamento de força

Abstract

The expression of androgen receptors (AR) has been highlighted as a potential mechanism for muscle hypertrophy. However, little is known about the associations between acute and chronic changes in total AR, cytoplasmic AR (cAR), nuclear AR (nAR), and AR-DNA content induced by resistance training (RT) and muscle hypertrophy in women and men. Furthermore, it is unknown whether these acute and chronic changes can explain the differences in the magnitude of hypertrophic responses between non-responders and responders to RT. The aim of this thesis was to investigate the acute and chronic effects of RT on total AR, cAR, nAR, and AR-DNA content in women and men. Additionally, it was investigated whether these acute and chronic changes in AR molecular markers are associated with muscle hypertrophy in both sexes. Finally, we sought to identify if there are differences between nonresponders and responders in both baseline contents and acute and chronic changes in AR markers resulting from RT. Thirty-eight untrained young individuals (19 women and 19 men) underwent 10 weeks of RT. Participants that did not present increases in muscle cross-sectional area (mCSA) greater than 2 typical errors, considering two mCSA measurements, were considered nonresponders and responders were numerically matched accordingly. Biopsies of the vastus lateralis muscle were performed at baseline (i.e., before the training period), 24 hours after the first RT session (acute responses), and 96-120 hours after the last training session (chronic responses). AR, cAR, and nAR protein contents were analyzed by Western blotting, while AR-DNA was analyzed by oligonucleotide-ELISA assay. Immunohistochemistry was used for fiber type analysis and cross-sectional area (fCSA), and ultrasonography was used to determine the mCSA. At baseline, men showed greater nAR content compared to women. Additionally, there was a significant association between baseline cAR and type II fCSA hypertrophy for men. Regarding acute results, both sexes showed decreased AR, cAR, and nAR, while men demonstrated greater decreases in nAR. After 10 weeks of RT, men showed greater cAR compared to women, while both sexes decreased AR-DNA levels, and AR or nAR remained unchanged. Acute or chronic responses of AR, cAR, nAR, and AR-DNA did not correlate with hypertrophy in women or men. There were no significant differences between nonresponders and responders for most AR markers in baseline contents or acute and chronic changes induced by RT. However, there was a significant difference between nonresponders (+19.5%) and responders (-14.4%) in acute AR-DNA activity (ES = -1.39; 95% CI: -2.53 to -0.16). Baseline cAR content potentially influences hypertrophy in men, whereas acute or chronic changes in AR or its fractions are not associated with muscle hypertrophy in women or men. Finally, the present findings study do not support AR markers as a mechanism capable of explaining differences in the magnitude of hypertrophic responses to RT in untrained young women and men.