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Aerobic exercise modulates intracortical inhibition and facilitation in a nonexercised upper limb muscle.

ABSTRACT: BACKGROUND:Despite growing interest in the relationship between exercise and short-term neural plasticity, the effects of exercise on motor cortical (M1) excitability are not well studied. Acute, lower-limb aerobic exercise may potentially modulate M1 excitability in working muscles, but the effects on muscles not involved in the exercise are unknown. Here we examined the excitability changes in an upper limb muscle representation following a single session of lower body aerobic exercise. Investigating the response to exercise in a non-exercised muscle may help to determine the clinical usefulness of lower-body exercise interventions for upper limb neurorehabilitation. METHODS:In this study, transcranial magnetic stimulation was used to assess input-output curves, short-interval intracortical inhibition (SICI), long-interval intracortical inhibition (LICI) and intracortical facilitation (ICF) in the extensor carpi radialis muscle in twelve healthy individuals following a single session of moderate stationary biking. Additionally, we examined whether the presence of a common polymorphism of the brain-derived neurotrophic factor (BDNF) gene would affect the response of these measures to exercise. RESULTS:We observed significant increases in ICF and decreases in SICI following exercise. No changes in LICI were detected, and no differences were observed in input-output curves following exercise, or between BDNF groups. CONCLUSIONS:The current results demonstrate that the modulation of intracortical excitability following aerobic exercise is not limited to those muscles involved in the exercise, and that while exercise does not directly modulate the excitability of motor neurons, it may facilitate the induction of experience-dependent plasticity via a decrease in intracortical inhibition and increase in intracortical facilitation. These findings indicate that exercise may create favourable conditions for adaptive plasticity in M1 and may be an effective adjunct to traditional training or rehabilitation methods.

SUBMITTER: Singh AM

PROVIDER: S-EPMC4100033 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Aerobic exercise modulates intracortical inhibition and facilitation in a nonexercised upper limb muscle.

Singh Amaya M AM Duncan Robin E RE Neva Jason L JL Staines W Richard WR

BMC sports science, medicine & rehabilitation 20140621

<h4>Background</h4>Despite growing interest in the relationship between exercise and short-term neural plasticity, the effects of exercise on motor cortical (M1) excitability are not well studied. Acute, lower-limb aerobic exercise may potentially modulate M1 excitability in working muscles, but the effects on muscles not involved in the exercise are unknown. Here we examined the excitability changes in an upper limb muscle representation following a single session of lower body aerobic exercise ...[more]

PMID: 25031838

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Project description:The molecular mechanisms underlying skeletal muscle mitochondrial adaptations induced by aerobic exercise (AE) are not fully understood. We have previously shown that AE induces mitochondrial adaptations in cardiac muscle, mediated by sympathetic stimulation. Since direct sympathetic innervation of neuromuscular junctions influences skeletal muscle homeostasis, we tested the hypothesis that ?2-adrenergic receptor (?2-AR)-mediated sympathetic activation induces mitochondrial adaptations to AE in skeletal muscle. Male FVB mice were subjected to a single bout of AE on a treadmill (80% Vmax, 60 min) under ?2-AR blockade with ICI 118,551 (ICI) or vehicle, and parameters of mitochondrial function and morphology/dynamics were evaluated. An acute bout of AE significantly increased maximal mitochondrial respiration in tibialis anterior (TA) isolated fiber bundles, which was prevented by ?2-AR blockade. This increased mitochondrial function after AE was accompanied by a change in mitochondrial morphology towards fusion, associated with increased Mfn1 protein expression and activity. ?2-AR blockade fully prevented the increase in Mfn1 activity and reduced mitochondrial elongation. To determine the mechanisms involved in mitochondrial modulation by ?2-AR activation in skeletal muscle during AE, we used C2C12 myotubes, treated with the non-selective ?-AR agonist isoproterenol (ISO) in the presence of the specific ?2-AR antagonist ICI or during protein kinase A (PKA) and G?i protein blockade. Our in vitro data show that ?-AR activation significantly increases mitochondrial respiration in myotubes, and this response was dependent on ?2-AR activation through a G?s-PKA signaling cascade. In conclusion, we provide evidence for AE-induced ?2-AR activation as a major mechanism leading to alterations in mitochondria function and morphology/dynamics. ?2-AR signaling is thus a key-signaling pathway that contributes to skeletal muscle plasticity in response to exercise.

Dataset Information

Aerobic exercise modulates intracortical inhibition and facilitation in a nonexercised upper limb muscle.

Publications

Aerobic exercise modulates intracortical inhibition and facilitation in a nonexercised upper limb muscle.

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