Introduction: The neurophysiological effects after acute endurance or aerobic exercise
(AE) has emerging evidence that has shown some trends but it is somewhat conflicting.
The combined directional findings of post-AE changes in measurements using
transcranial magnetic stimulation (TMS) can provide insight into exercise fatigue and
neuroplasticity modeling as it relates to the fields of motor learning, motor control,
psychological disorders, and neurological disorders. This meta-analysis was written
with a focus on TMS measurements of inhibitory cortical neural networks: long-interval cortical inhibition (LICI), short-interval cortical inhibition (SICI), cortical silent period (CSP), long-latency afferent inhibition (LAI), short-latency afferent inhibition (SAI), interhemispheric inhibition (IHI), cerebellar brain inhibition (CBI). Changes in these measures are associated with GABA-mediated inhibition, neurodegenerative disorders, motor learning, and many other physiological and behavioral outcomes.
Purpose: This study was conducted with the goal of evaluating the changes in neuro-
inhibitory measurements resulting from AE exposure in humans. Additionally, exercise intensity and post-exercise test timing were evaluated as covariates influencing neuro-
inhibitory changes post-AE.
Methods: The PRISMA guidelines were followed for this thesis. Subgroup divisions for the meta-analysis was carefully considered based on previous findings reported in the literature and preliminary correlation analysis. Mean difference (MD) was used to estimate effect size for each study, and Chi2, Z, I2 values were evaluated to determine between group difference, within group difference, and heterogeneity,
Results: The studies found to meet inclusion criteria included: six studies evaluating
LICI, 10 studies evaluating SICI, 11 studies evaluating CSP. LAI, SAI, IHI, and CBI
did not have sufficient evidence to conduct a meta-analysis. All analyses were performed with small number of available studies and small total sample sizes.
However, there was significant evidence supporting an overall disinhibition after AE
exposure when measured using LICI (MD = 8.5%, 95% confidence interval [CI] = 0.5,
16.5; Z = 2.08, p = .04) and SICI (MD = 8.0%, 95% CI = 3.2, 12.8; Z = 3.27, p = .001). CSP was observed to have similar post-AE trends as LICI and SICI, but did not reach significance (MD = 7.3 ms, 95% CI = -0.2, 14.8; Z = 1.90, p = .06). These findings were largely driven by studies evaluating vigorous and moderate intensity exercise, not those evaluating light intensity exercise.
Conclusions: GABAA- and GABAB-mediated inhibitory neural networks are altered (disinhibited) as a result of AE exercise. Although inconclusive at this time, it is possible that differences in exercise intensity prescription may result in differential changes in neuro-inhibitory measurements. Although differences in TMS methods, post-exercise test timing, and other variables were not the primary focus of the presented analysis, they may also be important in understanding the post-AE variance in TMS measurements. Future research should focus on performing randomized control trials (RCTs), establishing valid and consistent TMS methods, and evaluating the interaction between exercise intensity and post-AE test timing.