Comparison of single bout effects of bicycle training versus locomotor training on paired reflex depression of the soleus H-reflex after motor incomplete spinal cord injury.
ABSTRACT To examine paired reflex depression changes post 20-minute bout each of 2 training environments: stationary bicycle ergometer training (bicycle training) and treadmill with body weight support and manual assistance (locomotor training).
Motor incomplete SCI (n=12; mean, 44+/-16y); noninjured subjects (n=11; mean, 30.8+/-8.3y).
All subjects received each type of training on 2 separate days.
Paired reflex depression at different interstimulus intervals (10 s, 1 s, 500 ms, 200 ms, and 100 ms) was measured before and after both types of training.
(1) Depression was significantly less post-SCI compared with noninjured subjects at all interstimulus intervals and (2) post-SCI at 100-millisecond interstimulus interval: reflex depression significantly increased postbicycle training in all SCI subjects and in the chronic and spastic subgroups (P<.05).
Phase-dependent regulation of reflex excitability, essential to normal locomotion, coordinated by pre- and postsynaptic inhibitory processes (convergent action of descending and segmental inputs onto spinal circuits) is impaired post-SCI. Paired reflex depression provides a quantitative assay of inhibitory processes contributing to phase-dependent changes in reflex excitability. Because bicycle training normalized reflex depression, we propose that bicycling may have a potential role in walking rehabilitation, and future studies should examine the long-term effects on subclinical measures of reflex activity and its relationship to functional outcomes.
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ABSTRACT: Physical exercise promotes neural plasticity in the brain of healthy subjects and modulates pathophysiological neural plasticity after sensorimotor loss, but the mechanisms of this action are not fully understood. After spinal cord injury, cortical reorganization can be maximized by exercising the non-affected body or the residual functions of the affected body. However, exercise per se also produces systemic changes - such as increased cardiovascular fitness, improved circulation and neuroendocrine changes - that have a great impact on brain function and plasticity. It is therefore possible that passive exercise therapies typically applied below the level of the lesion in patients with spinal cord injury could put the brain in a more plastic state and promote cortical reorganization. To directly test this hypothesis, we applied passive hindlimb bike exercise after complete thoracic transection of the spinal cord in adult rats. Using western blot analysis, we found that the level of proteins associated with plasticity - specifically ADCY1 and BDNF - increased in the somatosensory cortex of transected animals that received passive bike exercise compared to transected animals that received sham exercise. Using electrophysiological techniques, we then verified that neurons in the deafferented hindlimb cortex increased their responsiveness to tactile stimuli delivered to the forelimb in transected animals that received passive bike exercise compared to transected animals that received sham exercise. Passive exercise below the level of the lesion, therefore, promotes cortical reorganization after spinal cord injury, uncovering a brain-body interaction that does not rely on intact sensorimotor pathways connecting the exercised body parts and the brain.PLoS ONE 01/2013; 8(1):e54350. · 3.53 Impact Factor
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ABSTRACT: Postactivation depression is decreased in patients with spasticity and partially restored by physical exercise in spinal cord injured patients. Up until now, the possibility to modulate postactivation depression with motor training has never been explored in subjects with spasticity following brain lesions. Postactivation depression, assessed as frequency related depression of soleus H-reflex, was investigated before and after robotic-assisted gait training in a group of seven subjects with spastic hemiparesis following hemispheric stroke. Patients received three sessions per week of robotic-assisted gait training for a period of 4 weeks (12 sessions in total). Postactivation depression was measured before the treatment (T0), after the first session (T1) and after the last session (T2). Postactivation depression was quantified as the ratio between H-reflex amplitude at 1Hz and at 0.1Hz. The greater the 1Hz/0.1Hz ratio, the smaller the postactivation depression. Following robotic-assisted gait training, the 1Hz/0.1Hz ratio decreased from 0.79±0.26 at T0 to 0.56±0.18 at T1 and 0.58±0.13 at T2. Post hoc analysis showed a significant difference between T0 and T1 and between T0 and T2, stating an increase of postactivation depression. No significant differences were found between T1 and T2. This study provides the first demonstration that physical exercise can determine a partial normalization of postactivation depression in hemiparetic patients with spasticity following unilateral hemispheric stroke.Gait & posture 04/2013; · 2.58 Impact Factor
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ABSTRACT: We examined gene expression in the lumbar spinal cord and the specific response of motoneurons, intermediate gray and proprioceptive sensory neurons after spinal cord injury and exercise of hindlimbs to identify potential molecular processes involved in activity dependent plasticity. Adult female rats received a low thoracic transection and passive cycling exercise for 1 or 4weeks. Gene expression analysis focused on the neurotrophic factors: brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), and their receptors because of their potential roles in neural plasticity. We also examined expression of genes involved in the cellular response to injury: heat shock proteins (HSP) -27 and -70, glial fibrillary acidic protein (GFAP) and caspases -3, -7, and -9. In lumbar cord samples, injury increased the expression of mRNA for TrkB, all three caspases and the HSPs. Acute and prolonged exercise increased expression of mRNA for the neurotrophic factors BDNF and GDNF, but not their receptors. It also increased HSP expression and decreased caspase-7 expression, with changes in protein levels complimentary to these changes in mRNA expression. Motoneurons and intermediate gray displayed little change in mRNA expression following injury, but acute and prolonged exercise increased levels of mRNA for BDNF, GDNF and NT-4. In large DRG neurons, mRNA for neurotrophic factors and their receptors were largely unaffected by either injury or exercise. However, caspase mRNA expression was increased by injury and decreased by exercise. Our results demonstrate that exercise affects expression of genes involved in plasticity and apoptosis in a cell specific manner and that these change with increased post-injury intervals and/or prolonged periods of exercise.Brain research 02/2012; 1438:8-21. · 2.46 Impact Factor