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.
Full-textDOI: · Available from: Chetan P Phadke, Mar 12, 2015
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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. DOI:10.1016/j.brainres.2011.12.015 · 2.83 Impact Factor
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ABSTRACT: Activity-based therapies such as passive bicycling and step-training on a treadmill contribute to motor recovery after spinal cord injury (SCI), leading to a greater number of steps performed, improved gait kinematics, recovery of phase-dependent modulation of spinal reflexes, and prevention of decrease in muscle mass. Both tasks consist of alternating movements that rhythmically stretch and shorten hindlimb muscles. However, the paralyzed hindlimbs are passively moved by a motorized apparatus during bike-training, whereas locomotor movements during step-training are generated by spinal networks triggered by afferent feedback. Our objective was to compare the task-dependent effect of bike- and step-training after SCI on physiological measures of spinal cord plasticity in relation to changes in levels of neurotrophic factors. Thirty adult female Sprague-Dawley rats underwent complete spinal transection at a low thoracic level (T12). The rats were assigned to one of three groups: bike-training, step-training, or no training. The exercise regimen consisted of 15 min/d, 5 days/week, for 4 weeks, beginning 5 days after SCI. During a terminal experiment, H-reflexes were recorded from interosseus foot muscles following stimulation of the tibial nerve at 0.3, 5, or 10 Hz. The animals were sacrificed and the spinal cords were harvested for Western blot analysis of the expression of neurotrophic factors in the lumbar spinal cord. We provide evidence that bike- and step-training significantly increase the levels of brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and NT-4 in the lumbar enlargement of SCI rats, whereas only step-training increased glial cell-derived neurotrophic factor (GDNF) levels. An increase in neurotrophic factor protein levels that positively correlated with the recovery of H-reflex frequency-dependent depression suggests a role for neurotrophic factors in reflex normalization.Journal of neurotrauma 11/2010; 28(2):299-309. DOI:10.1089/neu.2010.1594 · 3.97 Impact Factor
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ABSTRACT: Spasticity is evident in both humans and animals following spinal cord injury (SCI) and can contribute to significant functional limitation and disruption in quality of life of patients with this disorder. This mini-review describes a number of preclinical and clinical studies that promise to improve outcomes for, especially in terms of spasticity and hyper-reflexia, patients with SCI. A gold standard for the quantification of spasticity has proved elusive, but the combination of H-reflex frequency dependent depression and a novel stretch reflex (SR) windup protocol have the potential to provide new insights. As the pathophysiology of hyper-reflexia and spasticity continue to be investigated, the documented onset in the animal model of SCI provides critical time points for further study into these complex mechanisms. The positive effects of a passive exercise protocol and several potential pharmacological interventions are reviewed as well as a novel potential mechanism of action. Further work is needed to determine additional mechanisms that are involved in SCI, and how to optimize multiple therapies to overcome some of the deficits induced by SCI.06/2010; 1(2):160-169. DOI:10.2478/v10134-010-0021-z