Effect of exercise training on insulin sensitivity, mitochondria and computed tomography muscle attenuation in overweight women with and without polycystic ovary syndrome

Abstract

Aims/hypothesis Polycystic ovary syndrome (PCOS) is an insulin resistant (IR) state. Increased skeletal muscle lipid content and impaired mitochondrial biogenesis have been implicated in the pathogenesis of IR. We investigated whether differences in these variables explain the IR of women affected by PCOS and whether improvements in IR with exercise are reflected by changes in these variables. Methods Sixteen PCOS and 13 non-PCOS overweight women were assessed, and eight PCOS and seven non-PCOS women were reassessed after 12 weeks of moderate and vigorous exercise training. Outcomes included insulin sensitivity (glucose infusion rate [GIR]), skeletal muscle gene expression and protein abundance, enzyme activity of selected mitochondrial components, and computed tomography (CT) attenuation-estimated muscle lipid. Results GIR was lower in women with PCOS versus those without (p 00.01) and increased with exercise in both groups. Baseline CT muscle attenuation suggested a trend to less muscle lipid in PCOS, which increased with exercise training, with a difference in the change in muscle lipid (p00.01, age-corrected), compared with non-PCOS women. GIR correlated with PGC1A gene expression across the whole group; skeletal muscle expression of mitochondrial biogenesis markers was not different between groups at baseline, or after training. Neither lipid changes nor mitochondrial changes correlated with changes in GIR. Conclusions/interpretation Differences in IR in women with and without PCOS were not explained by differences in skeletal muscle lipid or mitochondrial parameters. Improvements in IR with exercise were dissociated from mitochondrial parameters. CT muscle attenuation suggested a differential capacity of PCOS muscle to store lipid compared with non-PCOS.

Aerobic exercise but not resistance exercise reduces intrahepatic lipid content and visceral fat and improves insulin sensitivity in obese adolescent girls: a randomized controlled trial

“…Our finding that both AE and RE are associated with reductions in IMAT in obese adolescent girls is of importance given that IMAT is inversely associated with insulin sensitivity in adolescents (23). That regular exercise is effective in reducing IMAT in obese girls is consistent with adult studies (13,26) demonstrating the beneficial effects of exercise in reducing skeletal muscle lipid content measured by CT. However, these observations differ from studies employing 1 H-MRS, which report no significant changes in intramyocellular lipid (IMCL) in response to regular exercise in obese adolescents (22,39) and obese adults (15).…”

Peripheral insulin resistance in obese girls with hyperandrogenism is related to oxidative phosphorylation and elevated serum free fatty acids

“…However, data examining the role of mitochondria in IR in HAS are limited and conflicting. Muscle mitochondrial oxidation gene expression for oxidative enzymes such as citrate synthase, or ␤-hydroxyacyl-CoA dehydrogenase were similar between women with and without HAS despite worse IR in the women with HAS, and gene expression did not change with exercise training, whereas IR improved (26). Furthermore, neither stage 1 or stage 3 oxidation was different in biopsy samples from women with PCOS compared with controls, again despite worse IR in the women with HAS (48).…”

The MRC1/CD68 Ratio Is Positively Associated with Adipose Tissue Lipogenesis and with Muscle Mitochondrial Gene Expression in Humans

“…Muscle mitochondrial dysfunction, which has been defined as a reduction in muscle oxidative capacity and mitochondrial biogenesis, has been associated with obesity, insulin resistance and type 2 diabetes [12]–[16]. Reduced levels of muscle PPARGC1A, TFAM and MT-CO3 mRNA levels have been used to evaluate muscle mitochondrial dysfunction [12], [13], [16].…”