Human inflammatory and resolving lipid mediator responses to resistance exercise and ibuprofen treatment

Markworth, James F., Vella, Luke, Lingard, Benjamin S., Tull, Dedreia L., Rupasinghe, Thusitha W., Sinclair, Andrew J., Maddipati, Krishana Rao and Cameron-Smith, David 2013, Human inflammatory and resolving lipid mediator responses to resistance exercise and ibuprofen treatment, American journal of physiology - regulatory integrative and comparative physiology, vol. 305, no. 11, pp. R1281-R1296.

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Title Human inflammatory and resolving lipid mediator responses to resistance exercise and ibuprofen treatment
Author(s) Markworth, James F.
Vella, Luke
Lingard, Benjamin S.
Tull, Dedreia L.
Rupasinghe, Thusitha W.
Sinclair, Andrew J.
Maddipati, Krishana Rao
Cameron-Smith, David
Journal name American journal of physiology - regulatory integrative and comparative physiology
Volume number 305
Issue number 11
Start page R1281
End page R1296
Total pages 16
Publisher American Physiological Society
Place of publication Bethesda, Maryland
Publication date 2013-12
ISSN 0363-6119
1522-1490
Keyword(s) eicosanoid
exercise
inflammation
nonsteroidal anti-inflammatory drug
resolution
Summary Classical proinflammatory eicosanoids, and more recently discovered lipid mediators with anti-inflammatory and proresolving bioactivity, exert a complex role in the initiation, control, and resolution of inflammation. Using a targeted lipidomics approach, we investigated circulating lipid mediator responses to resistance exercise and treatment with the NSAID ibuprofen. Human subjects undertook a single bout of unaccustomed resistance exercise (80% of one repetition maximum) following oral ingestion of ibuprofen (400 mg) or placebo control. Venous blood was collected during early recovery (0–3 h and 24 h postexercise), and serum lipid mediator composition was analyzed by LC-MS-based targeted lipidomics. Postexercise recovery was characterized by elevated levels of cyclooxygenase (COX)-1 and 2-derived prostanoids (TXB2, PGE2, PGD2, PGF2α, and PGI2), lipooxygenase (5-LOX, 12-LOX, and 15-LOX)-derived hydroxyeicosatetraenoic acids (HETEs), and leukotrienes (e.g., LTB4), and epoxygenase (CYP)-derived epoxy/dihydroxy eicosatrienoic acids (EpETrEs/DiHETrEs). Additionally, we detected elevated levels of bioactive lipid mediators with anti-inflammatory and proresolving properties, including arachidonic acid-derived lipoxins (LXA4 and LXB4), and the EPA (E-series) and DHA (D-series)-derived resolvins (RvD1 and RvE1), and protectins (PD1 isomer 10S, 17S-diHDoHE). Ibuprofen treatment blocked exercise-induced increases in COX-1 and COX-2-derived prostanoids but also resulted in off-target reductions in leukotriene biosynthesis, and a diminished proresolving lipid mediator response. CYP pathway product metabolism was also altered by ibuprofen treatment, as indicated by elevated postexercise serum 5,6-DiHETrE and 8,9-DiHETrE only in those receiving ibuprofen. These findings characterize the blood inflammatory lipid mediator response to unaccustomed resistance exercise in humans and show that acute proinflammatory signals are mechanistically linked to the induction of a biological active inflammatory resolution program, regulated by proresolving lipid mediators during postexercise recovery.
Language eng
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2013, American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30060432

Document type: Journal Article
Collections: School of Exercise and Nutrition Sciences
School of Medicine
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