Are acute and chronic responses in estrogen receptors induced by resistance training associated to muscle hypertrophy in women?

• Grant number: 24/12893-4
• Support Opportunities: Scholarships in Brazil - Support Program for Fixating Young Doctors
• Start date: August 01, 2024
• End date: July 31, 2025
• Field of knowledge: Health Sciences - Physical Education
• Agreement: CNPq
• Principal Investigator: Cleiton Augusto Libardi
• Grantee: João Guilherme Almeida Bergamasco
• Host Institution: Centro de Ciências Biológicas e da Saúde (CCBS). Universidade Federal de São Carlos (UFSCAR). São Carlos , SP, Brazil
• Associated research grant: 24/02221-9 - Are acute and chronic responses in estrogen receptors induced by resistance training associated to muscle hypertrophy in women?, AP.R

Abstract

Among the adaptations to resistance training (RT), increased muscle cross-sectional area (i.e., muscle hypertrophy) has been associated with several health benefits in both women and men. A recent meta-analysis indicated that although there is no difference in relative hypertrophy, the mechanisms underlying hypertrophy may differ between sexes. Among these mechanisms, RT-induced androgen receptor (AR) expression has been significantly associated with muscle hypertrophy in men, but not in women. Conversely, it is unclear whether estrogen receptors (ER) may play a similar role in women. Animal studies have suggested a potential association between ERs and satellite cells (SCs), which are responsible for muscle damage repair and play a crucial role in muscle hypertrophy through myonuclear addition. In humans, only one study has investigated the acute effects of ST on ERs, demonstrating that ER activation regulates myogenic regulatory factors responsible for SC proliferation and differentiation, such as MyoD and myogenin (MioG). Thus, acute (i.e., after a ST session) and chronic (i.e., after multiple ST sessions) changes induced by ST in ERs may be associated with muscle hypertrophy, both resulting from increased muscle growth factors (i.e., MyoD, MioG) involved in the SC cycle and myonuclear addition. Therefore, the aim of this study is to investigate the acute and chronic effects of ST on total ER, cytoplasmic ER (cER), nuclear ER (nER), ER-DNA, MyoD, MioG, and CD1 contents in women and men. Additionally, we will investigate whether these acute and chronic changes in ER markers are associated with SC activation, myonuclear quantity, and muscle hypertrophy in both sexes. Methods: Healthy young women (n = 20) and men (n = 20) will undergo 10 weeks of RT. Muscle biopsies performed on the vastus lateralis muscle will be conducted at baseline (i.e., before the training period), 24 hours after the first RT session, and between 96-120 hours after the last training session. The protein contents of ER, cER, and nER, MyoD, MioG, and CD1 will be analyzed by Western blotting, while ER-DNA will be assessed by ELISA-oligonucleotide assay. Immunohistochemical analysis will be used for muscle fiber type and cross-sectional area (fCSA) analysis. Unpaired t-tests will be used to compare ER markers and muscle fibers at baseline between women and men. In case of differences in baseline contents, ANCOVA will be applied with baseline values as covariates. In the absence of baseline differences, mixed-model analysis will be used. In both tests, in case of significant F-values, Tukey's post hoc test will be adopted. The significance level will be set at P < 0.05. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

BERGAMASCO, JOAO GUILHERME ALMEIDA; BITTENCOURT, DIEGO; SILVA, DEIVID GOMES; BIAZON, THAIS MARINA PIRES DE CAMPOS; SOLIGON, SAMUEL DOMINGOS; OLIVEIRA, RAMON MARTINS; LIBARDI, CLEITON AUGUSTO. Individual muscle hypertrophy in high-load resistance training with and without blood flow restriction: A near-infrared spectroscopy approach. JOURNAL OF SPORTS SCIENCES, v. N/A, p. 7-pg., 2024-12-16. (24/12893-4)