Postexercise skeletal muscle signaling responses to moderate- to high-intensity steady-state exercise in the fed or fasted state

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.

Graded reductions in preexercise muscle glycogen impair exercise capacity but do not augment skeletal muscle cell signaling: implications for CHO periodization

“…In contrast to AMPK and ACC, we did not observe any change in the phosphorylation status of p38MAPK Thr180/Tyr182 or CAMKII Thr286 either in response to exercise or muscle glycogen concentration, though we note the large inter-individual variability and recommend the use of larger sample sizes in future. These data are in agreement with previous work that demonstrate no change in p38MAPK or CAMKII phosphorylation using a variety of train-low methodologies, including sleep-low, train-low (3,25), twice-per day training (46) and fasted training (42). Whilst augmented p38MAPK phosphorylation has been observed when preexercise muscle glycogen is reduced (163 vs. 375 mmol kg -1 dw), this is only apparent within the nucleus and not the cytoplasm (7).…”

Protein-carbohydrate ingestion alters Vps34 cellular localization independent of changes in kinase activity in human skeletal muscle

“…Immunoblotting analysis was conducted as described previously (29). Briefly, equal amounts of protein were loaded into 8-15% polyacrylamide gels and separated by SDS-PAGE.…”

Carbohydrate Restriction in Type 1 Diabetes: A Realistic Therapy for Improved Glycaemic Control and Athletic Performance?

“…Fasted exercise, whereby breakfast is consumed after a morning training session, is a simpler model of train low that may lead to superior metabolic adaptations to training in the fed state (see Wallis and Gonzalez [161] for a recent review of non-diabetes studies). Exercising in the overnight fasted vs. fed state in people without diabetes has been linked to a number of responses that may translate to long-term improvements in lipid and glucose metabolism [162]. During fasted exercise, there is increased fat utilisation, improved plasma lipid profiles and enhanced activation of the molecular signalling pathways, leading to increased mitochondrial content and capacity to oxidise fat while supressing glucose metabolism compared to fed exercise [163,164,165].…”