The grizzly bear does something very special in that it hardly loses any strength during hibernation,’ says Professor Michael Gotthardt, head of the Neuromuscular and Cardiovascular Cell Biology group at the Max Delbrueck Center for Molecular Medicine in Berlin. These bears go into hibernation sometime between November and January, during which time their metabolism and heart rate drop rapidly and they stop excreting urine and faeces. When the bears emerge from their dens they might be a bit groggy, but their muscles are still largely intact. ‘If a human patient was bedridden for four and a half months, you would lose something like 80 per cent of your muscle mass,’ says Gotthardt. ‘But in the grizzly bear, it’s maybe 20 per cent. If you could learn from the grizzly how it does that, it would be really helpful.’

Gotthardt and his team have been trying to learn just that. The idea is that if humans could mimic grizzlies, serious issues of muscle atrophy in patients suffering from illness or recovering from accidents could potentially be avoided. The team examined muscle samples from grizzly bears, which they had received from Washington State University. They approached the tissue in two ways, firstly looking at the bears’ metabolic pathways while hibernating. These studies revealed that grizzlies can generate non-essential amino acids (NEAAs) without needing to break down their existing muscles. Humans don’t have this ability, but if muscle cells could be induced to produce NEAAs it could stimulate cell growth and reverse atrophy.

The team then looked at the bears' genes and compared them to those found in atrophied mice (such as those with limbs in a plaster cast) and bed-ridden patients. They wanted to work out which genes increase in sensitivity and activity and which shut down during hibernation, and how these compare to the genes of animals that don’t hibernate. There were a whole series of relevant genes but the team was able to narrow down the pool to a small handful of possible candidates which could be a starting point for muscle atrophy therapy.

There’s still a long road ahead, but with the research ongoing there might come a day when learning from bears provides humans with relief. ‘The next step is to see if we can convince human muscles to produce the amino acids that they need on site,’ explains Gotthardt. ‘Or alternatively, to see if one of the genes that we have identified as a potential target is non-essential, so that if we want to interfere with its function, we don’t cause a lot of side effects.’