Regulation of extracellular matrix elements and sarcomerogenesis in response to different periods of passive stretching in the soleus muscle of rats.

Stretching is a common method used to prevent muscle shortening and improve limited mobility. However, the effect of different time periods on stretching-induced adaptation of the extracellular matrix and its regulatory elements have yet to be investigated. We aimed to evaluate the expression of fibrillar collagens, sarcomerogenesis, metalloproteinase (MMP) activity and gene expression of the extracellular matrix (ECM) regulators in the soleus (SOL) muscle of rats submitted to different stretching periods. The soleus muscles were submitted to 10 sets of passive stretching over 10 (St 10d) or 15 days (St 15d) (1 min per set, with 30 seconds' rest between sets). Sarcomerogenesis, muscle cross-sectional area (CSA), and MMP activity and mRNA levels in collagen (type I, III and IV), connective tissue growth factor (CTGF), growth factor-beta (TGF-ß), and lysyl oxidase (LOX) were analyzed. Passive stretching over both time periods mitigated COL-I deposition in the SOL muscle of rats. Paradoxically, 10 days of passive stretching induced COL-I and COL-III synthesis, with concomitant upregulation of TGF-ß1 and CTGF at a transcriptional level. These responses may be associated with lower LOX mRNA levels in SOL muscles submitted to 10 passive stretching sessions. Moreover, sarcomerogenesis was observed after 15 days of stretching, suggesting that stretching-induced muscle adaptations are time-dependent responses.

Insulin treatment reverses the increase in atrogin-1 expression in atrophied skeletal muscles of diabetic rats with acute joint inflammation.

BACKGROUND: The aim of this study was to evaluate the changes in biomarkers of skeletal muscle proteolysis (atrogin-1, muscle RING finger-1 protein [MuRF-1]) and inflammation (nuclear factor kappa-B) in skeletal muscles of rats under two catabolic conditions, diabetes mellitus (DM) and acute joint inflammation, and the effects of insulin therapy. MATERIALS AND METHODS: Male Wistar rats were divided into groups without diabetes - normal (N), saline (NS), or ι-carrageenan (NCa) injection into the tibiotarsal joint - and groups with diabetes - diabetes (D), plus insulin (DI), saline (DS), or ι-carrageenan (DCa) injection into the tibiotarsal joint, or ι-carrageenan injection and treatment with insulin (DCaI). Three days after ι-carrageenan injection (17 days after diabetes induction), tibialis anterior (TA) and soleus (SO) skeletal muscles were used for analysis. RESULTS: DM alone caused a significant decrease in the mass of TA and SO muscles, even with low levels of atrogenes (atrogin-1, MuRF-1), which could be interpreted as an adaptive mechanism to spare muscle proteins under this catabolic condition. The loss of muscle mass was exacerbated when ι-carrageenan was administered in the joints of diabetic rats, in association with increased expression of atrogin-1, MuRF-1, and nuclear factor kappa-B. Treatment with insulin prevented the increase in atrogin-1 (TA, SO) and the loss of muscle mass (SO) in diabetic-carrageenan rats; in comparison with TA, SO muscle was more responsive to the anabolic actions of insulin. CONCLUSION: Acute joint inflammation overcame the adaptive mechanism in diabetic rats to prevent excessive loss of muscle mass, worsening the catabolic state. The treatment of diabetic-carrageenan rats with insulin prevented the loss of skeletal muscle mass mainly via atrogin-1 inhibition. Under the condition of DM and inflammation, muscles with the prevalence of slow-twitch, type 1 fibers were more responsive to insulin treatment, recovering the ability to grow.

Cryotherapy Reduces Inflammatory Response Without Altering Muscle Regeneration Process and Extracellular Matrix Remodeling of Rat Muscle.

The application of cryotherapy is widely used in sports medicine today. Cooling could minimize secondary hypoxic injury through the reduction of cellular metabolism and injury area. Conflicting results have also suggested cryotherapy could delay and impair the regeneration process. There are no definitive findings about the effects of cryotherapy on the process of muscle regeneration. The aim of the present study was to evaluate the effects of a clinical-like cryotherapy on inflammation, regeneration and extracellular matrix (ECM) remodeling on the Tibialis anterior (TA) muscle of rats 3, 7 and 14 days post-injury. It was observed that the intermittent application of cryotherapy (three 30-minute sessions, every 2 h) in the first 48 h post-injury decreased inflammatory processes (mRNA levels of TNF-α, NF-κB, TGF-ß and MMP-9 and macrophage percentage). Cryotherapy did not alter regeneration markers such as injury area, desmin and Myod expression. Despite regulating Collagen I and III and their growth factors, cryotherapy did not alter collagen deposition. In summary, clinical-like cryotherapy reduces the inflammatory process through the decrease of macrophage infiltration and the accumulation of the inflammatory key markers without influencing muscle injury area and ECM remodeling.

Neuromuscular electrical stimulation induces beneficial adaptations in the extracellular matrix of quadriceps muscle after anterior cruciate ligament transection of rats.

OBJECTIVE: The aim of this study was to assess the effect of neuromuscular electrical stimulation (NMES) on the extracellular matrix remodeling of the quadriceps muscle after anterior cruciate ligament (ACL) transection in rats. The hypothesis of this study was that ACL transection would induce maladaptive modifications in the extracellular matrix through the increase in connective tissue (CT) accumulation and net degradation of type IV collagen of the quadriceps muscle. In addition, clinical-like NMES, applied to the quadriceps muscle immediately after the ACL transection, would reduce the accumulation of the CT content and net degradation of type IV collagen. DESIGN: Wistar male rats were randomized into five different groups: ACL (surgery and ACL transection), Sham (surgery without ACL transection), ACLES (surgery, ACL transection, and NMES), ShamES (surgery without ACL transection, but NMES), and Control (intact animals). The vastus medialis, rectus femoris, and vastus lateralis muscles of the quadriceps were harvested 1, 2, 3, 7, and 15 days after surgery. Matrix metalloproteinase-2 (MMP-2) (messenger RNA [mRNA] levels and activity), collagen IV (mRNA and protein levels), and CT density were assessed. RESULTS: The ACL transection increased the CT content and MMP-2 mRNA levels and decreased collagen IV mRNA and protein levels. NMES minimized the CT density in all muscles and reduced the MMP-2 mRNA levels mainly in the vastus lateralis muscle at 7 days. Moreover, type IV collagen mRNA levels were increased in all muscles at 7 days, as was the protein level only at 15 days, in the NMES groups. CONCLUSIONS: This study showed that ACL transection increases CT content and MMP-2 mRNA levels and induces rapid changes in basement membranes, causing net degradation of type IV collagen during the first 2 wks after ACL injury. Furthermore, clinical-like NMES minimized the accumulation of CT density, regulated the MMP-2 mRNA levels, and increased both type IV collagen mRNA and protein levels.

Neuromuscular electrical stimulation alters gene expression and delays quadriceps muscle atrophy of rats after anterior cruciate ligament transection.

INTRODUCTION: Neuromuscular electrical stimulation (NMES) is used to improve quadriceps mass after anterior cruciate ligament (ACL) injury. We studied the effect of NMES on mRNA levels of atrophy genes in the quadriceps muscle of rats after ACL transection. METHODS: mRNA levels of atrogin-1, MuRF-1, and myostatin were assessed by quantitative PCR and the polyubiquitinated proteins by Western blot at 1, 2, 3, 7, and 15 days postinjury. RESULTS: NMES minimized the accumulation of atrogenes and myostatin according to time period. NMES also prevented reduction in muscle mass in all muscles of the ACLES group at 3 days. CONCLUSIONS: Use of NMES decreased the accumulation of atrogenes and myostatin mRNA in the quadriceps muscles, inhibiting early atrophy at 3 days, although it did not prevent atrophy at 7 and 15 days after ACL transection. This study highlights the importance of therapeutic NMES interventions in the acute phase after ACL transection.

Effect of tibiotarsal joint inflammation on gene expression and cross-sectional area in rat soleus muscle.

BACKGROUND: Joint inflammation is a common clinical problem in patients treated by physical therapists. The hypothesis of this study is that joint inflammation induces molecular and structural changes in the soleus muscle, which is composed mainly of slow-twitch muscle fibers. OBJECTIVE: To study the effect of tibiotarsal joint inflammation on muscle fiber cross-sectional area (CSA), gene expression levels (atrogin-1, MuRF1, MyoD, myostatin, p38MAPK, NFκB, TNF-alpha), and TNF-alpha protein in the soleus muscle. METHOD: Wistar rats were randomly divided into 3 periods (2, 7 and 15 days) and assigned to 4 groups (control, sham, inflammation, and immobilization). RESULTS: In the inflammation group at 2 days, MuRF1 and p38MAPK expression had increased, and NFκB mRNA levels had decreased. At 7 days, myostatin expression had decreased. At 7 and 15 days, this group had muscle fiber CSA reduction. At 2 days, the immobilization group showed increased atrogin-1, MuRF1, NFκB, MyoD, and p38MAPK expressions and reduced muscle fiber CSA. At 7 and 15 days, myostatin mRNA levels had increased, and the CSA had decreased. The sham group showed increased p38MAPK and myostatin expressions at 2 and 7 days, respectively. No changes occurred in TNF-alpha gene or protein expression. CONCLUSION: Acute joint inflammation induces gene expression related to the proteolytic pathway without reduction in muscle fiber CSA. Chronic joint inflammation induced muscle atrophy without up-regulation of important genes belonging to the proteolytic pathway. Thus, muscle adaptation may differ according to the stage of joint inflammation, which suggests that the therapeutic modalities used by physical therapists at each stage should also be different.

Quadriceps muscle atrophy after anterior cruciate ligament transection involves increased mRNA levels of atrogin-1, muscle ring finger 1, and myostatin.

OBJECTIVE: The aim of this study was to assess the mRNA levels of atrogin-1, muscle ring finger 1, and myostatin in rat quadriceps after anterior cruciate ligament (ACL) transection. DESIGN: Wistar rats were randomized into three different groups: ACL (surgery and ACL transection), sham (surgery without ACL transection), and control. Vastus medialis, rectus femoris, and vastus lateralis muscles were harvested at 1, 2, 3, 7, and 15 days after ACL transection. The mRNA levels of atrogin-1, muscle ring finger 1, and myostatin, as well as the ubiquitinated protein content, muscle mass, and cross-sectional area of the muscle fibers, were evaluated. RESULTS: Elevated levels of atrogin-1, muscle ring finger 1, and myostatin mRNA were detected in all tested muscles at most time points. The ubiquitinated protein content was increased at 3 days in the ACL and sham groups. The muscle mass of the ACL group was reduced at 3, 7, and 15 days (vastus lateralis and vastus medialis) and at 7 and 15 days (rectus femoris), whereas it was reduced in the sham group at 3 and 7 days (vastus lateralis and vastus medialis) and at 7 days (rectus femoris). The cross-sectional area of vastus medialis was reduced at 3, 7, and 15 days in the ACL group and at 3 and 7 days in the sham group. The cross-sectional area of the vastus lateralis was reduced at 7 and 15 days in the ACL group and at 7 days in the sham group. Whereas muscle mass and cross-sectional area recovery was noted in the sham group, no recovery was observed in the ACL group. CONCLUSIONS: Quadriceps atrophy after ACL transection involves increased levels of myostatin, atrogin-1, and muscle ring finger 1 mRNA and the accumulation of ubiquitinated protein.

Proposal of non-invasive experimental model to induce scoliosis in rats / Proposta de modelo experimental não-invasivo para indução de escoliose em ratos

BACKGROUND: In the literature, there are several experimental models that induce scoliosis in rats; however, they make use of drugs or invasive interventions to generate a scoliotic curve. OBJECTIVES: To design and apply a non-invasive immobilization model to induce scoliosis in rats. METHODS: Four-week old male Wistar rats (85±3.3g) were divided into two groups: control (CG) and scoliosis (SG). The animals in the SG were immobilized by two vests (scapular and pelvic) made from polyvinyl chloride (PVC) and externally attached to each other by a retainer that regulated the scoliosis angle for twelve weeks with left convexity. After immobilization, the abdominal, intercostal, paravertebral, and pectoral muscles were collected for chemical and metabolic analyses. Radiographic reports were performed every 30 days over a 16-week period. RESULTS: The model was effective in the induction of scoliosis, even 30 days after immobilization, with a stable angle of 28±5º. The chemical and metabolic analyses showed a decrease (p<0.05) in the glycogenic reserves and in the relationship between DNA and total protein reserves of all the muscles analyzed in the scoliosis group, being lower (p<0.05) in the convex side. The values for the Homeostatic Model Assessment of Insulin Resistance indicated a resistance condition to insulin (p<0.05) in the scoliosis group (0.66±0.03), when compared to the control group (0.81±0.02). CONCLUSIONS: The scoliosis curvature remained stable 30 days after immobilization. The chemical and metabolic analyses suggest changes in muscular homeostasis during the induced scoliosis process.

CONTEXTUALIZAÇÃO: Encontram-se na literatura diversos modelos experimentais de indução de escoliose em ratos, porém evidencia-se o uso de drogas ou intervenções invasivas para a geração da curvatura escoliótica. OBJETIVOS: Projetar e aplicar um modelo de imobilização não-invasiva para a indução de escoliose em ratos. MÉTODOS: Ratos Wistar machos com idade inicial de quatro semanas (85±3,3g) foram divididos nos grupos controle (GC) e escoliose (GE). Os animais do GE foram imobilizados por dois cintos (escapular e pélvico) de policloreto de vinila (PVC), interligados externamente por um limitador que regulava o ângulo da escoliose durante 12 semanas, com convexidade à esquerda. Após a imobilização, os músculos abdominais, intercostais, paravertebrais e peitorais bilateralmente foram coletados para as análises químio-metabólicas. Os registros radiológicos foram realizados a cada 30 dias, num total de 16 semanas. RESULTADOS: O modelo foi eficiente e eficaz na indução da escoliose, mesmo após 30 dias da desmobilização, mantendo um ângulo estável de 28±5 graus. Quanto às análises químio-metabólicas, observou-se diminuição (p<0,05) nas reservas glicogênicas e na relação proteína total/DNA de todos os músculos analisados do GE, sendo menores (p<0,05) no lado da convexidade. Os valores do HOMA-IR indicaram um quadro de resistência à insulina (p<0,05) no GE (0,66±0,03) quando comparado ao GC (0,81±0,02). CONCLUSÕES: A curvatura escoliótica manteve-se estável após 30 dias da desmobilização, e as alterações químio-metabólicas sugeriram a ocorrência de modificações na homeostasia muscular durante o processo indutor da escoliose.

Proposal of non-invasive experimental model to induce scoliosis in rats.

BACKGROUND: In the literature, there are several experimental models that induce scoliosis in rats; however, they make use of drugs or invasive interventions to generate a scoliotic curve. OBJECTIVES: To design and apply a non-invasive immobilization model to induce scoliosis in rats. METHODS: Four-week old male Wistar rats (85±3.3g) were divided into two groups: control (CG) and scoliosis (SG). The animals in the SG were immobilized by two vests (scapular and pelvic) made from polyvinyl chloride (PVC) and externally attached to each other by a retainer that regulated the scoliosis angle for twelve weeks with left convexity. After immobilization, the abdominal, intercostal, paravertebral, and pectoral muscles were collected for chemical and metabolic analyses. Radiographic reports were performed every 30 days over a 16-week period. RESULTS: The model was effective in the induction of scoliosis, even 30 days after immobilization, with a stable angle of 28±5º. The chemical and metabolic analyses showed a decrease (p<0.05) in the glycogenic reserves and in the relationship between DNA and total protein reserves of all the muscles analyzed in the scoliosis group, being lower (p<0.05) in the convex side. The values for the Homeostatic Model Assessment of Insulin Resistance indicated a resistance condition to insulin (p<0.05) in the scoliosis group (0.66±0.03), when compared to the control group (0.81±0.02). CONCLUSIONS: The scoliosis curvature remained stable 30 days after immobilization. The chemical and metabolic analyses suggest changes in muscular homeostasis during the induced scoliosis process.

Stretching and electrical stimulation reduce the accumulation of MyoD, myostatin and atrogin-1 in denervated rat skeletal muscle.

Denervation causes muscle atrophy and incapacity in humans. Although electrical stimulation (ES) and stretching (St) are commonly used in rehabilitation, it is still unclear whether they stimulate or impair muscle recovery and reinnervation. The purpose of this study was to evaluate the effects of ES and St, alone and combined (ES + St), on the expression of genes that regulate muscle mass (MyoD, Runx1, atrogin-1, MuRF1 and myostatin), on muscle fibre cross-sectional area and excitability, and on the expression of the neural cell adhesion molecule (N-CAM) in denervated rat muscle. ES, St and ES + St reduced the accumulation of MyoD, atrogin-1 and MuRF1 and maintained Runx1 and myostatin expressions at normal levels in denervated muscles. None of the physical interventions prevented muscle fibre atrophy or N-CAM expression in denervated muscles. In conclusion, although ES, St and ES + St changed gene expression, they were insufficient to avoid muscle fibre atrophy due to denervation.

Metabolic and morphometric alterations inherent to neuromuscular electric stimulation in the antagonist muscle submitted to ankle joint immobilization

The aim of this work was to investigate the effect of the neuromuscular electrical stimulation (ES) on the metabolic and morfometric profile of the tibialis anterior muscle, antagonist to the soleus muscle which was stimulate, under the joint immobilization condition of the ankle for 7 and 15 days. The immobilization promoted the reduction in the muscle mass (I7: 17.36 percent, I15: 20.83 percent), in the glycogen content (I7: 48 percent, I15: 48 percent), in the muscle fibers areas (I7: 27 percent, I15: 40 percent) and increase in intramuscular connective tissue density (I7: 122 percent, I15: 206 percent). The EE didn't promote significant alterations in the mass of the immobilized groups, however, promoted increase in the glycogen (IEE7: 31.25 percent; IEE15: 56.25 percent), reduction in the muscle fibers areas (IEE7: 14 percent, IEE15: 24.69 percent) and reduction in the connective tissue density (IEE7: 25.63 percent, IEE15: 49.09 percent) when compared with the respective immobilized groups.

O objetivo desse trabalho foi investigar o efeito da estimulação elétrica neuromuscular (EE) sobre o perfil metabólico e morfométrico do músculo tibial anterior, antagonista ao músculo sóleo, o qual foi estimulado, sob a condição de imobilização articular de tornozelo durante 7 e 15 dias. A imobilização promoveu redução na massa muscular (I7: 17,36 por cento, I15: 20,83 por cento), no conteúdo de glicogênio (I7: 48 por cento, I15: 48 por cento), na área das fibras musculares (I7: 27 por cento, I15: 40 por cento) e aumento na densidade do tecido conjuntivo intramuscular (I7: 122 por cento, I15: 206 por cento). A EE não promoveu alterações significativas na massa muscular dos grupos imobilizados, porém, promoveu aumento no glicogênio (IEE7: 31,25 por cento; IEE15: 56,25 por cento), redução na área das fibras musculares (IEE7: 14 por cento, IEE15: 24,69 por cento) e redução na densidade do tecido conjuntivo de (IEE7: 25,63 por cento, IEE15: 49,09 por cento) quando comparado aos respectivos grupos imobilizados.

Metformina minimiza as alterações morfométricas no músculo sóleo de ratos submetidos à imobilização articular / Metformin minimizes the morphometric alterations in the soleus muscle of rats submitted to articular immobilization

A proposta deste trabalho foi avaliar o músculo sóleo (S) de ratos submetidos à imobilização articular por sete dias, associado ou não ao tratamento com metformina (MET, 1,4mg.ml-1) por meio de análises morfométricas. Ratos adultos Wistar (n = 5) foram divididos nos grupos: controle (C), imobilizado em posição neutra do tornozelo (I), tratado com metformina (M), imobilizado tratado com metformina (I + MET). Foram avaliadas a área das fibras, a densidade de área do tecido conjuntivo intramuscular e a massa muscular do S. A análise estatística foi realizada pelo teste de normalidade, ANOVA e de Tukey (p < 0,05). A imobilização reduziu o peso muscular (mg) do S (34 por cento). No grupo M não houve alteração significativa do peso muscular quando comparado com o grupo C. Já no grupo I + MET foi observado aumento do peso muscular em 29,6 por cento quando comparado com o grupo I. O tratamento com metformina não alterou a área da fibra muscular quando comparado com grupo C. Já no grupo I, houve redução de 44 por cento na área da fibra. Com relação ao grupo I + MET, houve aumento de 22 por cento quando comparado com o grupo I. Por outro lado, ao compararmos o grupo C com o grupo I + MET, houve redução de 31 por cento. Ao avaliar a densidade de área do tecido conjuntivo, observou-se que o grupo I apresentou elevação de 216 por cento quando comparado com o grupo C. No grupo I + MET, houve redução de 67 por cento comparado com o grupo I. O tratamento com metformina em músculos submetidos à imobilização minimizou a redução da área das fibras do S, bem como o aumento do tecido conjuntivo. Esses resultados sugerem que a metformina pode favorecer recuperação mais rápida na fase pós-imobilização.

The aim of this study was to evaluate the effect of metformin treatment on the muscle mass, fibers area and connective tissue area density in soleus (S) muscle under articular immobilization. METHODS AND RESULTS: Male Wistar rats (250-300g) were divided in 4 groups (n=5): control, treated with metformin, immobilized and immobilized treated with metformin. Immobilization was performed by acrylic resin orthoses on the left hindlimb keeping the ankle in neutral position during 7 days. The animals were euthanatized and the S muscle was dissected and weighed. Samples of its ventral portion were treated for inclusion in paraffin and stained in Hematoxylin-Eosin (H:E). The results were obtained through analyses of the muscular fiber area (images analyzed - Image Pró-plus 4,0), as well as of intramuscular connective tissue by means of planimetry. The statistical analysis was performed by normality test followed by ANOVA and Tukey (p<0.05). Hindlimb immobilization during 7 days promoted significant reduction (p<0.05) of 35 percent in the muscular mass; 44 percent (p<0.05) in the fiber area and increase of 216 percent (p<0.05) in the intramuscular connective tissue. The metformin in immobilized group promoted significant alterations (p<0.05) in the muscular mass. In addiction, it was observed significant increase (p<0.05) of 29.6 percent in the fibers area and significant reduction (p<0.05) of 67 percent in the intramuscular connective tissue. CONCLUSION: The metformin treatment minimized the reduction of muscle fibers area, as well as the increase of connective tissue in hindlimb immobilized muscle. These results suggest that metformin should be used to increase fast muscle recovery after hindlimb immobilization.

Effects of alternagin-C from Bothrops alternatus on gene expression and activity of metalloproteinases in regenerating skeletal muscle.

This study evaluated the effects of alternagin-C (ALT-C) on mRNA levels of VEGF, MyoD and matrix metalloproteinase 2 (MMP-2) and on activity of MMPs in injured tibialis anterior (TA) muscle induced by cryolesioning in rats. Thirty-six Wistar rats (3 months old, 258.9+/-27 g) were divided into five groups: (1) control group; (2) injured TA and analyzed 3 days later; (3) injured TA treated with ALT-C and analyzed 3 days later; (4) injured TA and analyzed 7 days later and (5) injured TA treated with ALT-C and analyzed 7 days later. The injured muscle received 25 microl of ALT-C (50 nM). The injured and uninjured muscle areas were quantified by light microscopy. The MMP activity was evaluated through zymography, and mRNA of MyoD, VEGF and MMP-2 was assessed by quantitative polymerase chain reaction. ALT-C neither reduced the muscle injury area nor altered the pattern of MyoD and VEGF expression in injured muscles. However, ALT-C reduces both MMP-2 mRNA and gelatinolytic activity in injured muscles. The study indicates that ALT-C, at the tested concentrations, did not improve muscle regeneration process in rats. The effect on MMP-2 mRNA and gelatinolytic activity suggests that ALT-C changes the overall balance of ECM protein turnover during muscle regeneration.

Efeito do sulfato de vanadil sobre o comprometimento metabólico muscular induzido pela imobilização de membro posterior de ratos / Efecto del sulfato de vanadil sobre comprometimiento metabólico muscular inducido por la inmovilización del miembro posterior en ratones / Effect of the vanadyl sulphate on the muscular metabolic compromising induced by immobilization of posterior limb of rats

A proposta deste trabalho foi avaliar o efeito do sulfato de vanadil (SV) no perfil metabólico muscular de membro posterior imobilizado de ratos. Ratos Wistar foram divididos nos grupos (n = 6): controle (C), imobilizado em posição neutra do tornozelo (I), tratado com sulfato de vanadil (SV, 0,25mM, VO) e imobilizado tratado com SV (I + SV) durante sete dias. Após o período experimental, foram avaliadas as reservas de glicogênio (RG) dos músculos sóleo (S), gastrocnêmio branco (GB) e vermelho (GV), tibial anterior (TA) e extensor longo dos dedos (ELD), além do peso do S e ELD. A análise estatística foi realizada pela ANOVA seguida pelo teste de Tukey (p < 0,05). No grupo SV, os resultados mostraram elevação significativa nas RG (S 110 por cento, GB 71 por cento, GV 85 por cento, TA 125 por cento, EDL 108 por cento) e no peso (S 9 por cento, EDL 11 por cento). A imobilização reduziu significativamente as RG (S 31,6 por cento, GB 56,6 por cento, GV 39,1 por cento, ELD 41,7 por cento, TA 45,2 por cento) e peso (S 34,2 por cento e ELD 27 por cento); já no grupo I + SV, houve o aumento das RG em todos os músculos (S 211 por cento, GB 115 por cento, GV 148 por cento, ELD 161,9 por cento, TA 147 por cento), além de impedir a perda de peso do S (75 por cento) e ELD (46 por cento). O tratamento com sulfato de vanadil promoveu elevação nas reservas de glicogênio do grupo controle e imobilizado, além de impedir a perda de peso, demonstrando que seu efeito insulino-mimético é representado pela ação glicogênica associado a uma possível ação anticatabólica.

The purpose of this study was to evaluate the metabolic performance of immobilized skeletal muscle in rats treated with vanadyl sulphate. Male Wistar rats were divided in groups (n = 6): control (C), immobilized (I), treated with vanadyl sulphate (VS, 0,25 mM) and immobilized treated with vanadyl sulphate (I + VS) during seven days. The concentration of vanadyl sulphate diluted in water was 0,25 mM. After experimental stage, the glycogen content (GC) was evaluated in soleus (S), white gastrocnemius (WG), red gastrocnemius (RG), tibialis anterior (TA) and extensor digitorum longus (EDL) muscles, besides S and EDL weight. The statistical analysis was realized by the ANOVA followed by Tukey test (p < 0,05). In VS group, the results showed a significant increase in GC (S 110 percent, WG 71 percent, RG 85 percent, TA 125 percent, EDL 108 percent) and in the weight (S 9 percent, EDL 11 percent). The immobilization reduced significantly the GC (S 31.6 percent, WG 56.6 percent, RG 39.1 percent, EDL 41.7 percent, TA 45.2 percent) and weight (S 34.2 percent and ELD 27 percent), and in I + VS group, there was a increase of the GC in all muscles (S 211 percent, WG 115 percent, RG 148 percent, EDL 161.9 percent, TA 147 percent), besides hindering the weight loss in S (75 percent) and EDL (46 percent). The vanadyl sulphate treatment promoted an increase in the glycogen content of control and immobilized groups, besides hindering the weight loss, showing that the insulino-mimetic effect is represented by glycogenic action associate to a possible anti-catabolic action.

La propuesta de este trabajo ha sido la de evaluar el efecto del sulfato de vanadil (SV) en el perfil metabólico muscular de miembro posterior inmovilizado de ratones. Ratones Wistar fueron divididos en grupos (n = 6): control (C), inmovilizado en posición neutra de tobillo (I), tratado con sulfato de vanadil (SV, 0,25mM, VO) e inmovilizado tratado con SV (I + SV) durante 7 días. Después del periodo experimental, fueron evaluadas las reservas de glicógeno (RG) de los músculos soleo (S), gastrocnemio blanco (GB) y colorado (GV), tibial anterior (TA) y extensor largo de los dedos (ELD), además del peso de S y ELD. El análisis estadístico fue realizado por ANOVA seguido del test de Tukey (p < 0,05). En el grupo SV, los resultados mostraron elevación significativa en las RG (S 110 por ciento, GB 71 por ciento, GV 85 por ciento, TA 125 por ciento, EDL 108 por ciento) y en el peso (S 9 por ciento, EDL 11 por ciento). La inmovilización redujo significativamente las RG (S 31,6 por ciento, GB 56,6 por ciento, GV 39,1 por ciento, ELD 41,7 por ciento, TA 45,2 por ciento) y peso (S 34,2 por ciento e ELD 27 por ciento), por otro lado en el grupo I + SV, hubo aumento de las RG en todos los músculos (S 211 por ciento, GB 115 por ciento, GV 148 por ciento, ELD 161,9 por ciento, TA 147 por ciento), además de impedir la pérdida de peso de S (75 por ciento) y ELD (46 por ciento). El tratamiento con sulfato de vanadil promovió una elevación en las reservas de glicógeno del grupo control e inmovilizado, además de impedir la pérdida de peso, lo que demuestra que su efecto insulina mimético está representado por la acción glicogénica asociado a una posible acción anticatabólica.