Abstract

Corticospinal excitability, and particularly the balance between cortical inhibitory and excitatory processes (assessed in a muscle using single and paired-pulse transcranial magnetic stimulation), are affected by neurodegenerative pathologies or following a stroke. This review describes how locomotor exercises may counterbalance these neuroplastic alterations, either when performed under its conventional form (e.g., walking or cycling) or when comprising eccentric (i.e., active lengthening) muscle contractions. Non-fatiguing conventional locomotor exercise decreases intracortical inhibition and/or increases intracortical facilitation. These modifications notably seem to be a consequence of neurotrophic factors (e.g., brain-derived neurotrophic factor) resulting from the hemodynamic solicitation. Furthermore, it can be inferred from non-invasive brain and peripheral stimulation studies that repeated activation of neural networks can endogenously shape neuroplasticity. Such mechanisms could also occur following eccentric exercises (lengthening of the muscle), during which motor-related cortical potential (electroencephalography) is of greater magnitude and lasts longer than during concentric exercises (i.e., muscle shortening). As single-joint eccentric exercise decreased short- and long-interval intracortical inhibition and increased intracortical facilitation, locomotor eccentric exercise (e.g., downhill walking or eccentric cycling) may be even more potent by adding hemodynamic-related neuroplastic processes to endogenous processes. Besides, eccentric exercise is especially useful to develop relatively high force levels at low cardiorespiratory and perceived intensities, which can be a training goal alongside the induction of neuroplastic changes. Even though indirect evidence let us think that locomotor eccentric exercise could shape neuroplasticity in ways relevant to neurorehabilitation, its efficacy remains speculative. We provide future research directions on the neuroplastic effects and underlying mechanisms of locomotor exercise.

Highlights

  • During exercise, the primary motor cortex sends electrical impulses to trigger voluntary muscle contractions

  • Pathological populations may not be capable of exercising at sufficient intensities to trigger these beneficial neuroplastic modulations and an alternative method is needed. As it can be inferred from noninvasive brain and peripheral stimulation studies, a high neural activity can directly result in neuroplastic changes

  • This article provides a review of 1) the impact of conventional locomotor exercise on neuroplasticity assessed in non-exercised or exercised muscles; 2) likely underlying neuroplastic processes triggered by the hemodynamic flow; 3) insights from non-invasive brain and peripheral stimulation studies on the nervous mechanisms resulting in neuroplastic changes ; 4) eccentric exercise and locomotor tasks within this category as a way to merge neural and hemodynamic factors associated with neuroplastic changes

Read more

Summary

Introduction

The primary motor cortex sends electrical impulses to trigger voluntary muscle contractions. CS excitability, tested by transcranial magnetic stimulation (TMS) applied over the primary motor cortex, refers to “the efficacy of the corticospinal pathway to relay neural signals from higher brain areas to the muscle” [1]. [12, 13]) show changes in this balance, which could impair motor or executive functions In this context, neurorehabilitation protocols using non-invasive brain stimulation techniques such as repetitive. This article provides a review of 1) the impact of conventional locomotor exercise on neuroplasticity assessed in non-exercised or exercised muscles; 2) likely underlying neuroplastic processes triggered by the hemodynamic flow; 3) insights from non-invasive brain and peripheral stimulation studies on the nervous mechanisms resulting in neuroplastic changes ; 4) eccentric exercise and locomotor tasks within this category as a way to merge neural and hemodynamic factors associated with neuroplastic changes

Physical exercise induces neuroplasticity
Non-exercised muscles
Exercised muscles
Exercise intensity affects hemodynamic processes underlying neuroplasticity
Non-invasive stimulation studies hint at neural mechanisms of neuroplasticity
Conclusion
Funding source
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call