| Summary: | Spinal cord injury (SCI) is a devastating insult to the nervous system with implications for locomotor, autonomic and sensory function. Past studies indicate that passively moving the lower limbs may be beneficial for locomotor recovery after SCI, however the literature lacks in studies addressing autonomic and sensory ramifications of passive exercise. I used a well-established passive exercise model, which consists of cycling the hind-limbs of adult male Wistar rats with complete transection SCI at the third thoracic segment (T3), beginning 5 days after injury and continuing for 4 weeks (5 days / week, 1 hour total cycling/day). I measured Hoffman (H)-reflex latency and motoneuron recruitment after the cycling intervention. Latency of the H-wave was shorter in duration and motoneuron recruitment was enhanced after SCI when compared to uninjured controls. Exercise did not affect these properties. I performed histological analysis of parvalbumin-expressing neurons of lumbar (L) and sacral (S) dorsal root ganaglia (DRGs). Proprioceptive neurons at L1/L2 and L4/L5 levels demonstrated somal size decreases after SCI and further decreases with exercise, while there was no change at the L6/S1 level. This effect may be due to exercise-induced changes in neurotrophic support of proprioceptive neurons by target tissues. The autonomic/cardiovascular effects of passive exercise are largely unknown. I focused on two common cardiovascular conditions associated with SCI, autonomic dysreflexia (AD) and orthostatic hypotension (OH). AD occurs in individuals with an injury above T6, and is marked by massive spikes in blood pressure (BP) due to a normally-innocuous stimulus below the injury level. OH is a large drop in BP upon being seated upright, assessed via tilting the animal to a 90 degree head-up position. Passive exercise led to a 50% reduction in AD severity, as measured by beat-to-beat BP measurements and an established method for inducing AD. In contrast, I found no change in OH severity with exercise. Lumbosacral nociceptors expressing the capsaicin receptor (TRPV1), which have previously been implicated in AD and demonstrate hypertrophy after SCI, decrease in soma size after the exercise intervention. This may also indicate exercise-induced altered neurotrophic support.
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