Postexercise skeletal muscle signaling responses to moderate- to high-intensity steady-state exercise in the fed or
Ben Stocks1, Jessica R Dent1, Henry B Ogden1
1School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham , Birmingham , United Kingdom.
Abstract:
Exercise performed in the fasted state acutely increases fatty acid availability and utilization. Furthermore, activation of energy-sensing pathways and fatty acid metabolic genes can be augmented by fasting and fasted exercise. However, whether a similar effect occurs at higher exercise intensities remains poorly understood. This study aimed to assess the effect of fed and fasted exercise upon postexercise signaling and mRNA responses during moderate- to high-intensity steady-state exercise. Eight male participants [age: 25 (SD 2) yr, V̇o2peak: 47.9 (SD 3.8) ml·kg-1·min-1] performed 1 h of cycling at 70% Wmax in the fasted (FAST) state or 2 h following ingestion of a carbohydrate-rich mixed-macronutrient breakfast (FED). Muscle biopsies were collected pre-, immediately, and 3 h postexercise from the medial vastus lateralis, while venous blood samples were collected throughout the trial. Plasma, nonesterified fatty acid, and glycerol concentrations were elevated during FAST compared with FED, although substrate utilization during exercise was similar. AMPKThr172 phosphorylation was ~2.5-fold elevated postexercise in both trials and was significantly augmented by ~30% during FAST. CREBSer133 phosphorylation was elevated approximately twofold during FAST, although CREBSer133 phosphorylation acutely decreased by ~50% immediately postexercise. mRNA expression of PDK4 was approximately three- to fourfold augmented by exercise and approximately twofold elevated throughout FAST, while expression of PPARGC1A mRNA was similarly activated (~10-fold) by exercise in both FED and FAST. In summary, performing moderate- to high-intensity steady-state exercise in the fasted state increases systemic lipid availability, elevates phosphorylation of AMPKThr172 and CREBSer133, and augments PDK4 mRNA expression without corresponding increases in whole body fat oxidation and the mRNA expression of PPARGC1A.
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