Ten-year resistance training background modulates somatosensory P3 cognitive brain resonse in older men: A...

The brain electrophysiological component P3, associated with good cognitive abilities, deteriorates during healthy aging. Both cognitive functions and P3 component amplitude respond positively to exercise, but the effects of resistance training on P3 are much less studied. Short-term resistance training interventions in older adults indicate modulation towards larger P3 amplitude, but this association has not been studied with a longitudinal study design. We investigated magnetoencephalographically recorded P3 (P3m) in a unique study design of nine aged men (mean age 77.7 y) with quasi-supervised resistance training background over a 10-year period and eight controls of similar age (mean age 77.5 y) with no training background. We elicited P3m utilizing lower limb electrical stimulation, as the resistance training program was mostly directed to lower limbs. Somatosensory oddball paradigm was performed with the right foot's fourth toe as standard (90%) and hallux as deviant (10%). Participants were asked to respond to deviants with a button press using their left index finger. Topographic maps showed bilateral temporoparietal activation for P3m in both groups. No amplitude differences were found in active P3m regions between groups. However, the groups differed in hemispheric activity of P3m. The exercise group showed stronger activation in the right frontotemporal and parietal sensor-groups compared to the left sensor-groups, and the control group showed stronger activation in right frontotemporal sensor-group compared to left. The control group showed shorter P3m latency in the right temporal sensor-group than the exercise group, but the latencies in other sensor-groups were similar. In aging, the brain utilizes compensatory areas to perform cognitive tasks. Our results suggest modulation in topographic distribution of P3m activity in aging men with long-term resistance training background compared to their controls. This might arise from a difference in age-related compensatory mechanisms in P3m generation.