DOES AEROBIC EXERCISE TRAINING PROMOTE CHANGES IN STRUCTURAL AND BIOMECHANICAL PROPERTIES OF THE TENDONS IN EXPERIMENTAL ANIMALS? A SYSTEMATIC REVIEW

To develop a systematic review to evaluate, through the best scientific evidence available, the effectiveness of aerobic exercise in improving the biomechanical characteristics of tendons in experimental animals. Two independent assessors conducted a systematic search in the databases Medline/PUBMED and Lilacs/BIREME, using the following descriptors of Mesh in animal models. The ultimate load of traction and the elastic modulus tendon were used as primary outcomes and transverse section area, ultimate stress and tendon strain as secondary outcomes. The assessment of risk of bias in the studies was carried out using the following methodological components: light/dark cycle, temperature, nutrition, housing, research undertaken in conjunction with an ethics committee, randomization, adaptation of the animals to the training and preparation for the mechanical test. Eight studies, comprising 384 animals, were selected; it was not possible to combine them into one meta-analysis due to the heterogeneity of the samples. There was a trend to increasing ultimate load without changes in the other outcomes studied. Only one study met more than 80% of the quality criteria. Physical training performed in a structured way with imposition of overloads seems to be able to promote changes in tendon structure of experimental models by increasing the ultimate load supported. However, the results of the influence of exercise on the elastic modulus parameters, strain, transverse section area and ultimate stress, remain controversial and inconclusive. Such a conclusion must be evaluated with reservation as there was low methodological control in the studies included in this review

Involvement of the Fcγ receptor in a chronic N-methyl-4-phenyl-1,,2, 3,6-tetrahydropyridine mouse model of dopaminergic loss

Although there is growing evidence for a role of the innate immune response in Parkinson's disease, the nature of any humoral response in dopaminergic degeneration is uncertain. Here we report on a protracted N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of dopaminergic death that potentially allows a more full adaptive humoral response to develop. Rag2 mutant mice that lack the full adaptive response (deficient in both T and B cells) are resistant to dopaminergic death and behavioral deficiencies in this model. These mice are resensitized after reconstitution with WT splenocytes. To more directly provide evidence for humoral/IgG involvement, we show that deficiency of Fcγ receptors, which are critical for activation of macrophages/microglia by binding to IgGs, is also protective in this protracted model. FcγR-deficient mice display improved behavior and impaired microglial activation. Interestingly, however, Rag2 mutant but not FcγR-deficient mice are resistant to a more standard N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine paradigm where death is more rapid. Taken together, these data indicate that, provided sufficient time, the humoral arm of the adaptive immune system can play a critical functional role in modulating the microglial response to dopaminergic degeneration and suggest that this humoral component may participate in degeneration in Parkinson's disease