Submitted on April 18, 2008
Revised on September 2, 2008
Accepted on September 11, 2008
Fat-adaptation followed by carbohydrate restoration increases AMPK activity in skeletal muscle from trained humans
Wee Kian Yeo1, Sarah J. Lessard1, Zhi-Ping Chen2, Andrew P. Garnham3, Louise M. Burke4, Donato A. Rivas1, Bruce E. Kemp2, and John A. Hawley1*
1 RMIT University
2 St. Vincent's Institute
3 Deakin University
4 Australian Institute of Sport
* To whom correspondence should be addressed. E-mail: john.hawley{at}rmit.edu.au.
We have previously reported that 5 d of a high-fat diet followed by 1 d high carbohydrate intake (FAT-adapt) increased rates of fat oxidation and decreased rates of muscle glycogenolysis during submaximal cycling compared to consumption of an isoenergetic high-carbohydrate diet (HCHO) for 6 d. To determine potential mechanisms underlying shifts in substrate selection, 8 trained subjects performed FAT-adapt and HCHO. On day 7 subjects performed 1 hr 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 (TG) levels were higher after FAT-adapt (p<0.05). Resting AMPK
1 and -2 activity were 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 Ser 221) 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 AMPK1 activity after HCHO (p=0.03) but not FAT-adapt. Exercise was associated with an increase in pACC at Ser 221 for both dietary treatments (p<0.05), with post-exercise pACC Ser 221 higher after FAT-adapt (p=0.02). In conclusion, compared to HCHO, FAT-adapt increased resting muscle TG stores and resting AMPK2 activity. FAT-adapt also resulted in higher rates of whole-body fat oxidation, reduced muscle glycogenolysis and attenuated the exercise-induced rise in AMPK1 and AMPK2 activity compared to HCHO. Our results demonstrate that AMPK1 and AMPK2 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.
