The Effect of Omega-3 Fatty Acid Supplementation on Skeletal Muscle Membrane Composition and Cellular Metabolism
NCT ID: NCT01732003
Last Updated: 2012-11-28
Study Results
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Basic Information
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UNKNOWN
NA
24 participants
INTERVENTIONAL
2011-11-30
2013-02-28
Brief Summary
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Compared to research investigating other body tissues, the effect of EPA and DHA on skeletal muscle membranes and cellular function has received little attention. Of the studies done, EPA and DHA supplementation consistently results in increased EPA, DHA, and total omega-3 fatty acid content in the skeletal muscle membranes of rodents. One study has also demonstrated this effect in humans. These studies, however, have been limited to whole muscle measurements, yet cells contain numerous subcellular membranes with diverse functions. Two membranes of key importance to the metabolic function of a skeletal muscle cell are the membrane that surrounds the cell (plasma membrane), and the membrane that surrounds the mitochondria.
The plasma and mitochondrial membranes are responsible for taking up nutrients and converting them into useable energy for the muscle. Recent findings suggest that physiological changes in these processes may occur following EPA and DHA supplementation. At rest and during exercise, there is potential for a shift in substrate selection that favors fat utilization following EPA and DHA supplementation. Several membrane proteins are responsible for transporting fat into the cell and mitochondria. The presence of EPA and DHA within membranes has the potential to affect the membrane integration and function of proteins. The investigators aim to determine whether fat utilization increases following EPA and DHA supplementation, and if there is a concurrent change in the concentrations of fat transport proteins within plasma and mitochondrial membranes. Supplementation with EPA and DHA may also affect oxygen consumption, an important process in energy production that is regulated by mitochondrial membrane proteins. Evidence from human and rodent studies shows a decrease in whole body oxygen consumption following supplementation. The investigators aim to examine these changes directly by measuring mitochondrial respiration following EPA and DHA supplementation.
Therefore, the primary purpose of this study is to examine how plasma and mitochondrial membrane fatty acid composition change individually in response to EPA and DHA supplementation in humans. The secondary purpose of this study is to examine functional metabolic changes that occur in skeletal muscle in response to EPA and DHA supplementation, and to investigate correlational relationships between these changes and any compositional alterations in plasma and mitochondrial membranes. The investigators hypothesize that supplementation with EPA and DHA will alter fuel selection at rest and during exercise, and this will correspond to an increase in the concentration of membrane fatty acid transport proteins, and that these changes will correlate to an increase in the EPA, DHA, and total omega-3 content of plasma and mitochondrial membranes.
Detailed Description
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Conditions
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Keywords
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Study Design
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NON_RANDOMIZED
PARALLEL
BASIC_SCIENCE
SINGLE
Study Groups
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Omega-3 Complete
Oral ingestion of 3000 mg (5 capsules) of Omega-3 Complete (Jamieson Laboratories Ltd., Windsor, Ontario, Canada) per day for 12 weeks
Omega-3 Complete
Placebo Pill
Oral ingestion of 5 capsules of a placebo oil pill (Jamieson Laboratories Ltd., Windsor, Ontario, Canada) per day for 12 weeks
Placebo Pill
Interventions
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Omega-3 Complete
Placebo Pill
Eligibility Criteria
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Inclusion Criteria
* Must currently practice a consistent diet, and exercise regimen, and maintain this throughout the duration of the study
Exclusion Criteria
* Average fish intake greater than two times per week
* Sedentary
* Highly active/trained
* Diagnosed respiratory problem
* Diagnosed heart problem/condition
* Lightheadedness, shortness of breath, chest pain, numbness, fatigue, coughing, or wheezing during at rest of with low to moderate physical activity
* Cardiovascular disease risk factors: Family history of heart attacks, hypertension, hypercholesterolemia, diabetes mellitus, smoking, obesity
* Allergies to lidocaine, fish/fish oil, gelatine, glycerin, or mixed tocopherols
* Currently taking any medications or supplements that may increase the chance of bleeding (e.g. Aspirin, Coumadin, Anti-inflammatories, Plavix, Vitamin C or E, high doses of garlic, ginkgo biloba, willow bark products)
* Tendency toward easy bleeding or bruising
18 Years
30 Years
MALE
Yes
Sponsors
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McMaster University
OTHER
Medical University of Bialystok
OTHER
University of Guelph
OTHER
Responsible Party
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Lawrence Spriet
Professor and Chair
Principal Investigators
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Lawrence L Spriet, PhD
Role: PRINCIPAL_INVESTIGATOR
University of Guelph
Locations
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University of Guelph
Guelph, Ontario, Canada
Countries
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Central Contacts
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References
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Ayre KJ, Hulbert AJ. Dietary fatty acid profile influences the composition of skeletal muscle phospholipids in rats. J Nutr. 1996 Mar;126(3):653-62. doi: 10.1093/jn/126.3.653.
Peoples GE, McLennan PL. Dietary fish oil reduces skeletal muscle oxygen consumption, provides fatigue resistance and improves contractile recovery in the rat in vivo hindlimb. Br J Nutr. 2010 Dec;104(12):1771-9. doi: 10.1017/S0007114510002928. Epub 2010 Aug 9.
Andersson A, Nalsen C, Tengblad S, Vessby B. Fatty acid composition of skeletal muscle reflects dietary fat composition in humans. Am J Clin Nutr. 2002 Dec;76(6):1222-9. doi: 10.1093/ajcn/76.6.1222.
Couet C, Delarue J, Ritz P, Antoine JM, Lamisse F. Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults. Int J Obes Relat Metab Disord. 1997 Aug;21(8):637-43. doi: 10.1038/sj.ijo.0800451.
Delarue J, Labarthe F, Cohen R. Fish-oil supplementation reduces stimulation of plasma glucose fluxes during exercise in untrained males. Br J Nutr. 2003 Oct;90(4):777-86. doi: 10.1079/bjn2003964.
Peoples GE, McLennan PL, Howe PR, Groeller H. Fish oil reduces heart rate and oxygen consumption during exercise. J Cardiovasc Pharmacol. 2008 Dec;52(6):540-7. doi: 10.1097/FJC.0b013e3181911913.
Other Identifiers
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11SE032
Identifier Type: -
Identifier Source: org_study_id