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Fat adaptation followed by carbohydrate restoration increases AMPK activity in skeletal muscle from trained humans

¹Exercise Metabolism Group, School of Medical Sciences, RMIT University, Victoria; ²St. Vincent's Institute, University of Melbourne, Victoria; ³Exercise, Muscle and Metabolism Unit, School of Exercise and Nutrition Sciences, Deakin University, Victoria; and ⁴Department of Sports Nutrition, Australian Institute of Sport, Belconnen, Australian Capital Territory, Australia

Submitted 18 April 2008 ; accepted in final form 11 September 2008

We have previously reported that 5 days of a high-fat diet followed by 1 day of high-carbohydrate intake (Fat-adapt) increased rates of fat oxidation and decreased rates of muscle glycogenolysis during submaximal cycling compared with consumption of an isoenergetic high-carbohydrate diet (HCHO) for 6 days (Burke et al. J Appl Physiol 89: 2413–2421, 2000; Stellingwerff et al. Am J Physiol Endocrinol Metab 290: E380–E388, 2006). To determine potential mechanisms underlying shifts in substrate selection, eight trained subjects performed Fat-adapt and HCHO. On day 7, subjects performed 1-h cycling at 70% peak O₂ uptake. Muscle biopsies were taken immediately before and after exercise. Resting muscle glycogen content was similar between treatments, but muscle triglyceride levels were higher after Fat-adapt (P < 0.05). Resting AMPK-₁ and -₂ activity was higher after Fat-adapt (P = 0.02 and P = 0.05, respectively), while the phosphorylation of AMPK's downstream target, acetyl-CoA carboxylase (pACC at Ser²²¹), tended to be elevated after Fat-adapt (P = 0.09). Both the respiratory exchange ratio (P < 0.01) and muscle glycogen utilization (P < 0.05) were lower during exercise after Fat-adapt. Exercise increased AMPK-₁ activity after HCHO (P = 0.03) but not Fat-adapt. Exercise was associated with an increase in pACC at Ser²²¹ for both dietary treatments (P < 0.05), with postexercise pACC Ser²²¹ higher after Fat-adapt (P = 0.02). In conclusion, compared with HCHO, Fat-adapt increased resting muscle triglyceride stores and resting AMPK-₁ and -₂ activity. Fat-adapt also resulted in higher rates of whole body fat oxidation, reduced muscle glycogenolysis, and attenuated the exercise-induced rise in AMPK-₁ and AMPK-₂ activity compared with HCHO. Our results demonstrate that AMPK-₁ and AMPK-₂ activity and fuel selection in skeletal muscle in response to exercise can be manipulated by diet and/or the interactive effects of diet and exercise training.

acetyl-coenzyme A carboxylase; fat oxidation; muscle glycogen; skeletal muscle metabolism