Oral Presentation Australian Diabetes Society and the Australian Diabetes Educators Association Annual Scientific Meeting 2017

Differential metabolic effects of moderate vs. high intensity interval exercise may be related to muscle adiponectin in high-fat fed mice. (#177)

Sergio F Martinez Huenchullan 1 , Babu Raja Maharjan 1 , Charmaine S Tam 2 , Susan V McLennan 1 3 , Stephen M Twigg 1 4
  1. Sydney Medical School, and Charles Perkins Centre, University of Sydney, Sydney, New South Wales, Australia
  2. Charles Perkins Centre and School of Life and Environmental Sciences, University of Sydney, Sydney, New South Wales, Australia
  3. NSW Health Pathology, Sydney, Australia
  4. Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia

Adiponectin has recently been described as a myokine that regulates insulin sensitivity in an autocrine/paracrine manner. This feature is thought to be one of the mechanisms behind exercise-related metabolic benefits in obesity. However, whether skeletal muscle adiponectin varies between different exercise modalities is unclear. This study investigated effects of 10 weeks endurance(END/moderate intensity) or high intensity interval training (HIIT) on metabolic profiles and muscle adiponectin in a mouse model of diet-induced obesity.

Ten week-old male C57BL/6 mice were fed HFD(45% FAT) ab libitum and underwent either END or HIIT for 10 weeks(3x40min sessions/week). Chow-fed mice acted as controls. Compared with HFD alone, both training programs similarly protected against body weight(BW) gain (final weight (g) HFD=45±2;END=37±2;HIIT=36±2), preserved lean tissue mass(%BW) (HFD=58±2.9;END=72±6.6;HIIT=72±7.3), improved blood glucoseAUC during an insulin tolerance test(0.65IU/kg*BW) (HFD=411±54;END=350±57;HIIT=320±66 A.U.), and prevented muscle triglyceride  accumulation ((mg/ml per mg tissue) HFD=0.39±0.1;END=0.14±0.1;HIIT=0.13±0.1). Fasting hyperglycaemia, hyperinsulinaemia, and altered AST/ALT ratio (HFD=1.7±0.5;END=3.3±1.3;HIIT=2.2±0.2) were prevented only by END. END, but not HIIT, increased skeletal muscle adiponectin mRNA (14-fold; p<0.05) and increased protein content of high molecular weight (HMW) adiponectin (3.3-fold), whereas HIIT induced a milder increase (2.4-fold). Interestingly, END (irrespective of diet) and HFD alone induced downregulation in muscle adiponectin receptor 1 (ADIPOR1) protein which was not seen with HIIT (fold change from Chow: HFD=0.50±0.2;END=0.48±0.1;HIIT=0.72±0.3; p<0.05). Furthermore, only END prevented the HFD downregulation in mRNA level of PGC1α (p<0.05), which is downstream of adiponectin signaling. Compared with HFD, neither END or HIIT altered circulating low(LMW) or high(HMW) molecular weight adiponectin forms.

While further investigation is needed, differences between training programs might be related to differential induction of muscle adiponectin, particularly in its isoforms and muscle receptor content. Together these results suggest that END is a more effective regimen to prevent HFD induced metabolic disturbances.