Blood flow restriction training and HI-RT were similarly effective in increasing muscle strength, quadriceps muscle mass, and functionality in knee OA patients. Importantly, BFRT was also able to improve pain while inducing less joint stress, emerging as a feasible and effective therapeutic adjuvant in OA management.

Objective. To evaluate the effects of a low-load resistance training program associated with partial blood-flow restriction in patients with rheumatoid arthritis (RA).Methods. Forty-eight women with RA were randomized into 1 of 3 groups: high-load resistance training (HL-RT; 70% 1 repetition maximum [1RM]), low-load resistance training (30% 1RM) with partial blood-flow restriction training (BFRT), and a control group. Patients completed a 12-week supervised training program and were assessed for lower-extremity 1RM, quadriceps cross-sectional area (CSA), physical function (timed-stands test [TST], timedup-and-go test [TUG], and Health Assessment Questionnaire [HAQ]), and quality of life (Short Form 36 health survey ) at baseline and after the intervention.Results. BFRT and HL-RT were similarly effective in increasing maximum dynamic strength in both leg press (22.8% and 24.2%, respectively; P < 0.0001 for all) and knee extension (19.7% and 23.8%, respectively; P < 0.0001 for all). Quadriceps CSA was also significantly increased in both BFRT and HL-RT (9.5% and 10.8%, respectively; P < 0.0001 for all). Comparable improvements in TST (11.2% and 14.7%; P < 0.0001 for all) and TUG (-6.8% [P < 0.0053] and -8.7% [P < 0.0001]) were also observed in BFRT and HL-RT, respectively. Improvements in both groups were significantly greater than those of the control group (P < 0.05 for all). SF-36 role physical and bodily pain and HAQ scores were improved only in BFRT (45.7%,22.5%, and -55.9%, respectively; P < 0.05 for all). HL-RT resulted in 1 case of withdrawal and several cases of exercise-induced pain, which did not occur in BFRT.Conclusion. BFRT was effective in improving muscle strength, mass, function, and health-related quality of life in patients with RA, emerging as a viable therapeutic modality in RA management.Clinicaltrials.gov identifier: NCT01483157.

Astroglial and microglial activation was analyzed in adult male Wistar rats after a unilateral striatal injection of different doses (8, 4 and 1 micrograms) of 6-hydroxydopamine (6-OHDA). Control animals received the injection of the same volume of the solvent. The rotational behavior was registered by a rotometer 24 and 72 hours, 7, 10, 14 and 22 days after lesion. Following, animals were sacrificed and the tyrosine hydroxylase (TH) positive dopamine cells, the glial fibrillary acidic protein (GFAP) immunolabeled astrocytes and the OX42 immunoreactive microglia were visualized by mean of immunohistochemistry and quantified by stereologic method employing the optical disector and the point intercepts. The apomorphine (0.5 mg/kg)-induced circling behavior was seen only after 8 micrograms of 6-OHDA from 72 hours postlesion until sacrifice. Decreases of the TH immunoreactive terminals and cell bodies were found in the sampled fields of the striatum and pars compacta of the substantia nigra (SNc), respectively, after 8 and 4 micrograms of 6-OHDA. The GFAP immunohistochemistry revealed increases in the number/density of astroglial cells in the ipsilateral neostriatum (137% of control) and ipsilateral SNc (83% of control) and also in the volumeal fraction of the astroglial processes in the ipsilateral neostriatum (30% of control) and ipsilateral SNc (38% of control) in the rats with higher dose of the neurotoxin. Increases in the number of OX42 microglial labeled profiles and in the volumeal fraction of microglial processes were found in the ipsilateral neostriatum (67% and 27%, respectively, of control) and ipsilateral SNc (100% and 50%, respectively, of control) in the 8 micrograms 6-OHDA injected rats. These results suggest that the retrograde degeneration induced by a intrastriatal injection of a small dose of the 6-OHDA leads to an astroglial and microglial reaction in the nigrostriatal dopamine pathway. The interaction between activated glial cells may be involved in the wounding and repair events in the partial lesioned nigrostriatal system as well as in the paracrine responses to surviving dopamine neurons.

Astroglial and microglial activation were analyzed in the ventral tegmental area (VTA) in adult male Wistar rats, after an unilateral striatal 6-hydroxydopamine (6-OHDA) injection. Different doses (8, 4, and 1 microg) of 6-OHDA were injected in the left side of the neostriatum; animals were sacrificed 22 days later. Control animals received an injection of the same volume of the solvent. The tyrosine hydroxylase (TH) positive dopamine cells, the glial fibrillary acidic protein (GFAP) immuno -labeled astrocytes, and the OX42 immunoreactive microglia were visualized by means of immunohistochemistry and quantified by stereologic methods employing the optical dissector and the point intercepts. The number and the density of TH immunoreactive cell bodies were decreased by 45% and 46%, respectively, in the sampled field of the ipsilateral VTA of 8 microg 6-OHDA injected rats. The GFAP immunohistochemistry revealed in the ipsilateral VTA increases the number and density of astroglial cells (154% and 166% of control, respectively) in the rats with a higher dose of the 6-OHDA, and also in the volume fraction of the astroglial processes after 8 microg (41% of control) and 4 microg (24% of control) of 6-OHDA. Increased number (76% of control) and density (77% of control) of OX42 microglial labeled profiles and microglial processes (51% of control) were found in the ipsilateral VTA of the 8 microg 6-OHDA injected animals. These results suggest that the retrograde degeneration of the mesostriatal dopamine pathways, induced by a striatal injection of 6-OHDA, leads to astroglial and microglial reactions in the VTA. The interaction between activated glial cells may be involved in the wounding and repair events in the partial lesioned system, and also in the trophic paracrine responses in the surviving VTA dopamine neurons.

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Patients with RA showed reduced chronotropic response to exercise and slower postexercise HRR. These abnormal autonomic responses to exercise indicate the presence of cardiac autonomic dysfunction and increased cardiovascular risk in this population.

Resumo. O termo plasticidade cerebral abrange os possíveis mecanismos de reorganização neuronal, recrutamento de vias funcionalmente homólogas, sinaptogenese, arborização dendrÌtica e ativação de áreas secundárias. A reorganização cerebral inicia-se ainda na fase aguda após a lesão cortical, com melhora progressiva até a estabilização do quadro. Apesar das remodelações corticais serem mais proeminentes nas fases iniciais, mudanças na atividade cerebral continuam até um ano após a lesão. Os processos de reparação e reorganização do sistema nervoso central que se iniciam logo após a lesão, se somados à reabilitação fisioterapêutica intensificada na fase inicial, favorecerão o aprendizado ou reaprendizado motor do paciente pós lesão neuronal, pois o processo de reabilitação acontecerá no pico da plasticidade cerebral, favorecendo, assim, suas respostas motoras. Diversas técnicas têm sido utilizadas para a recuperação da função motora nesses pacientes, entretanto existem controvérsias quanto à efetividade das mesmas e há necessidade de novas pesquisas baseadas nos princípios da neuroplasticidade. No entanto, a relação entre eficiência sináptica e ativação microglial ainda não está bem descrita na literatura, acreditam que durante uma tarefa específica, a atividade fagocitária da microglia faz com que sinapses mais fracas sejam eliminadas, levando a uma maior ativação de sinapses mais fortes, portanto a fisioterapia precoce na fase inicial pode promover o processo de reparo e cicatrização nas áreas lesadas bem como favorecer o trofismo e a plasticidade dos neurônios remanescentes. Neste sentido, esse trabalho objetivou revisar sobre a interação neuro-glial e a plasticidade neuronal, relacionado com os aspectos da fisioterapia precoce.

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