Muscle oxygenation of the paralyzed lower limb in spinal cord-injured persons.
Kawashima N, Nakazawa K, Akai M.
Department of Rehabilitation for Movement Functions, Research Institute, National Rehabilitation Center for Persons with Disabilities, Saitama, Japan. nori@rehab.go.jp
PURPOSE: Even in the paralyzed lower limb muscle, EMG activity can be induced by imposing passive leg movement in standing posture in persons with spinal cord injury (SCI). The purpose of the present study was to ascertain whether the oxygenation level of the paralyzed lower limb muscle covaried with the muscle EMG activity during imposed passive leg movement. METHODS: Six motor-complete SCI subjects and four neurologically normal controls were placed on a gait-training apparatus that enabled the SCI subjects to stand and move their legs passively. After a 1-min resting stage, consecutive passive alternate leg movements were performed at different frequencies (0.8, 1, 1.2, and 1 Hz, for 3 min at each stage). To obtain postexercise data, subjects were kept in a standing posture for 5 min after passive movement ceased. The EMG activity and concentration changes in the oxygenated (oxy-) and deoxygenated hemoglobin (Hb) (deoxy-Hb) were continuously measured using near-infrared spectroscopy (NIRS) from the gastrocnemius muscle. RESULTS: In all SCI subjects, muscle EMG activity was observed during passive leg movement. The oxy-Hb level gradually increased, whereas the deoxy-Hb decreased, and these changes were independent of the total Hb changes. In the recovery stage, the total Hb level was found to exceed the preexercise level. In contrast to the SCI patients, the normal subjects showed neither EMG activity nor changes in oxy- or deoxy-Hb. CONCLUSION: The present results demonstrate that passive leg movement can induce not only muscular activity but also alteration of muscle oxygenation level in the paralyzed lower leg. Particularly, induced muscular activity seems to correlate with increased perfusion of the muscle.

Relevance

This study shows that muscle activity and oxygenation can be increased through passive exercise while standing. Why is this important? Muscle activity is crucial for maintaining muscle mass and joint stability. Increasing the oxygen content of the muscles helps keep these tissues healthy and can decrease the incidence of pressure sores.

At Project Walk® we use passive and active movement to stimulate the nervous system. Many of our exercises are performed in a weight bearing environment. From this study we can theorize that our program also increases the muscle activity and oxygen content in the paralyzed areas of the body involved in these exercises. This is one area of our program we hope to begin research on in the near future.

Exercise-induced gene expression changes in the rat spinal cord.

Perreau VM, Adlard PA, Anderson AJ, Cotman CW.

Institute for Brain Aging and Dementia, 1113 Gillespie N.R.F., University of California Irvine, Irvine, CA 92697, USA. vperreau@uci.edu

There is growing evidence that exercise benefits recovery of neuromuscular function from spinal cord injury (SCI). However, the effect of exercise on gene expression in the spinal cord is poorly understood. We used oligonucleotide microarrays to compare thoracic and lumbar regions of spinal cord of either exercising (voluntary wheel running for 21 days) or sedentary rats. The expression data were filtered using statistical tests for significance, and K-means clustering was then used to segregate lists of significantly changed genes into sets based upon expression patterns across all experimental groups. Levels of brain-derived neurotrophic factor (BDNF) protein were also measured after voluntary exercise, across different regions of the spinal cord. BDNF mRNA increased with voluntary exercise, as has been previously shown for other forms of exercise, contributed to by increases in both exon I and exon III. The exercise-induced gene expression changes identified by microarray analysis are consistent with increases in pathways promoting neuronal health, signaling, remodeling, cellular transport, and development of oligodendrocytes. Taken together these data suggest cellular pathways through which exercise may promote recovery in the SCI population.

Relevance

Although this study is done on healthy uninjured rats, it shows the changes that occur within the spinal cord due to exercise. Exercise alone increases the pathways promoting neuronal health, remodeling/reorganization, and development of oligodendrocytes. Why is the development of oligodendrocytes important? Oligodendrocytes are responsible for myelinating axons. Myelin is the insulating sheath that surrounds axons and allows for proper transmission of the nerve signal. Each oligodendrocyte myelinates between 10-20 axons. Demyelination of axons is one factor in the loss of function from SCI. Therefore if it is possible to develop more oligodendrocytes, these cells may be able to remyelinate these axons.

These molecular changes that occur are extremely important to functional recovery after spinal cord injury. As shown in the following study:

Exercise restores levels of neurotrophins and synaptic plasticity following spinal cord injury.

Ying Z, Roy RR, Edgerton VR, Gomez-Pinilla F.

Department of Physiological Science, UCLA, Los Angeles, CA 90095-1527, USA; Division of Neurosurgery, UCLA Brain Injury Research Center, Los Angeles, CA 90095-1527, USA.

We have conducted studies to determine the potential of exercise to benefit the injured spinal cord using neurotrophins. Adult rats were randomly assigned to one of three groups: (1) intact control (Con); (2) sedentary, hemisected at a mid-thoracic level (Sed-Hx), or (3) exercised, hemisected (Ex-Hx). One week after surgery, the Ex-Hx rats were exposed to voluntary running wheels for 3, 7, or 28 days. BDNF mRNA levels on the lesioned side of the spinal cord lumbar region of Sed-Hx rats were approximately 80% of Con values at all time points and BDNF protein levels were approximately 40% of Con at 28 days. Exercise compensated for the reductions in BDNF after hemisection, such that BDNF mRNA levels in the Ex-Hx rats were similar to Con after 3 days and higher than Con after 7 (17%) and 28 (27%) days of exercise. After 28 days of exercise, BDNF protein levels were 33% higher in Ex-Hx than Con rats and were highly correlated (r=0.86) to running distance. The levels of the downstream effectors for the action of BDNF on synaptic plasticity synapsin I and CREB were lower in Sed-Hx than Con rats at all time points. Synapsin I mRNA and protein levels were higher in Ex-Hx rats than Sed-Hx rats and similar to Con rats at 28 days. CREB mRNA values were higher in Ex-Hx than Sed-Hx rats at all time points. Hemisection had no significant effects on the levels of NT-3 mRNA or protein; however, voluntary exercise resulted in an increase in NT-3 mRNA levels after 28 days (145%). These results are consistent with the concept that synaptic pathways under the regulatory role of BDNF induced by exercise can play a role in facilitating recovery of locomotion following spinal cord injury.

Relevance

The important points to take away from this study are that the levels of neurotrophins within the spinal cord are depressed by as much as 40% after SCI. Through exercise we can raise these levels up to 33% above baseline. So we are not just bringing them back to normal but actually going above normal levels. These elevated levels are associated with increased recovery of function.

Both of these studies together show why exercise is a key component in recovery today and will be in the future.