Oestrogen's regulation of fat metabolism during exercise and gender specific effects

Early animal, menstrual phase and gender comparative studies inconsistently support an oestrogen-induced increase in fat oxidation during exercise. Recent advances from studies of cellular signalling and gene expression provide evidence for inter-tissue and intramuscular mechanisms that demonstrate oestrogen's promotion of skeletal muscle fat oxidative capacity. Oestrogen or oestrogen-analogues act mainly through oestrogen receptor-alpha in skeletal muscle to stimulate the genomic expression of certain other nuclear hormone receptors and downstream targets to promote long chain fatty acid (LCFA) uptake, mitochondrial shuttling and β oxidation. Oestrogen increases the availability of LCFA substrate by enhancing adipocyte lipolysis and expression of genes promoting intramyocellular lipid storage. Oestrogen acts by non-genomic means to increase the activation of AMPK that may reinforce some direct genomic actions.

► In muscle oestrogen increases the expression and protein content of PPARα and PPARδ⋅ ► Oestrogen's direct/indirect genomic action increases LCFA transport and oxidation. ► During exercise, oestrogen promotes the mobilisation of adipose stores. ► Oestrogen increases gene expression for IMCL storage to enhance LCFA availability. ► Oestrogen and catechol-oestrogen metabolite activates AMPK via non-genomic means.