Obesity is highly associated with the development of metabolic disorders in insulin sensitive tissues (muscle, adipose tissue, liver). To determine if different exercise prescriptions could exert differential metabolic benefits on insulin sensitive tissues, we compared two isocaloric programs; constant-moderate endurance (END) and high intensity interval training (HIIT), in a mouse model of diet-induced obesity.
Ten week-old male 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. After 20 weeks mice were sacrificed and quadriceps muscle, subcutaneous adipose tissue (SAT) and liver were extracted for analysis.
Results showed that END and HIIT did not change the body weight or the fat/lean mass proportion in HFD groups (p>0.05). Interestingly, after an insulin tolerance test (0.65 IU/kg*BW), only HIIT improved insulin sensitivity in HFD mice (p<0.05 versus untrained). In quadriceps, HFD induced a down-regulation of muscle high-molecular weight (HMW) adiponectin which was similarly normalized by END and HIIT. However, only HIIT was able to reverse the HFD-driven downregulation of adiponectin receptor 1 (AdipoR1; p<0.05). In SAT, both exercise programs tended to decrease collagen VI (protein; p=0.08), whereas HIIT induced an upregulation in transcription (3-fold vs HFD untrained) and translation (2-fold vs untrained) of UCP1. In liver, only END was able to reverse collagen I accumulation (2-fold; p<0.05) and downregulation of CTGF (0.5-fold; protein) seen in HFD untrained mice (p<0.05).
In the light of these results, HIIT seems to promote better systemic metabolic effects, 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 in an obesity-context.