As we age, bones respond worse to sport

American researchers from the University of Arkansas set out to find out why in older people even regular exercise does not have the same effect on bones. It was usually thought that the reason was the accumulation of cellular damage and disorders in the processes of self-cleaning of cells. But fresh data casts doubt on this version.

The work is based on observing how bones respond to stress. When a person moves, bones receive microscopic shocks and pressures – this triggers the process of their renewal and strengthening. However, as we age, this response wanes. To understand why this happens, the team modeled aging conditions in mice and tested how their bones respond to exercise.

The bone cells in the older mice were indeed weaker in responding to exercise. But when the scientists “aged” the cells in young animals artificially – by adding oxidative stress or disrupting their self-cleaning processes – the expected deterioration did not occur. The bones continued to respond to physical activity in almost the same way as normal. This greatly surprised the researchers.

They also found that damage to the bone sensor cell system did not prevent bones from repairing themselves. Previously, it was the destruction of the osteocyte network that was thought to be one of the key causes of age-related osteoporosis. But even when this system was damaged in some mice, bones were successfully incorporated into the repair process.

If earlier everything was written off to free radicals and weakness of cells, now it is clear – these factors are not enough to explain the decline in bone activity in the elderly.

The authors suggest that new approaches to the prevention of age-related bone fragility should take into account not only biochemistry, but also more subtle mechanisms, such as how bone cells exchange signals or redistribute energy.

Simply reducing oxidative stress or supporting cellular “housekeeping” will not have a sustained effect. More subtle methods are needed to help preserve bone mass even when normal mechanisms begin to fail.

Combating age-related bone fragility and bone density decline will require a rethinking of the very understanding of what exactly happens within bone tissue as we age. And this is a step towards new strategies for maintaining mobility and strength at any age.