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The purpose of this study was to determine whether or not chronic exercise could cause long-term metabolic plasticity in cerebellum. The activity of cytochrome oxidase (COX), coupled to ATP production, reflects long-term plasticity in metabolic capacity. The present study examined whether or not 10 weeks of voluntary exercise would increase COX activity in the cerebellum. Adult male Sprague-Dawley rats were randomly assigned to a control or exercise condition. Exercising rats had running wheels attached to their home cages. COX activity was measured using histochemical methods and optical densitometry. Rats in the exercise condition had significantly higher optical density in spinocerebellum (mainly in lobules 3, 4, 5, 8, 9 and in the copula), but not in neocerebellar crura I and II.

By proteomic analysis we found an up-regulation of four carbonic anhydrase-3 (CA3) isoforms and a down-regulation of superoxide dismutase [Cu-Zn] (SODC) in quadriceps of sedentary X-linked muscular dystrophy (mdx) mice as compared with wild–type (WT) mice and the levels were significantly restored to WT values following low-intensity endurance exercise., In our recent study was shown a significant recovery of damaged skeletal muscle of mice with X-linked muscular dystrophy (mdx) following low-intensity endurance exercise, probably by reducing the degeneration of dystrophic muscle. Consequently, in the present work, we aimed to identify proteins involved in the observed reduction in degenerating fibres. To this end, we used proteomic analysis to evaluate changes in the protein profile of quadriceps dystrophic muscles of exercised compared with sedentary mdx mice. Four protein spots were found to be significantly changed and were identified as three isoforms of carbonic anhydrase 3 (CA3) and superoxide dismutase [Cu-Zn] (SODC). Protein levels of CA3 isoforms were significantly up-regulated in quadriceps of sedentary mdx mice and were completely restored to wild–type (WT) mice values, both sedentary and exercised, in quadriceps of exercised mdx mice. Protein levels of SODC were down-regulated in quadriceps of sedentary mdx mice and were significantly restored to WT mice values, both sedentary and exercised, in quadriceps of exercised mdx mice. Western blot data were in agreement with those obtained using proteomic analysis and revealed the presence of one more CA3 isoform that was significantly changed. Based on data found in the present study, it seems that low-intensity endurance exercise may in part contribute to reduce cell degeneration process in mdx muscles, by counteracting oxidative stress.

The lack of dystrophin in mdx mice leads to cycles of muscle degeneration and regeneration processes. Various strategies have been proposed in order to reduce the muscle-wasting component of muscular dystrophy, including implementation of an exercise programme. The aim of this study was to examine how low-intensity endurance exercise affects the degeneration-regeneration process in dystrophic muscle of male mdx mice. Mice were subjected to low-intensity endurance exercise by running on a motorized Rota-Rod for 5 days/week for 6 weeks. Histomorphological analysis showed a signifi cant reduction of measured inflammatory-necrotic areas in both gastrocnemius and quadriceps muscle of exercised mdx mice as compared to matched sedentary mdx mice. The degenerative-regenerative process was also evaluated by examining the protein levels of connexin 39 (Cx39), a specifi c gene expressed in injured muscles. Cx39 was not detected in sedentary wild type mice, whereas it was found markedly increased in sedentary mdx mice, revealing active muscle degeneration-regeneration process. These Cx39 protein levels were signifi cantly reduced in muscles of mdx mice exercised for 30 and 40 days, revealing together with histomorphological analysis a strong reduction of degeneration process in mice subjected to low-intensity endurance exercise. Muscles of exercised mdx mice did not show significant changes in force and fatigue resistance as compared to sedentary mdx mice. Overall in this study we found that specifi c lowintensity endurance exercise induces a beneficial effect probably by reducing the degeneration of dystrophic muscle.

Neuroplasticity represents a common phenomenon after spinal cord (SC) injury or deafferentation that compensates for the loss of modulatory inputs to the cord. Neurotrophins play a crucial role in cell survival and anatomical reorganization of damaged spinal cord, and are known to exert an activity-dependent modulation of neuroplasticity. Little is known about their role in the earliest plastic events, probably involving synaptic plasticity, which are responsible for the rapid recovery of hindlimb motility after hemisection, in the rat. In order to gain further insight, we evaluated the changes in BDNF and NT-4 expression by lumbar motoneurons after low-thoracic spinal cord hemisection. Early after lesion (30 min), the immunostaining density within lumbar motoneurons decreased markedly on both ipsilateral and contralateral sides of the spinal cord. This reduction was statistically significant and was then followed by a significant recovery along the experimental period (14 days), during which a substantial recovery of hindlimb motility was observed. Our data indicate that BDNF and NT-4 expression could be modulated by activity of spinal circuitry and further support putative involvement of the endogenous neurotrophins in mechanisms of spinal neuroplasticity.