Postexercise High-Fat Feeding Suppresses p70S6K1 Activity in Human Skeletal Muscle
Open accessAbstract
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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High-fat feeding may impair muscle protein synthesis, potentially via reduced activation of mammalian target of rapamycin (mTOR) and ribosomal protein S6 kinase (p70S6K) signalling.
“Emerging data also suggest that high-fat feeding may impair muscle protein synthesis [46], potentially via reduced activation of mammalian target of rapamycin (mTOR) and ribosomal protein S6 kinase (p70S6K) signalling [43].”
From Fuel for the Work Required: A Theoretical Framework for Carbohydrate Periodization and the Glycogen Threshold Hypothesis (2018) · cites this paper as [43]
The Discussion (p. 14) reports suppressed p70S6K1 activity after postexercise high-fat feeding and suggests this may impair regulation of muscle protein synthesis. It does not report reduced mTOR activation in the studied human muscle; the Discussion (p. 19) mentions possible impaired mTORC signalling in a cited rat-liver study. The muscle-protein-synthesis claim carries a separate citation [46], so the unsupported part of the claim attributed to this paper is reduced mTOR activation. (LLM, conf=0.86)
Experimental — accuracy not yet measured1-5 days of high-fat feeding reduces the expression of the pyruvate dehydrogenase (PDH) complex.
“Indeed, 1–5 days of high-fat feeding reduces the expression [43] and activity of the pyruvate dehydrogenase (PDH) complex [44], ultimately impairing CHO oxidation and high-intensity performance.”
From Fuel for the Work Required: A Theoretical Framework for Carbohydrate Periodization and the Glycogen Threshold Hypothesis (2018) · cites this paper as [43]
The Results (p. 13) report increased PDK4 mRNA expression after high-fat feeding, not reduced expression of the PDH complex. The Discussion (p. 17) suggests that, if the dietary protocol were followed long term, it might suppress the PDH complex; it does not establish the claimed reduction in PDH expression after 1–5 days. (LLM, conf=0.84)
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- Authors
- HAMMOND, K. M., IMPEY, S. G., CURRELL, K., MITCHELL, N., SHEPHERD, S. O., JEROMSON, S., HAWLEY, J. A., CLOSE, G. L., HAMILTON, L. D., SHARPLES, A. P., & MORTON, J. P.
- Affiliations
- University of Stirling (GB)
- ORCID
- Venue
- Medicine & Science in Sports & Exercise
- Published
- 2016-11
- Volume
- 48
- Issue
- 11
- Pages
- 2108-2117
- ISSN
- 0195-9131 (ISSN-L)
- OpenAlex
- W2471933862
- Cited by
- 30
- References
- 39
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 4 · 2022: 3 · 2021: 4 · 2020: 3 · 2019: 6 · 2018: 5 · 2017: 3
- FWCI
- 3.21
- Type
- journal article
- Language
- en
- Open access
- green
- eprints.keele.ac.uk
- Licence
- cc-by
- Locations
- Medicine & Science in Sports & Exercise (publishedVersion)
- PubMed (publishedVersion)
- Keele Research Repository (Keele University) (submittedVersion, cc-by)
- Liverpool John Moores University (submittedVersion)
- Stirling Online Research Repository (University of Stirling) (submittedVersion, public-domain)
- Figshare (submittedVersion, cc-by)
- Funders
- English Institute of Sport
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- skeletal muscle, p70S6K1, S6K, mitochondrial biogenesis, lipid metabolism, muscle protein synthesis, muscle glycogen, PGC-1α, PDK4, CD36, carnitine palmitoyltransferase 1, high-intensity interval training, dietary fat
- MeSH terms
- Organelle Biogenesis, Dietary Carbohydrates, Dietary Fats, Glycogen, Humans, Male, Muscle Proteins, Signal Transduction, Exercise, Gene Expression, Muscle, Skeletal, Cross-Over Studies, Ribosomal Protein S6 Kinases, Lipid Metabolism, Young Adult
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