Exercise slows ovarian aging via fat-tissue hormone

Ovaries age faster than most organs. As they do, the pool of primordial follicles declines. These are the dormant, immature egg cells every female is born with. Once that reserve is depleted, fertility ends. But ovarian aging also affects the brain, bones, muscles and heart through hormonal changes that extend well beyond the menopause itself.

The authors of the study, published in Nature Aging, analyzed data from more than 150,000 women. Postmenopausal women were less physically active than premenopausal women. That correlation may have multiple causes, but the researchers hypothesized that ovarian aging itself contributes to the decline.

One month on a treadmill changes the ovaries

To test the causal link, they put adult female mice through one month of treadmill training. Those mice had more primordial follicles afterward than the control group. AMH, a standard marker of ovarian reserve, was also higher, as were levels of growth factors produced by the egg cells.

The key molecule turned out to be adiponectin, a hormone made by fat tissue that improves insulin sensitivity and reduces inflammation. Adiponectin rose after training. In aging ovaries of model animals, adiponectin expression is reduced. When the researchers pharmacologically activated adiponectin receptors without exercise, that extended the reproductive span of the mice.

Beyond fertility

These are mouse data for now. Whether the findings translate directly to humans has not been demonstrated. But the link between exercise, adiponectin and ovarian health is notable from a longevity perspective, because adiponectin has previously been associated with longer lifespan in mice and with slower aging of muscle and brain. The mechanism may therefore affect multiple organ aging clocks simultaneously. Hormone therapy alleviates menopausal symptoms but does not stop ovarian aging. An intervention targeting the adiponectin system might, in principle, do so.

Read the original article