Resistance Training and Ovariectomy: Antagonic Effects in Mitochondrial Biogenesis Markers in Rat Skeletal Muscle.

Estrogen reduction is associated with a decline in skeletal muscle mitochondrial biogenesis. Molecular events associated with improvements in markers of mitochondrial biogenesis after resistance training and estradiol replacement are unknown. This study aimed to investigate the effects of ovariectomy, resistance training, and estradiol replacement on markers of mitochondrial biogenesis and protein expression related to oxidative capacity in the rat gastrocnemius pool. Estradiol replacement was performed using Silastic(®) capsules. During the 12-week resistance training, animals climbed a ladder with weights attached to their tails. Gene expression was analysed by RT-PCR, and protein content was determined by western blotting. Ovariectomy decreased the gene expression of the mitochondrial biogenesis markers PGC-1α (~73%), NRF-1 (~44%), and TFAM (~53%) (p<0.05) and decreased the protein expression of phosphorylated AMPK, CREB and AKT, which are related to oxidative capacity. Resistance training increased PGC-1α (~59%) and TFAM (~48%) expression compared to the Ovariectomy-Sedentary group. The combination of resistance training and estradiol replacement was superior to the ovariectomy-sedentary and ovariectomy-resistance training treatments regarding the gastrocnemius muscle. Estrogen deficiency altered the expression of genes and proteins that favour the development of a mitochondrial dysfunction phenotype, which was improved with resistance training and was partially improved by estradiol replacement.

Resistance training suppresses intra-abdominal fatty acid synthesis in ovariectomized rats.

Ovarian hormone loss is associated with a shift in fat distribution to intra-abdomin al adipose tissue (intra-AAT) depots and with lipid metabolism disorders, which predisposes individuals to developing insulin resistance. Resistance training (RT) prevents increases in intra-AAT after ovarian hormone loss. However, the molecular mechanisms underlying these changes remain unclear. We investigated the effects of ovariectomy and RT on gene expression related to lipogenesis and fat oxidation in the intra-AAT of ovariectomized rats. Sprague-Dawley rats (n=6/group) were divided into the groups: sham-sedentary, ovariectomized-sedentary, sham-RT and ovariectomized-RT. RT groups performed a 10-week climbing program on a ladder with progressive overload. Intra-AAT was subjected to morphometric and mRNA analysis. Ovariectomized-sedentary group had larger adipocytes and higher expression of peroxisome proliferator-activated receptor-γ (PPAR-γ), sterol regulatory element-binding protein-1c (SREBP-1c), stearoyl-CoA desaturase-1 (SCD-1), acetyl-CoA carboxylase (ACC), hormone-sensitive lipase (HSL) and lower expression of the oxidative carnitinepalmitoyltransferase-I (CPT-1). RT counteracted OVX-induced increases in PPAR-γ and SCD-1 and decreased SREBP-1c. ACC and HSL were downregulated in ovariectomized-RT compared with the ovariectomized-sedentary group. Ovariectomized-RT group had the highest CPT-1 gene expression. Adipocyte size decreased in ovariectomized-RT group. Results suggest that RT reduces intra-AAT adipocyte size in ovariectomized rats by suppressing intra-AAT fatty acid synthesis and enhancing fatty acid ß-oxidation.