Abnormalities in muscle lipid metabolism in obesity have been linked to insulin resistance. Exercise training alters skeletal muscle lipid abundance and localization, but the direct effects of exercise training (independent of weight loss) on skeletal muscle lipolytic proteins are not clearly understood, and data are lacking regarding influence of training intensity on factors regulating muscle lipid metabolism in obesity. Our aim was to examine the effects of high-intensity interval training (HIIT) vs. moderate-intensity continuous training (MICT) on skeletal muscle lipolytic proteins in obese humans. Eighteen sedentary, obese adults completed 12 weeks (4 sessions weekly) of either HIIT (10 x 1 min at 90% HRmax, 1 min recovery; n=8) or MICT (45 min at 70% HRmax; n=10). Muscle biopsies (vastus lateralis) were collected before and after training. Subjects maintained body weight and fat mass and the post-training biopsy occurred 3 days after the final exercise session. Both exercise training programs increased aerobic capacity (VO2max) by ~10% (p=0.003), with no significant difference between HIIT and MICT. In muscle samples, hormone-sensitive lipase (HSL) protein abundance increased ~2-fold after training in HIIT (P<0.05), but not MICT. Training did not affect muscle abundance of adipose triglyceride lipase (ATGL) in either group but interestingly, the abundance of both CGI-58 (a positive regulator of ATGL lipolytic activity) and G0S2 (a negative regulator of ATGL lipolytic activity) increased ~15-20% after training (p<0.02), with no difference between HIIT and MICT.

In summary, HIIT and MICT result in similar modifications to lipolytic proteins in skeletal muscle, although our findings suggest that HIIT may be a more potent stimulus for increasing HSL abundance. Future work is needed to determine if the concomitant increases in protein abundance of CGI-58 and G0S2 with training may improve lipid handling in obesity.

Disclosure

B.J. Ryan: None. M.W. Schleh: None. P. Varshney: None. A. Ludzki: None. J.B. Gillen: None. K. Foug: None. B.D. Carr: None. J.F. Horowitz: Research Support; Self; American Diabetes Association.

Funding

National Institutes of Health (R01DK077966, P30DK089503, T32DK007245); Canadian Institutes of Health Research (DFS146190)

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