Resting metabolic rate (RMR) declines by 1-2% per decade after 20 years of age. This reduction is linked to a decrease in fat free mass (FFM) (10-20%) and the rate of energy expenditure of tissues (Manini 2010). It has also been shown that as we age there is a: * Concomitant reduction in basal fat and carbohydrate oxidation, most likely due to the decrease in RMR than to a change in respiratory exchange ratio (RER) (St-Onge and Gallagher 2010). * A change towards a more saturated membrane of different tissues (Rabini et al 2002). Incorporation of omega-3s, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), into cell membranes may alter energy metabolism by: * Increasing the rate at which proteins operate (Hulbert 2007). * Promoting the release of EPA and DHA into the cytosol which will act as ligands for peroxisome proliferator-activated receptors (PPARs) (Calder 2011). PPARs play an important role in energy homeostasis by regulating genes involved in lipid metabolism (Kota et al 2005). * Augmenting protein synthesis through activation of the mTOR-p70s6k pathway (Di Girolamo et al 2014). Supplementation with fish oil in older males and females: * Increases whole muscle phospholipid profile of EPA and DHA (Smith et al 2011). * Increases lean body mass (LBM), RMR, and fatty acid oxidation (Logan et al unpublished) * Decreases carbohydrate oxidation (Logan et al unplubished). Skeletal muscle (SM) accounts for 20-30% of RMR (Zurlo et al 1990, Manini 2010), therefore it is tempting to speculate that these changes may occur by some of the mechanisms described earlier, with skeletal muscle being an important contributor. To date there are no studies that have examined the effect of n-3 supplementation (3g/day)\* on plasma membrane fatty acid composition, RMR and substrate oxidation, and the possible mechanisms behind it. Therefore the purpose of this study is to determine whether in older adults (female and male), supplementation with n-3 alters: 1. RMR and fatty acid oxidation. 2. Membrane composition of whole muscle and sarcolemma. 3. Content of skeletal muscle membrane fatty acid transport proteins. 4. Dose response of NaKATPase and SERCA efficiency 5. Content of mitochondrial proteins 6. Expression and content of PPARs and proteins involved in translocation of FA transporters (AMPK, ERK1/2, CamKII). 7. Phosphorylation of AMPKα(THR172), ERK1/2(THR202 TYR204) and CaMKII(THR286). 8. Proteomic profile of skeletal muscle. 9. Body composition
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
DOUBLE
Enrollment
30
Fish Oil Capsules
Olive Oil Capsules
University of Guelph
Guelph, Ontario, Canada
Change in skeletal muscle whole muscle membrane fatty acid composition from baseline
Time frame: Baseline and 12 weeks
Change in skeletal muscle sodium pump (Na/K ATPase) activity (umol/mg protein/hour)
Time frame: Baseline and 12 weeks
Change in skeletal muscle sarcoplasmic reticulum calcium (SERCA) ATPase activity (umol/mg protein/hour)
Time frame: Baseline and 12 weeks
Change in whole body resting metabolic rate
Time frame: Baseline, 6 and 12 weeks
Change in skeletal muscle membrane fatty acid transporter content
Time frame: Baseline and 12 weeks
Change in skeletal muscle content of mitochondrial proteins
Time frame: Baseline and 12 weeks
Change in skeletal muscle phosphorylation of AMPKα(THR172), ERK1/2(THR202 TYR204) and CaMKII(THR286)
Time frame: Baseline and 12 weeks
Change in skeletal muscle PPARs content
Time frame: Baseline and 12 weeks
Change in body composition
Time frame: Baseline, 6 and 12 weeks
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