Effects of respiratory muscle training on parasympathetic activity in diabetes mellitus

This study verified the effects of respiratory muscle training (RMT) on hemodynamics, heart rate (HR) variability, and muscle morphology in rats with streptozotocin-induced diabetes mellitus (DM). Thirty-six male Wistar rats were randomized into 4 groups and 34 completed the study: i) sham-sedentary (Sham-ST; n=9); ii) sham-RMT (Sham-RMT; n=9); iii) DM-sedentary (DM-ST; n=8); and iv) DM-RMT (DM-RMT; n=8). Hemodynamics were assessed by central cannulation, and R-R intervals were measured by electrocardiogram. In addition, the effects of RMT on the cross-sectional area of the diaphragm, anterior tibial, and soleus muscles were analyzed. The induction of DM by streptozotocin resulted in weight loss, hyperglycemia, reduced blood pressure, and attenuated left ventricular contraction and relaxation (P<0.05). We also observed a decrease in root mean square of successive differences between adjacent RR intervals (RMSSD) index and in the cross-sectional area of the muscles assessed, specifically the diaphragm, soleus, and anterior tibial muscles in diabetic rats (P<0.05). Interestingly, RMT led to an increase in RMSSD in rats with DM (P<0.05). The induction of DM produced profound deleterious changes in the diaphragmatic and peripheral muscles, as well as impairments in cardiovascular hemodynamics and autonomic control. Nevertheless, RMT may beneficially attenuate autonomic changes and improve parasympathetic modulation.

Reaching task performance is associated to neuromuscular junction adaptations in rats with induced diabetes mellitus

Upper limb performance is affected by diabetes mellitus (DM). Neuromuscular junction (NMJ) is a key structure to understand the relationship between performance and morphology in DM. The aim of the study was to analyze NMJ plasticity due to DM in an animal model and its relationship with the function of forelimbs in rats. Twelve Wistar rats were divided into control (C) and DM groups. Animals were trained to perform a grasping task, following procedures of habituation, shaping, and reaching task. DM was induced using streptozotocin. Forelimb neuromuscular performance for dexterity was evaluated one day before DM induction and five weeks following induction. After that, biceps, triceps, and finger flexors and extensors were removed. Connective tissue and muscle fiber cross-sectional area (CSA) were measured. NMJ was assessed by its morphometric characteristics (area, perimeter, and maximum diameter), using ImageJ software. Motor performance analyses were made using single pellet retrieval task performance test. Student's t-test was used for comparisons between groups. A significant decrease in all NMJ morphometric parameters was observed in the DM group compared with the C group. Results showed that DM generated NMJ retraction in muscles involved in a reaching task. These alterations are related to signs of muscular atrophy and to poor reaching task performance. In conclusion, induced DM caused NMJ retraction and muscular atrophy in muscles involved in reaching task performance. Induced DM caused significantly lower motor performance, especially in the final moments of evaluation, when DM compromised the tropism of the muscular tissue.

Effects of exercise training on atrophy gene expression in skeletal muscle of mice with chronic allergic lung inflammation

We evaluated the effects of chronic allergic airway inflammation and of treadmill training (12 weeks) of low and moderate intensity on muscle fiber cross-sectional area and mRNA levels of atrogin-1 and MuRF1 in the mouse tibialis anterior muscle. Six 4-month-old male BALB/c mice (28.5 ± 0.8 g) per group were examined: 1) control, non-sensitized and non-trained (C); 2) ovalbumin sensitized (OA, 20 µg per mouse); 3) non-sensitized and trained at 50 percent maximum speed _ low intensity (PT50 percent); 4) non-sensitized and trained at 75 percent maximum speed _ moderate intensity (PT75 percent); 5) OA-sensitized and trained at 50 percent (OA+PT50 percent), 6) OA-sensitized and trained at 75 percent (OA+PT75 percent). There was no difference in muscle fiber cross-sectional area among groups and no difference in atrogin-1 and MuRF1 expression between C and OA groups. All exercised groups showed significantly decreased expression of atrogin-1 compared to C (1.01 ± 0.2-fold): PT50 percent = 0.71 ± 0.12-fold; OA+PT50 percent = 0.74 ± 0.03-fold; PT75 percent = 0.71 ± 0.09-fold; OA+PT75 percent = 0.74 ± 0.09-fold. Similarly significant results were obtained regarding MuRF1 gene expression compared to C (1.01 ± 0.23-fold): PT50 percent = 0.53 ± 0.20-fold; OA+PT50 percent = 0.55 ± 0.11-fold; PT75 percent = 0.35 ± 0.15-fold; OA+PT75 percent = 0.37 ± 0.08-fold. A short period of OA did not induce skeletal muscle atrophy in the mouse tibialis anterior muscle and aerobic training at low and moderate intensity negatively regulates the atrophy pathway in skeletal muscle of healthy mice or mice with allergic lung inflammation.

Alteracoes da cronaxia, da reobase e da acomodacao no musculo esqueletico desnervado submetido a eletroestimulacao / Alterations of the chronaxie, reobase and accomodation in denervated skeletal muscle submitted to electrical stimulation

O uso da eletroestimulacao (EE) no tratamento das lesoes nervosas perifericas e controverso. Este estudo avaliou a alteracao da cronaxia, da reobase e da acomodacao no musculo tibial anterior (TA) desnervado de ratos submetidos a EE. Quatro grupos de ratos forma divididos: TA desnervado com eletrodiagnostico (ED) semanal (DSN+ED); TA desnervado com EE em dias alternados (DSN+EE+ED); TA direito desnervado (DSN); e TA inervado (INV). O eletrodiagnostico do grupo DSN+EE+ED forneceu os parametros EE (20 contracoes intensas com corrente monopolar, exponencial; periodo de pulso igual a 2x o valor da cronaxia; frequencia de 20Hz; amplitude em nivel motor; e tempo ON 3,0 s e OFF 6,0 s). Apos 4 semanas, nota-se, em todos os musculos desnervados, diminuicao na reobase, caracterizando hiperexcitabilidade muscular. A reobase foi mairo no musculo so desnervado (1+0 mA), se comparada ao DSN+ED (0,5+0mA, p=0,00006) e ao DSN+EE+ED (0,58+0,19mA, P=0,0001). A cronaxia do grupo DSN+EE+ED foi melhor (4,06+2,1ms) se comparada aos grupos DNS+ED (8,4+0,93MS,P=0006) e DSN (5,31+0,53ms, p=0,45). A acomodacao diminuiu nos grupos DSN+ED (0,75+0,42mA) e DSN+EE+ED (0,75+0,6mA), mantendo-se com valores proximos a pre-desnervacao no grupo somente desnervado (DSN 1,8+0,45mA). Concluiu-se que, embora a EE e o ED tenha atrasado a recuperacao da reobase e da acomodacao, sua utilizacao conjunta favoreceu a rcuperacao da cronaxia. Esse resultado indica o efeito benefico no tratamento do musculo desnervado