Assessment of the passive and eccentric torque at knee and ankle flexion and extension in type 2 diabetics with and without peripheral neuropathy

Abstract

The type 2 diabetes mellitus (T2D) is a epidemic and chronic disease caused by an inflammatory mechanism associated with visceral obesity. Due to the inflammatory mechanism, individuals can present decrease in muscle strength and muscle mass from the onset of the disease. Moreover, the TD2M is associated with chronic complications, like diabetic peripheral neuropathy (DPN), collagen stiffening and oxidative stress, which can also affect the skeletal muscle. However, changes in musculoskeletal function were poorly investigated in individuals with T2D. In a recent study in our laboratory, we observed a decrease in concentric and isometric torques and maintenance in eccentric torque of knee and ankle joints in individuals with T2DM, regardless of the presence of DPN. The decrease in concentric and isometric torques has been associated with increasing inflammation that can lead to muscle atrophy. The maintenance of eccentric torque in these individuals could be associated with increasing in collagen stiffness and changes in muscle non-contractile structures. Thus, an assessment of passive torque can provide insights on the muscle elastic resistance characteristics of these individuals with T2DM. To verify if the maintenance of the eccentric torque is associated with others alterations in the contractile structures of the muscle, a electromyographic (EMG) analysis of the muscle would be important. Thus, the aim of this study is to analyze knee and ankle passive and eccentric torques, during flexion and extension at different motion speeds (5 ° / s, 30 ° / s and 60 ° / s), associated with EMG signals, of individuals with T2DM, with and without DPN, compared to a control group without diabetes. The hypothesis of the study is that T2DM individuals, with and without DPN, will present an increased passive torque and a maintenance in eccentric torque, of both joints, compared to the control group. Knee and ankle torques will be assessed using an isokinetic dynamometer (Biodex, system 3), synchronized to surface EMG (Trigno, Delsys). The presence of DPN will be assessed using the Michigan Neuropathy Screening Protocol and the DPN severity will be classified using a logic Fuzzy system. Glycemic control will be evaluated by the glycated hemoglobin test to confirm T2DM condition. The Kolmogorov-Smirnov and Levene test will be used to test the data distribution. One-way ANOVA test with a Tukey post hoc will be used to compare clinical and demographic characteristics, passive and eccentric torques and EMG signals between groups. A significance level of 5% will be considered. If necessary Kruskal-Wallis and Mann Whitney tests will be applied for non-moral data and the significance level will be adjusted.