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First published online February 13, 2009
Journal of Experimental Biology 212, 593-597 (2009)
Published by The Company of Biologists 2009
doi: 10.1242/jeb.015024
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The physiology of long-distance migration: extending the limits of endurance metabolism

Jean-Michel Weber

Department of Biology, University of Ottawa, Ontario, Canada


Figure 1
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Fig. 1. The semipalmated sandpiper (Calidris pusilla) stops in the Bay of Fundy (New Brunswick, Canada) during its fall migration from breeding areas in the Arctic. This crucial stopover allows the migrant to store large lipid reserves by eating seasonally abundant amphipods (Corophium volutator) buried in the mudflats. It is currently estimated that 75% (~1 million individuals) of the world population of semipalmated sandpipers stops at this location. The Corophium mudshrimp contains unusually large amounts of n-3 polyunsaturated fatty aids (45% of total lipids) and is found only in the Bay of Fundy and along the coast of Maine. Dietary n-3 fatty acids are not only used as an energy source but they also act as performance-enhancing substances to increase the capacity for endurance exercise, just before the sandpiper crosses the Atlantic ocean to South America (Maillet and Weber, 2006Go; Maillet and Weber, 2007Go). The remainder of the annual migration cycle appears to be achieved through multiple short flights over land and along coastal areas. Pollution and rising sea levels caused by global warming are major threats to strategic stopover sites such as the Bay of Fundy and to the future of this migrant bird. [Photographs adapted from: Ferrin 2004 (Calidris) and S. Mautner (Corophium).]

 

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Fig. 2. Figure showing the first mechanism of natural doping whereby dietary n-3 fatty acids are incorporated into membrane phospholipids. Before crossing the ocean, the semipalmated sandpiper (Calidris pusilla) doubles its body mass by eating n-3 eicosapentaenoic acid (EPA 20:5) and n-3 docosahexaenoic acid (DHA 22:6). These lipids are from the n-3 family of fatty acids because their first double bond is located after the third carbon from the terminal methyl group (n). The X:Y nomenclature indicates that these fatty acids have X carbon atoms and Y double bonds. EPA and DHA have multiple double bonds, imposing many angles upon their carbon chains. Therefore, their addition to phospholipids increases membrane fluidity and alters the properties of membrane-bound proteins. Carnitine palmitoyl transferase (CPT) is one of the enzymes activated by the presence of EPA in mitochondrial membrane phospholipids.

 

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Fig. 3. Figure showing a second mechanism of natural doping whereby the binding of dietary n-3 fatty acids to the transcription factors peroxisome proliferator-activated receptors {alpha} and β (PPAR{alpha} and β) activates genes regulating lipid metabolism. n-3 eicosapentaenoic acid (EPA) and n-3 docosahexaenoic acid (DHA) are natural ligands for PPARs. Ligand binding causes the dimerization of PPAR with the retinoid-X-receptor (RXR). The PPAR–RXR complex activates target genes by recognizing promoter regions called peroxisome proliferator response elements (PPREs). Target genes include the β-oxidation enzymes carnitine palmitoyl transferase (CPT) and hydroxyacyl dehydrogenase (HOAD), fatty acid binding proteins (FABPs) and the transmembrane fatty acid transporters CD36 and FAT.

 

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