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

Department of Physical Therapy, University of Florida, Gainesville, FL, USA.
Archives of physical medicine and rehabilitation (Impact Factor: 2.57). 08/2009; 90(7):1218-28. DOI: 10.1016/j.apmr.2009.01.022
Source: PubMed


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).
Pretest-posttest repeated-measures.
Locomotor laboratory.
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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Available from: Chetan P Phadke, Mar 12, 2015
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    • "A possible intriguing way to generically promote cortical plasticity is indirectly suggested by exercise therapies employed after spinal cord injury, which are often applied to the affected body in order to improve functions below the level of the lesion [30]. For example, passive exercise of the lower limbs after spinal cord injury has been shown to reduce spasticity [31], [32], [33], [34], reduce the rate of bone density loss [35], [36] and reduce lower limb blood pooling [37]. Interestingly, passive exercise also produces the systemic effects that are typical of exercise per se, such as increases in cardiovascular fitness [38], improved circulation [39] and neuroendocrine changes [40]. "
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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.
    Full-text · Article · Jan 2013 · PLoS ONE
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    • "Natural recovery mechanisms alone, such as sprouting, gliogenesis and synaptic reorganization are unable to overcome obstacles to regeneration, but treatment with rhythmic patterned activity or exercise (Ex), can enhance some recovery of function (de Leon et al., 1998; Lovely et al., 1986). Activity-dependent plasticity has been observed in animal models of SCI (Beaumont et al., 2004; De Leon et al., 1999; Sandrow-Feinberg et al., 2009) as well as in human studies (Astorino et al., 2008; Phadke et al., 2009). Indeed, beneficial aspects of exercise likely stem from its ability to stimulate spinal circuits (Edgerton and Roy, 2009; Ollivier-Lanvin et al., 2010) and to increase local levels of trophic factors (Gomez-Pinilla et al., 2001; Gomez-Pinilla et al., 2002; Sandrow-Feinberg et al., 2009; Côté et al., 2011). "
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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.
    Full-text · Article · Feb 2012 · Brain research
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    • "PICs are thought to be involved in the development of spasticity after SCI. Interestingly, the recovery of the H-reflex depression is associated with a decrease in spasticity (Kiser et al., 2005; Phadke et al., 2009). "
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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.
    Full-text · Article · Nov 2010 · Journal of neurotrauma
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