With tongue and tail wagging wildly, Larry the lead dog crossed the finish line in March in sunny Nome, Alaska—after running 1,131 miles to win the Iditarod Trail Sled Dog Race for the third year in a row. To most mortals, Larry looks like a happy but nondescript, scrawny mutt. To sled dog mushers, he is a mini legend that simply needs no introduction. To scientists, Larry may hold the key to a physiological mystery.
Specifically, sled dogs seem to flip an internal switch that acutely changes how they burn fat calories, allowing them to keep going and going and going with no obvious pain. Figuring out how that mechanism works may have implications for human diabetics and those battling obesity.
Researchers first discovered the metabolic switch in 2005, when a team headed by Oklahoma State University’s Michael Davis—who has been investigating the metabolic, gastrointestinal, respiratory and blood systems of sled dogs for 10 years—did a controlled study at a professional racing kennel in Alaska. Mushers ran the dogs in mock, 100-mile races for four to five days in a row. Every 100 miles the researchers took matchstick-size samples of leg muscle (about 60 milligrams apiece) from the dogs to test for protein levels, enzyme activity and glycogen, a starchlike compound that stores energy for quick release.
Glycogen turns out to be a crucial piece of the metabolic switch. During the first few days of racing, sled dogs draw energy from glycogen stored inside muscle cells. But instead of depleting glycogen stores and tiring the muscles, the animals suddenly switch to a glycogen-sparing metabolism. They start drawing energy from sources outside of the muscles.
Davis suggests that the muscle cells start extracting fat directly from the blood and somehow transport this fat across the cell membranes and into the cells, where it can be burned as fuel. During race times, fat builds up in a sled dog’s blood, most likely because of the high-fat racing diet. Each 50-pound canine consumes about 12,000 calories daily (typically 60 percent fat and 40 percent carbohydrate and protein).
According to Raymond Geor, an exercise physiologist at Michigan State University, sled dog muscle cells are well equipped to use this fat because they have a higher mitochondrial density—more cellular power plants—than other animals. The mystery is how the blood-borne fat gets into cells in the first place. Increasing evidence suggests that fat is transported into the cells along similar pathways as glucose, Davis says, with the hormone insulin playing a critical role. Researchers are exploring the sled dog’s sensitivity to insulin to better understand this pathway.
Breeding probably had much to do with the development of the metabolic switch. Larry is descended from a long line of racing dogs. “The bloodlines of my dogs date back 100 years,” says Lance Mackey, Larry’s owner and legendary racing musher, the only person to win the long-distance Iditarod and the Yukon Quest in the same year with the same dog team. “They are mixed breeds—mutts—but they’ve been bred to run.”
Selective breeding, though, may not be the whole story. The dogs may have learned to switch metabolic strategies on demand through intense training. If so, then researchers might have an easier time applying what they learn about the canines to humans training for an endurance event or those seeking treatment for diabetes or obesity. Such patients might benefit, for instance, if researchers could pinpoint the mechanisms that boost the body’s sensitivity to insulin or that better utilize fat that builds up in muscle tissue.
This year Mackey won the Iditarod by one of the widest margins ever, finishing a comfortable eight hours ahead of his closest competitor. That Iditarod, however, will be the last one for Larry, after participating for eight of his nine living years. He will officially retire from racing at the end of this year for a well-deserved, if unneeded, rest.