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      Neurophysiological responses and adaptation following repeated bouts of maximal lengthening contractions in young and older adults

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          Abstract

          A bout of maximal lengthening contractions is known to produce muscle damage, but confers protection against subsequent damaging bouts, with both tending to be lower in older adults. Neural factors contribute to this adaptation, but the role of the corticospinal pathway remains unclear. Twelve young (27 ± 5 yr) and 11 older adults (66 ± 4 yr) performed two bouts of 60 maximal lengthening dorsiflexions 2 weeks apart. Neuromuscular responses were measured preexercise, immediately postexercise, and at 24 and 72 h following both bouts. The initial bout resulted in prolonged reductions in maximal voluntary torque (MVC; immediately postexercise onward, P < 0.001) and increased creatine kinase (from 24 h onward, P = 0.001), with both responses being attenuated following the second bout ( P < 0.015), demonstrating adaptation. Smaller reductions in MVC following both bouts occurred in older adults ( P = 0.005). Intracortical facilitation showed no changes ( P ≥ 0.245). Motor-evoked potentials increased 24 and 72 h postexercise in young ( P ≤ 0.038). Torque variability ( P ≤ 0.041) and H-reflex size ( P = 0.024) increased, while short-interval intracortical inhibition (SICI; P = 0.019) and the silent period duration (SP) decreased ( P = 0.001) in both groups immediately postexercise. The SP decrease was smaller following the second bout ( P = 0.021), and there was an association between the change in SICI and reduction in MVC 24 h postexercise in young adults ( R = −0.47, P = 0.036). Changes in neurophysiological responses were mostly limited to immediately postexercise, suggesting a modest role in adaptation. In young adults, neural inhibitory changes are linked to the extent of MVC reduction, possibly mediated by the muscle damage–related afferent feedback. Older adults incurred less muscle damage, which has implications for exercise prescription.

          NEW & NOTEWORTHY This is the first study to have collectively assessed the role of corticospinal, spinal, and intracortical activity in muscle damage attenuation following repeated bouts of exercise in young and older adults. Lower levels of muscle damage in older adults are not related to their neurophysiological responses. Neural inhibition transiently changed, which might be related to the extent of muscle damage; however, the role of processes along the corticospinal pathway in the adaptive response is limited.

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          Most cited references73

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          The Role of GABA in Human Motor Learning

          Results There is considerable variability in motor learning behavior across individuals [7], and the present study aimed to test whether some of this variability could be explained by variation in responsiveness of the GABA system, because GABA modulation plays an important role in learning [1–4]. As a measure of GABA responsiveness, we used magnetic resonance spectroscopy (MRS) to quantify changes in GABA concentration following anodal transcranial direct current stimulation (tDCS), a noninvasive technique that decreases GABA within the motor cortex [5], increases cortical excitability [8], and enhances short-term learning [9]. We predicted that individuals who show less tDCS-mediated GABA modulation would show less behavioral evidence of motor learning and less modulation of fMRI responses during learning. Subjects participated in three experimental sessions on different days. The first two sessions were MRS sessions, during which GABA-edited spectra were acquired before and after 10 min of tDCS. In the third session, subjects performed an explicit sequence learning task during fMRI, and no tDCS was applied. Motor Behavior Motor learning was assessed via change in reaction times to a visually cued explicit sequence learning task performed with the four fingers of the right hand during fMRI acquisition in session 3. All subjects showed a significant reduction in reaction times across successive learning blocks (Figure 1A; repeated-measures analysis of variance, main effect of BLOCK F(15,150) = 19.95; p  2.0 and a (corrected) cluster significance threshold of p = 0.01.
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            Neuroplasticity in the context of motor rehabilitation after stroke.

            Approximately one-third of patients with stroke exhibit persistent disability after the initial cerebrovascular episode, with motor impairments accounting for most poststroke disability. Exercise and training have long been used to restore motor function after stroke. Better training strategies and therapies to enhance the effects of these rehabilitative protocols are currently being developed for poststroke disability. The advancement of our understanding of the neuroplastic changes associated with poststroke motor impairment and the innate mechanisms of repair is crucial to this endeavor. Pharmaceutical, biological and electrophysiological treatments that augment neuroplasticity are being explored to further extend the boundaries of poststroke rehabilitation. Potential motor rehabilitation therapies, such as stem cell therapy, exogenous tissue engineering and brain-computer interface technologies, could be integral in helping patients with stroke regain motor control. As the methods for providing motor rehabilitation change, the primary goals of poststroke rehabilitation will be driven by the activity and quality of life needs of individual patients. This Review aims to provide a focused overview of neuroplasticity associated with poststroke motor impairment, and the latest experimental interventions being developed to manipulate neuroplasticity to enhance motor rehabilitation.
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              The role of GABA(B) receptors in intracortical inhibition in the human motor cortex.

              While GABA(B) receptors are thought to have an important role in mediating long interval intracortical inhibition (LICI) in the human motor cortex, the effect of a selective GABA(B) receptor agonist on this measure has not been directly tested. Nine healthy volunteers ingested either 50 mg baclofen (BAC) or placebo (PBO) in a randomized, double blind crossover design, with the second session one week later. We used transcranial magnetic stimulation to assess motor threshold, motor evoked potential (MEP) amplitude, cortical silent period (CSP) duration, short interval intracortical inhibition (SICI) and LICI before and 90 min following drug intake. There was no specific effect of drug on motor threshold, MEP amplitude or CSP duration. BAC resulted in a significant increase in LICI (P=0.002) and a significant decrease in SICI (P=0.046) while PBO had no effect. Our findings demonstrate that the enhanced GABA(B) receptor activation results in differential effects on these two measures of intracortical inhibition in the human motor cortex. The increase in LICI is likely to be a result of increased GABA(B) receptor mediated inhibitory post-synaptic potentials, while the reduction in SICI may relate to the activation of pre-synaptic GABA(B) receptors reducing GABA release.
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                Author and article information

                Journal
                Journal of Applied Physiology
                Journal of Applied Physiology
                American Physiological Society
                8750-7587
                1522-1601
                November 01 2019
                November 01 2019
                : 127
                : 5
                : 1224-1237
                Affiliations
                [1 ]Faculty of Health and Life Sciences, Northumbria University, Newcastle Upon Tyne, England, United Kingdom
                [2 ]Water Research Group, School of Environmental Sciences and Development, Northwest University, Potchefstroom, South Africa
                Article
                10.1152/japplphysiol.00494.2019
                31513444
                573e880e-4ecb-4c57-aa9c-8e35053d655d
                © 2019
                History

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