Journal
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
Volume 128, Issue -, Pages 74-86Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.plefa.2017.12.003
Keywords
Skeletal muscle; Polyunsaturated fatty acids (PUFA); Omega-6 (n-6); Eicosanoid; Supplement
Funding
- Liggins Institute, University of Auckland, Faculty Research and Development Fund [3706927]
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Arachidonic acid (ARA), an omega-6 polyunsaturated fatty acid (PUFA), is the metabolic precursor to the eicosanoid family of lipid mediators. Eicosanoids have potent pro-inflammatory actions, but also act as important autocrine/paracrine signaling molecules in skeletal muscle growth and development. Whether dietary ARA is incorporated into skeletal muscle phospholipids and the resulting impact on intramuscular inflammatory and adaptive processes in-vivo is not known. In the current study, resistance trained men (>= 1 year) received dietary supplementation with 1.5 g/day ARA (n = 9, 24 +/- 1.5 years) or placebo (n = 10, 26 +/- 1.3 years) for 4-weeks while continuing their normal training regimen. Plasma and vastus lateralis muscle biopsies were collected in an overnight fasted state at baseline and week 4. ARA supplementation increased plasma content of ARA and gamma-linolenic acid, while decreasing relative abundance of linoleic acid, eicosapentaenoic acid, and dihomogamma-linolenic acid. In skeletal muscle, ARA and dihomo-gamma-linolenic acid content increased, whereas alpha-linolenic-acid was reduced. Compared to placebo, ARA supplementation reduced circulating platelet and monocyte number, and decreased the mRNA expression of the immune cell surface markers; neutrophil elastase/CD66b and interleukin 1-beta, in peripheral blood mononuclear cells. In muscle, ARA supplementation increased mRNA expression of the myogenic regulatory factors; MyoD and myogenin, but had no effect on a range of immune cell markers or inflammatory cytokines. These data show that dietary ARA supplementation can rapidly and safely modulate plasma and muscle fatty acid profile and promote myogenic gene expression in resistance trained men, without a risk of increasing basal systemic or intramuscular inflammation.
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