Neural Control of Movement with Aging and Effects of Activity

Aging is associated with reduced neuromuscular function, which may be due to central nervous system changes in corticospinal excitability and a reduced capacity of the human brain to re-organize the strength of its connections (neuroplasticity). PURPOSE: This symposium presentation will highlight two complementary studies that determined the influence of aging and physical activity (PA) on motor cortical excitability and neuroplasticity, elicited with Transcranial Magnetic Stimulation (TMS). METHODS: In study one, corticospinal excitability was assessed in 28 young (22.4 ± 2.2 yr; 14 women) and 50 old adults (70.2 ± 6.1 yr; 22 women) by measuring motor evoked potentials (MEPs) elicited in motor cortical areas and targeting the vastus lateralis (VL) muscle of the quadriceps. In the second study, the response to a continuous theta burst stimulation paradigm (cTBS) was assessed in 27 old adults (66.5 ± 4.5, 13 women) by measuring MEPs in the first dorsal interosseous (FDI) muscle elicited after a single and paired cTBS paradigm- targeting the primary motor cortex. PA was measured in both studies using accelerometry (Actigraph GT-3x or GENEActiv, respectively). RESULTS: In study 1, irrespective of age and sex, individuals who achieved >10,000 steps/day had reduced corticospinal excitability of the VL muscles (F[1.61, 85.6] = 3.49, p = 0.04). In study 2, when accounting for age and sex, more time engaging in PA was associated with a greater neuroplasticity response to the cTBS paradigm (r=-0.51, p=0.007). CONCLUSION: These studies provide evidence that PA in both young and old adults is associated with lower corticospinal excitability in the lower limb and an enhanced capacity of the motor cortex to re-organize the strength of its connections. Together these results suggest regular PA may protect against age-related movement decline through preservation of the inhibitory and excitatory networks within the primary motor cortex, resulting in maintenance of an optimal environment for neuroplasticity. Supported by NHMRC-ARC Dementia Research development fellowship awarded to Dr Ashleigh Smith (GNT 1097397) and NIH Grant R0I awarded to Dr Sandra K. Hunter.