 external fuel sources during long-term, high-intensity exercise because mammals preferentially burn carbohydrates to provide energy, and these reserves are rapidly used up. The body switches to a lipid fuel source after carbohydrate stores are depleted, but the fat-burning process is inefficient, limiting our ability to exercise continuously even if we have excess fat to burn. In contrast, migrating birds preferentially use fat for energy, and each bird bulks up before its long flight.
The accumulation and internal storage of fuel is necessary for long-distance avian migration. Songbirds double their body mass to prepare for migration, mostly due to increased subcutaneous fat stores. Premigratory fattening is controlled by a circannual timer in many species. Photoperiod and food availability also serve as cues to stimulate fattening. In some species, a change in metabolic efficiency prompts fat accumulation, even without increased food intake. For the most part, however, seasonal changes in appetite and satiety lead to increased food intake, accounting for a significant amount of the body mass in many species. The hypothalamic region of the brain controls appetite and satiety, and seasonal increases in neurotransmitters in the hypothalamus (for example, one called neuropeptide Y) are associated with seasonal hyperphagia in birds.
In mammals, a major signal for satiety, which basically indicates, “Stop eating, you’re full,” is a hormone called leptin. This hormone may be involved in seasonal changes in eating, fat storage and lipid utilization in migratory birds. Strangely, the gene that encodes leptin is absent from the avian genome. However, research from Christopher Guglielmo at University of Western Ontario shows that birds are responsive to leptin: They possess a functional receptor for the hormone, and injecting leptin has dramatic effects on their metabolism. Do birds make use of a signal other than leptin that serves to indicate the levels of fat stores? The answer is probably yes. One candidate is adiponectin, another hormone that, like leptin, is produced by adipose cells that make up body fat. This hormone exerts effects on metabolic activity via two different adiponectin receptors. Adiponectin promotes glucose and fatty acid mobilization and metabolism, so levels of this molecule are usually higher in lean animals. Like numerous other metabolic factors, adiponectin is rhythmically expressed in a circadian manner (see Figure 8, below). Work from our laboratory shows that when white-throated sparrows (Zonotrichia albicollis) migrate, peak levels of adiponectin are shifted from daytime to nighttime. Furthermore, adiponectin receptors in the liver of migrating birds increase in abundance during the night. Changing the adiponectin rhythm, in combination with increased levels of the receptors, promotes energy utilization during the night when birds are flying.
The initiation and duration of the fattening period is correlated with migration distance: The longer the migratory route, the more fat birds amass. How are they even able to get off the ground? The gain in body mass is partially offset by a premigratory reduction in digestive organ sizes, and bulking up flight muscles helps power the extra load. Still, the body condition of a premigratory bird is in stark contrast to the human athlete preparing for extended physical activity, for whom excess weight is undesirable. The premigratory increase in body mass, body-fat percentage, and levels of glucose and lipids in blood plasma are hallmarks of human obesity and metabolic syndrome, the constellation of metabolic imbalances associated with increased risk of diabetes and cardiovascular disease. By human standards, premigratory birds are obese, diabetic and likely to drop dead of a heart attack at any moment. However, unlike mammals, birds are exceptionally good at burning fat for energy, and their bodies are extremely resistant to metabolic disorders.
Fat provides the greatest energy per unit mass, making it an ideal fuel for flying animals. But its insolubility mak