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Promoting Motor Cortical Plasticity with Acute Aerobic Exercise: A Role for Cerebellar Circuits.

Mang CS, Brown KE, Neva JL, Snow NJ, Campbell KL, Boyd LA - Neural Plast. (2016)

Bottom Line: Here, we investigated the effect of acute aerobic exercise on cerebellar circuits, and their potential contribution to altered M1 plasticity in healthy individuals (age: 24.8 ± 4.1 years).In Experiment   1, acute aerobic exercise reduced cerebellar inhibition (CBI) (n = 10, p = 0.01), elicited by dual-coil paired-pulse transcranial magnetic stimulation.Thus, the results of these planned comparisons indirectly provide modest evidence that modulation of cerebellar circuits may contribute to exercise-induced increases in M1 plasticity.

View Article: PubMed Central - PubMed

Affiliation: Graduate Program in Rehabilitation Sciences, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3.

ABSTRACT
Acute aerobic exercise facilitated long-term potentiation-like plasticity in the human primary motor cortex (M1). Here, we investigated the effect of acute aerobic exercise on cerebellar circuits, and their potential contribution to altered M1 plasticity in healthy individuals (age: 24.8 ± 4.1 years). In Experiment   1, acute aerobic exercise reduced cerebellar inhibition (CBI) (n = 10, p = 0.01), elicited by dual-coil paired-pulse transcranial magnetic stimulation. In Experiment   2, we evaluated the facilitatory effects of aerobic exercise on responses to paired associative stimulation, delivered with a 25 ms (PAS25) or 21 ms (PAS21) interstimulus interval (n = 16 per group). Increased M1 excitability evoked by PAS25, but not PAS21, relies on trans-cerebellar sensory pathways. The magnitude of the aerobic exercise effect on PAS response was not significantly different between PAS protocols (interaction effect: p = 0.30); however, planned comparisons indicated that, relative to a period of rest, acute aerobic exercise enhanced the excitatory response to PAS25 (p = 0.02), but not PAS21 (p = 0.30). Thus, the results of these planned comparisons indirectly provide modest evidence that modulation of cerebellar circuits may contribute to exercise-induced increases in M1 plasticity. The findings have implications for developing aerobic exercise strategies to "prime" M1 plasticity for enhanced motor skill learning in applied settings.

No MeSH data available.


Related in: MedlinePlus

CBI ratios averaged across the group. A value of 1.0 on the y-axis (depicted by dashed line) indicates the amplitude of the TS alone. Asterisks indicate statistical significance (p < 0.05). Error bars represent one standard deviation. CBI: cerebellar inhibition.
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fig3: CBI ratios averaged across the group. A value of 1.0 on the y-axis (depicted by dashed line) indicates the amplitude of the TS alone. Asterisks indicate statistical significance (p < 0.05). Error bars represent one standard deviation. CBI: cerebellar inhibition.

Mentions: TS amplitude during CBI collection did not change across experimental time points (F(2,18) = 1.07, p = 0.37, baseline: 0.99 ± 0.51 mV, before: 1.22 ± 0.50 mV, and after: 1.12 ± 0.55 mV). Figure 2 shows mean MEP waveforms collected for CBI in a single participant at each time point. Figure 3 depicts the CBI ratios averaged across the group at each time point. The one-way RM-ANOVA conducted on CBI ratio detected a significant main effect of time (F(2,18) = 6.11, p = 0.01). Post hoc analyses indicated that CBI ratio was significantly higher following aerobic exercise compared to the baseline (p = 0.01) and preexercise time points (p = 0.04). In contrast, CBI ratio did not change from before to after the period of seated rest (baseline to before exercise, p = 0.84).


Promoting Motor Cortical Plasticity with Acute Aerobic Exercise: A Role for Cerebellar Circuits.

Mang CS, Brown KE, Neva JL, Snow NJ, Campbell KL, Boyd LA - Neural Plast. (2016)

CBI ratios averaged across the group. A value of 1.0 on the y-axis (depicted by dashed line) indicates the amplitude of the TS alone. Asterisks indicate statistical significance (p < 0.05). Error bars represent one standard deviation. CBI: cerebellar inhibition.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4834415&req=5

fig3: CBI ratios averaged across the group. A value of 1.0 on the y-axis (depicted by dashed line) indicates the amplitude of the TS alone. Asterisks indicate statistical significance (p < 0.05). Error bars represent one standard deviation. CBI: cerebellar inhibition.
Mentions: TS amplitude during CBI collection did not change across experimental time points (F(2,18) = 1.07, p = 0.37, baseline: 0.99 ± 0.51 mV, before: 1.22 ± 0.50 mV, and after: 1.12 ± 0.55 mV). Figure 2 shows mean MEP waveforms collected for CBI in a single participant at each time point. Figure 3 depicts the CBI ratios averaged across the group at each time point. The one-way RM-ANOVA conducted on CBI ratio detected a significant main effect of time (F(2,18) = 6.11, p = 0.01). Post hoc analyses indicated that CBI ratio was significantly higher following aerobic exercise compared to the baseline (p = 0.01) and preexercise time points (p = 0.04). In contrast, CBI ratio did not change from before to after the period of seated rest (baseline to before exercise, p = 0.84).

Bottom Line: Here, we investigated the effect of acute aerobic exercise on cerebellar circuits, and their potential contribution to altered M1 plasticity in healthy individuals (age: 24.8 ± 4.1 years).In Experiment   1, acute aerobic exercise reduced cerebellar inhibition (CBI) (n = 10, p = 0.01), elicited by dual-coil paired-pulse transcranial magnetic stimulation.Thus, the results of these planned comparisons indirectly provide modest evidence that modulation of cerebellar circuits may contribute to exercise-induced increases in M1 plasticity.

View Article: PubMed Central - PubMed

Affiliation: Graduate Program in Rehabilitation Sciences, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3.

ABSTRACT
Acute aerobic exercise facilitated long-term potentiation-like plasticity in the human primary motor cortex (M1). Here, we investigated the effect of acute aerobic exercise on cerebellar circuits, and their potential contribution to altered M1 plasticity in healthy individuals (age: 24.8 ± 4.1 years). In Experiment   1, acute aerobic exercise reduced cerebellar inhibition (CBI) (n = 10, p = 0.01), elicited by dual-coil paired-pulse transcranial magnetic stimulation. In Experiment   2, we evaluated the facilitatory effects of aerobic exercise on responses to paired associative stimulation, delivered with a 25 ms (PAS25) or 21 ms (PAS21) interstimulus interval (n = 16 per group). Increased M1 excitability evoked by PAS25, but not PAS21, relies on trans-cerebellar sensory pathways. The magnitude of the aerobic exercise effect on PAS response was not significantly different between PAS protocols (interaction effect: p = 0.30); however, planned comparisons indicated that, relative to a period of rest, acute aerobic exercise enhanced the excitatory response to PAS25 (p = 0.02), but not PAS21 (p = 0.30). Thus, the results of these planned comparisons indirectly provide modest evidence that modulation of cerebellar circuits may contribute to exercise-induced increases in M1 plasticity. The findings have implications for developing aerobic exercise strategies to "prime" M1 plasticity for enhanced motor skill learning in applied settings.

No MeSH data available.


Related in: MedlinePlus