In brief:

• Researchers attempted to identify changes in the brain among cognitively healthy adults 65 and older who engaged in a 12-week aerobic exercise program
• 53 participants were divided into exercise and non-exercise groups; chemical markers, proteins, cognitive function, and gray matter were evaluated at baseline and after 12 weeks
• At the end of the 12 weeks, the only measurable difference between the groups was related to levels of total choline (tCho), a chemical associated with membrane degeneration and inflammation—exercise group's tCho levels remained stable while the non-exercise group's tCho levels rose
• Researchers believe tCho levels could prove to be a useful marker to measure the effects of aerobic exercise on brain function of adults who are elderly

The connection between physical activity (PA) and the slowing or prevention of cognitive decline in the elderly has been widely recognized, but an explanation of just how PA works on the brain's chemistry has been more elusive. Now researchers in Germany believe they've isolated a chemical marker that helps identify PA's neuroprotective effects.

The research project itself was fairly straightforward: split 53 cognitively healthy individuals 65 and older into 2 groups—the first of which received 3 half-hour supervised cycle training sessions per week for 12 weeks, and the second of which did not increase their PA—and then measure a host of factors associated with cognitive decline at the beginning and end of the 12-week training program. Researchers didn't limit their investigation to chemical markers but also included evaluations of gray matter volume and cognitive performance tests. Results were published in Translational Psychiatry.

At the end of the 12 weeks, only 1 major difference between the 2 groups was found: the amount of total choline (tCho) present in the brains of participants. A combination of 2 types of choline, tChol is associated with pathological membrane turnover and inflammation, and is often present along with elevated creatine levels in the brains of individuals with Alzheimer's disease and dementia. The tCho levels of individuals who participated in the exercise program remained stable, while the non-exercise group's tCho levels rose over the 12-week timeframe.

Researchers were unable to identify significant differences in any other areas, including markers associated with neuronal energy reserve or brain-derived neurotrophic factor (BNF), a protein associated with brain plasticity. The study also found no changes to gray matter volume, a change other studies have noted. Authors noted, however, that those studies tended to take place over a longer time period—measurements at 12 weeks simply may be too soon to pick up those.

As for what it is about PA that helps to tamp down the increase in tCho, researchers were unable to pin it to aerobic capacity, which did not increase significantly for the exercise group compared with the non-exercise group. Instead, they believe the effect could be due to an increase in cardiac efficiency among the exercise group.

"Changes in fitness level … were positively associated with changes in metabolite concentrations … in the training group, thus suggesting that fitness is closely linked to cerebral brain metabolism," authors write. "Overall, the currently available data indicate that aerobic training interventions with moderate intensity may improve both brain metabolism and cardiopulmonary function."

Authors acknowledge that their study is limited by its sample size and short timeframe, and call for additional studies with larger groups and longer study periods.

Still, they assert, the notable difference in tCho levels could be a window into the chemistry behind the beneficial effects of PA.

"As choline is a marker of neurodegeneration, this finding suggests a neuroprotective effect of aerobic exercise," authors write. "Overall, our findings indicate that cerebral tCho might constitute a valid marker for an effect of aerobic exercise on the brain in healthy aging."

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