Maintenance of contractile properties despite impaired skeletal muscle oxidative metabolism in diet‐induced obesity.

Diet‐induced obesity (DIO) is increasing in prevalence among youth; a time where robust muscle growth occurs. We hypothesized that consumption of a high fat diet (HFD) in early adulthood would negatively impact mouse muscle metabolism and contractile function. HFD (~60% kcal fat for 8 weeks) induced an obese and insulin resistant phenotype with reduced relative muscle mass (72 ± 1.9%) compared to control. Using isolated single muscle fibers for analysis, HFD induced a significant impairment in palmitate and glucose oxidation (72.8 ± 6.6% and 61.8 ± 9.1% of control respectively). This novel technique was validated in intact muscle. Impaired insulin responses were noted for glucose metabolism and glycogen synthesis in HFD muscle vs. control, while glucose and palmitate uptake was not altered between groups. Preliminary RT‐PCR results demonstrate no difference in CPT‐1, PGC‐1α, PPARα or UCP‐2 expression. Further gene and protein analysis into the mechanisms underlying changes in fat uptake and oxidation are currently underway. Despite metabolic impairments, HFD muscle exhibited no loss of maximal contractile force or alteration in fatigue rates. Our data suggest that HFD skeletal muscle is highly adaptive in the face of impaired substrate oxidation, as demonstrated by the preservation of contractile properties. These findings contribute to our understanding of the impact of DIO on developing skeletal muscle.