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How grizzly bears prevent muscle atrophy during hibernation

By Brooks Hays
Despite spending most of the winter asleep, grizzly bears don't suffer from muscle atrophy. File photo by David Rasmus/Shutterstock
Despite spending most of the winter asleep, grizzly bears don't suffer from muscle atrophy. File photo by David Rasmus/Shutterstock

Dec. 30 (UPI) -- New research has revealed how grizzly bears hibernate for three months without suffering muscle atrophy.

Grizzly bears need their big, strong muscles to fight off rivals and catch fish. But from late fall until early spring, grizzlies don't use their muscles. During hibernation, their metabolism and heart rate drop, and their blood becomes flooded with nitrogen.

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Most other animals, including humans, experience muscle atrophy after just a few weeks of disuse, but not bears.

"Muscle atrophy is a real human problem that occurs in many circumstances," Dr. Douaa Mugahid, a postdoctoral researcher at Harvard Medical School, said in a news release. "We are still not very good at preventing it."

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For their study, researchers analyzed muscle samples, provided by Washington State University, collected from grizzly bears before, during and after hibernation.

"By combining cutting-edge sequencing techniques with mass spectrometry, we wanted to determine which genes and proteins are upregulated or shut down both during and between the times of hibernation," said lead researcher Michael Gotthardt, scientist at the Max Delbrueck Center for Molecular Medicine in Germany.

Researchers compared the patterns of gene expression and protein production with those observed in the tissue of humans, mice and nematode worms.

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The findings -- published this month in the journal Scientific Reports -- suggest grizzly bears possess a unique set of genes that boost amino acid metabolism during hibernation, resulting in greater concentrations of certain non-essential amino acids, which fuel muscle cell growth.

"In experiments with isolated muscle cells of humans and mice that exhibit muscle atrophy, cell growth could also be stimulated by NEAAs," said Gotthardt. "It is known, however, from earlier clinical studies that the administration of amino acids in the form of pills or powders is not enough to prevent muscle atrophy in elderly or bedridden people."

To prevent muscle atrophy in humans, authors of the latest study suggest scientists must find a way to get muscles to produce NEAAs on their own.

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Researchers were able to identify the genetic pathways enabling NEAA production by comparing the gene activity sequenced in tissue from bears, humans, mice and nematodes. The nematode worms, in particular, offered scientists a chance to isolate differences in genetic activity.

"In worms, individual genes can be deactivated relatively easily and one can quickly see what effects this has on muscle growth," said Gotthardt.

In followup studies, scientists plan to explore the functionality of several genes highlighted in the most recent study, including Pdk4 and Serpinf1, both of which appear to influence glucose and amino acid metabolism.

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"We will now examine the effects of deactivating these genes," said Gotthardt. "After all, they are only suitable as therapeutic targets if there are either limited side effects or none at all."

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