Postexercise High-Fat Feeding Suppresses p70S6K1 Activity in Human Skeletal Muscle

Jun 22, 2016Medicine and science in sports and exercise

High-Fat Meals After Exercise Reduce Muscle Protein-Building Activity in Humans

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Abstract

Muscle glycogen was significantly lower at 3 hours (251 vs 301 mmol·kg dry weight) and 15 hours (182 vs 312 mmol·kg dry weight) post-exercise in the high-fat recovery condition compared to the high-carbohydrate condition.

Adenosine monophosphate-activated protein kinase α2 activity did not show an increase post-exercise in either dietary condition.
Comparable increases in mRNA levels of several genes related to mitochondrial biogenesis and muscle function were observed in both high-carbohydrate and high-fat conditions.
Higher mRNA expression of lipid metabolism-related genes, such as PDK4, CD36, and carnitine palmitoyltransferase 1, was found in the high-fat condition during recovery.
Ribosomal protein S6 kinase activity was higher in the high-carbohydrate condition at 3 hours post-exercise, suggesting a potential impact on muscle remodeling under high-fat feeding.

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PURPOSE: This study aimed to examine the effects of reduced CHO but high postexercise fat availability on cell signaling and expression of genes with putative roles in regulation of mitochondrial biogenesis, lipid metabolism, and muscle protein synthesis.

METHODS: Ten males completed a twice per day exercise model (3.5 h between sessions) comprising morning high-intensity interval training (8 × 5 min at 85% V˙O2peak) and afternoon steady-state (SS) running (60 min at 70% V˙O2peak). In a repeated-measures design, runners exercised under different isoenergetic dietary conditions consisting of high-CHO (HCHO: 10 g·kg CHO, 2.5 g·kg protein, and 0.8 g·kg fat for the entire trial period) or reduced-CHO but high-fat availability in the postexercise recovery periods (HFAT: 2.5 g·kg CHO, 2.5 g·kg protein, and 3.5 g·kg fat for the entire trial period).

RESULTS: Muscle glycogen was lower (P < 0.05) at 3 h (251 vs 301 mmol·kg dry weight) and 15 h (182 vs 312 mmol·kg dry weight) post-SS exercise in HFAT compared with HCHO. Adenosine monophosphate-activated protein kinase α2 activity was not increased post-SS in either condition (P = 0.41), although comparable increases (all P < 0.05) in PGC-1α, p53, citrate synthase, Tfam, peroxisome proliferator-activated receptor, and estrogen-related receptor α mRNA were observed in HCHO and HFAT. By contrast, PDK4 (P = 0.003), CD36 (P = 0.05), and carnitine palmitoyltransferase 1 (P = 0.03) mRNA were greater in HFAT in the recovery period from SS exercise compared with HCHO. Ribosomal protein S6 kinase activity was higher (P = 0.08) at 3 h post-SS exercise in HCHO versus HFAT (72.7 ± 51.9 vs 44.7 ± 27 fmol·min·mg).

CONCLUSION: Postexercise high-fat feeding does not augment the mRNA expression of genes associated with regulatory roles in mitochondrial biogenesis, although it does increase lipid gene expression. However, postexercise ribosomal protein S6 kinase 1 activity is reduced under conditions of high-fat feeding, thus potentially impairing skeletal muscle remodeling processes.

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Postexercise High-Fat Feeding Suppresses p70S6K1 Activity in Human Skeletal Muscle

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