17β-estradiol (E2) and progesterone (P4) may influence exercise-induced muscle damage and repair during the menstrual cycle (MC), but their individual and combined effects remain unclear. This study investigated how hormones influence C2C12 myoblast proliferation, differentiation, and migration under basal conditions and after electrical pulse stimulation (EPS). Myoblasts were treated with E2 and P4 (alone or combined to mimic MC phases). Proliferation (MTT assay), migration (scratch assay), creatine kinase (CK), differentiation (immunohistochemistry), and protein expression (western blot) were assessed. Elevated E2 (>100 pg/mL) and P4 (>1.5 ng/ml) reduced proliferation, as well as in the early follicular phase (EFP) and mid-luteal phase (MLP) ( p < 0.05). Migration decreased in EFP and late follicular phase (LFP) ( p < 0.05), but not with isolated E2/P4 treatment. Differentiation was impaired across all MC phases (reduced myotube diameter; p < 0.05). While greater E2 accelerated CK recovery post-EPS, the presence of P4 (MC phases) influenced this effect. E2 upregulated HSP70 and myogenin protein content, but P4 counteracted these benefits during specific MC phases. ERɑ increased in all conditions, suggesting a potential role in mediating the EPS response. In conclusion, E2 and P4 independently decrease myoblast activity, but their combined effects vary across the MC, with a potential role of ERɑ in this process. These findings highlight the complex interplay of sex hormones in the myogenic response to contractile stress.
Wageh et al. (Thu,) studied this question.