What scientists are learning about oestrogen and exercise

These techniques showed, in real time, oestrogen binding to Mc4r genes in certain neurons, especially those in a part of the mouse brain involved in energy expenditure. These brain cells also shared connections with other neurons elsewhere in the brain that control the speed at which animals move. Taken together, this experiment showed oestrogen firing up a particular gene that turns on certain brain cells that then should be expected to nudge an animal to move.

But the scientists had not yet seen these genes and neurons in action, so, as a final aspect of the study, they used a sophisticated technique known as chemogenetics to directly galvanise the relevant neurons in female mice that had been bred to produce no oestrogen. Once physically sluggish, these mice now explored, stood, played and ran far more than they had before.

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Similarly, when the scientists used a form of the gene-editing technology CRISPR to gin up activity of the Mc4r gene in female animals’ brains, the mice became almost twice as active as before, a physical surge that persisted for weeks. Even male mice moved more when their Mc4r gene activity was dialled up by CRISPR, although not as much as the peripatetic females.

These results highlight the “complexity of physical activity behaviour,” Ingraham said, and how the willingness to spontaneously move — or not — for any animal probably involves an intricate interplay among genetics, endocrinology and neurology, along with conscious deliberation.

The study raises the intriguing possibility that the “timing of exercise, to have its most beneficial impact for women, might be fine-tuned by considering the changing hormonal milieu,” including the hormonal changes of menopause, said Dr. Tamas Horvath, a professor of neuroscience and obstetrics, gynaecology and reproductive sciences at the Yale School of Medicine and chair of the school’s department of comparative medicine.

“Of course, all these observations in mice need to be confirmed to operate in us, humans,” said Horvath, who was not involved in the current research. “However, the fact that this mechanism is found in an ancient part of the brain suggests that it will be applicable for most mammals, including humans.”

‘Knowledge is power’

Ingraham agreed. “We assume this circuit is working in humans, too,” she said, and, if so, the new study and any subsequent, related research could help to explain, in part, why inactivity is so common in women after menopause and also offer some potential strategies for overcoming the pull toward lassitude. Increasing oestrogen levels in older women, for instance, might, in theory, encourage more movement, although oestrogen-replacement therapy remains a complicated subject because of heightened cancer risks and other health concerns.

The study does hint, however, that it could, eventually, be possible to bypass oestrogen and re-create its effects with new therapies that would directly target the Mc4r gene or the relevant neurons in people’s brains and mimic the effects of oestrogen without the hormone itself. Any such medical advances are years in the future, Ingraham said.

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Already, though, by delving into “the interrelationship between hormones and physical activity in females, this study has significant implications for human research studying the menstrual cycle and hormonal contraceptives and also menopause,” said Paul Ansdel, a lecturer in exercise physiology at Northumbria University in England, who was not involved with the study but has extensively studied menstruation and physical performance. “We know the importance of exercising in later life for promoting and maintaining health,” he said, “so the challenge for us now is to understand the best ways to stay active throughout the major hormonal transition that is menopause.”

This article originally appeared in The New York Times.

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