Abstract
Obesity associates highly with metabolic disorders including insulin resistance. To determine if two exercise prescriptions exert differential metabolic benefits in insulin sensitive tissues, we compared isocaloric programs of constant-moderate endurance (END) and high intensity interval training (HIIT), in a mouse model of diet-induced obesity. Male 10 week old C57BL/6 mice were fed a high fat diet (HFD; 45% kcal fat) ab libitum for 10 weeks, achieving 25% excess weight, and for a further 10 weeks they then underwent isocaloric END or HIIT (3x40min sessions/week). Untrained HFD and chow-fed mice acted as controls. At 30 weeks of age, mice were sacrificed and quadriceps muscle, subcutaneous adipose tissue (SAT) and liver were excised. Neither END or HIIT altered the body weight or the fat/lean mass proportion in HFD mice. An insulin tolerance test (0.65 IU/kg*BW) showed HIIT but not END improved insulin sensitivity in HFD mice (p<0.vs. untrained). In quadricep, HFD induced down-regulation of high-molecular weight adiponectin protein, which was similarly normalized by END and HIIT. In contrast HIIT but not END reversed the HFD-driven downregulation of adiponectin receptor 1 (AdipoR1; p<0.05). In SAT, both programs tended to decrease collagen VI protein (p=0.08), whereas only HIIT induced an upregulation in mRNA (3-fold vs. HFD untrained) and protein (2-fold vs. HFD untrained) of UCP1. In liver, only END was able to reverse the collagen I accumulation (2-fold; p<0.05) and downregulation of CTGF (0.5-fold; protein) seen in HFD untrained mice (p<0.05). Our results suggest that HIIT may promote better systemic metabolic effects, compared to END during high-fat fed conditions, which could be explained by the normalization of muscle AdipoR1 and higher UCP1 induction in SAT. However, END was more effective in normalizing liver changes, suggesting differential metabolic effects of END and HIIT during obesity. Disclosure S.F. Martinez-Huenchullan: None. L.A. Ban: None. L.F. Olaya: None. B.R. Maharjan: None. C. Tam: None. S. McLennan: None. S.M. Twigg: Advisory Panel; Self; Abbott. Consultant; Self; Abbott. Advisory Panel; Self; Novo Nordisk Inc., Sanofi-Aventis, AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company. Speaker's Bureau; Self; AstraZeneca, Merck Sharp & Dohme Corp.. Other Relationship; Self; Abbott.
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