Effects of short-term strength training on body composition, muscle strength and functional capacity of elderly: a systematic review and meta-analysis / Efeitos do treinamento de força de curta duração sobre a composição corporal, a força muscular e a capacidade funcional de idosos: revisão sistemática e meta-análise

To examine the effects of short-term strength training (STST) on different manifestations of muscle strength in the lower limbs, functional capacity and body composition of people 65 years old or older. We searched the electronic databases (PubMed, Web of Science and Cochrane) to identify all publications using STST (up to 12 weeks) in people aged 65 or older, published in the last five years, prior to May 2018. Results were analyzed as continuous data using random effects to calculate the standardized mean difference (SMD) and the 95% confidence interval (95%CI). 28 studies with 921 subjects met the inclusion criteria and were analyzed. These works were grouped into three categories for analysis: Muscular Strength, Functional Capacity and Body Composition. In Muscular Strength category, the overall pooled effect estimate was 0.95 (95%CI: 0.63; 1.26), with a significant STST effect (Z= 5.93; p<0.001), over the different strength manifestations analyzed. In Functional Capacity category, the STST decreased the Time Up-and-Go test run time (SMD: -1.01; 95%CI: -1.56; -0.47) and increased the repetitions' number performed in 30-s chair-stand test (SMD: 1.07, 95% CI: 0.79, 1.34). In Body Composition category, the overall pooled effect estimate was 0.13 (95%CI: -0.16; 0.42), without finding a significant effect of STST (Z= 0.87; p= 0.38). STST has a moderate to large effect in improving the different manifestations of muscle strength and functional capacity. However, this type of intervention has no effect on body composition.

Examinar os efeitos do treinamento de força de curta duração (TFCD) em diferentes manifestações de força muscular nos membros inferiores, capacidade funcional e composição corporal de pessoas maiores de 65 anos. Foram pesquisadas bases de dados eletrônicas (PubMed, Web of Science e Cochrane) para identificar todas as publicações utilizando TFCD (até 12 semanas) em pessoas maiores de 65 anos, publicadas nos últimos cinco anos, antes de maio de 2018. Os resultados foram analisados como dados contínuos usando efeitos aleatórios para calcular a diferença padronizada da média (SMD) e o intervalo de confiança de 95% (IC95%). 28 estudos com 921 sujeitos preencheram os critérios de inclusão e foram analisados. Esses trabalhos foram agrupados em três categorias para análise: Força Muscular, Capacidade Funcional e Composição Corporal. Na categoria Força Muscular, a estimativa geral do efeito combinado foi de 0,95 (95% CI: 0,63; 1,26), com um efeito significativo do TFCD (Z = 5,93; p <0,001), sobre as diferentes manifestações de força analisadas. Na categoria Capacidade Funcional, o TFCD diminuiu o tempo de execução do teste Timed Up-and-Go (SMD: -1.01; 95% CI: -1.56; -0.47) e aumentou o número de repetições realizadas no teste de levantar e sentar na cadeira de 30 segundos (SMD: 1,07, IC 95%: 0,79, 1,34). Na categoria de Composição Corporal, a estimativa geral do efeito combinado foi de 0,13 (IC 95%: -0,16; 0,42), sem encontrar efeito significativo do TFCD (Z = 0,87; p = 0,38). O TFCD apresenta efeito moderado a grande na melhora das diferentes manifestações de força muscular e capacidade funcional. No entanto, este tipo de intervenção não tem efeito sobre a composição corporal.

Diclofenac pretreatment modulates exercise-induced inflammation in skeletal muscle of rats through the TLR4/NF-κB pathway.

Nonsteroidal anti-inflammatory drugs, such as diclofenac, are widely used to treat inflammation and pain in several conditions, including sports injuries. This study analyzes the influence of diclofenac on the toll-like receptor-nuclear factor kappa B (TLR-NF-κB) pathway in skeletal muscle of rats submitted to acute eccentric exercise. Twenty male Wistar rats were divided into 4 groups: control-saline, control-diclofenac, exercise-saline, and exercise-diclofenac. Diclofenac or saline were administered for 7 days prior to an acute eccentric exercise bout. The inflammatory status was evaluated through mRNA levels of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), IL-1ß, and tumor necrosis factor alpha (TNF-α), and protein content of COX-2, IL-6, and TNF-α in vastus lateralis muscle. Data obtained showed that a single bout of eccentric exercise significantly increased COX-2 gene expression. Similarly, mRNA expression and protein content of other inflammation-related genes also increased after the acute exercise. However, these effects were attenuated in the exercise + diclofenac group. TLR4, myeloid differentiation primary response gene 88 (MyD88), and p65 were also upregulated after the acute eccentric bout and the effect was blunted by the anti-inflammatory drug. These findings suggest that pretreatment with diclofenac may represent an effective tool to ameliorate the pro-inflammatory status induced by acute exercise in rat skeletal muscle possibly through an attenuation of the TLR4-NF-κB signaling pathway.

Efecto del ejercicio agudo sobre la expresión del receptor tipo Toll-4 y los mecanismos inflamatorios en corazón de rata / Effect of an acute exercise bout on Toll-like receptor 4 and inflammatory mechanisms in rat hear

Background: Toll like receptor 4 (TLR-4) is a protein located in the cell membrane with an important function in the immune response of the organism. Its activation decreases heart contractility and activates nuclear transcription factor kappa B (NF-kB ). This in turn, increases the synthesis of different pro-inflammatory cytokines and the inducible enzyme nitric oxide (iNOS), which plays an important role in the inflammatory processes when nitric oxide production is enhanced. Aim: To determine if, after one session of acute exercise, expression of TLR-4 and iNOS, and activation of NF-kB are induced in rat cardiac tissue. Material and Methods: Exercise and control groups of eight male Wistar rats each, were studied. The exercise group was subjected to an acute exercise bout lasting one hour. After the exercise, the heart was excised to measure the expression of iNOS and TLR-4 genes by quantitative polyme-rase chain reaction, NF-kB activation by electrophoretic mobility shift assay (EMSA) and p50 by Western blot. Results: After exercise, there was an increase in TLR-4 and of iNOS mRNA levels (+46.7 and +74.3% respectively). NF-kB activation and the nuclear expression of its p50 subunit also increased significantly (+240 and +306% respectively). Conclusions: Increased expression of TLR4 following a session of acute exercise may contribute to the activation of the NF-kB signaling route, promoting the synthesis of nitric oxide, which could influence negatively the cardiac response to high intensity physical exercise.

[Effect of an acute exercise bout on Toll-like receptor 4 and inflammatory mechanisms in rat heart]. / Efecto del ejercicio agudo sobre la expresión del receptor tipo Toll-4 y los mecanismos inflamatorios en corazón de rata.

BACKGROUND: Toll like receptor 4 (TLR-4) is a protein located in the cell membrane with an important function in the immune response of the organism. Its activation decreases heart contractility and activates nuclear transcription factor kappa B (NF-kB ). This in turn, increases the synthesis of different pro-inflammatory cytokines and the inducible enzyme nitric oxide (iNOS), which plays an important role in the inflammatory processes when nitric oxide production is enhanced. AIM: To determine if, after one session of acute exercise, expression of TLR-4 and iNOS, and activation of NF-kB are induced in rat cardiac tissue. MATERIAL AND METHODS: Exercise and control groups of eight male Wistar rats each, were studied. The exercise group was subjected to an acute exercise bout lasting one hour. After the exercise, the heart was excised to measure the expression of iNOS and TLR-4 genes by quantitative polyme-rase chain reaction, NF-kB activation by electrophoretic mobility shift assay (EMSA) and p50 by Western blot. RESULTS: After exercise, there was an increase in TLR-4 and of iNOS mRNA levels (+46.7 and +74.3% respectively). NF-kB activation and the nuclear expression of its p50 subunit also increased significantly (+240 and +306% respectively). CONCLUSIONS: Increased expression of TLR4 following a session of acute exercise may contribute to the activation of the NF-kB signaling route, promoting the synthesis of nitric oxide, which could influence negatively the cardiac response to high intensity physical exercise.

Nitric oxide regulates the repair of injured skeletal muscle.

Skeletal muscle repair can be understood as a balance between fibrosis and regeneration, the result of which may lead to complete recovery or loss of muscle function. To study the involvement of nitric oxide in post-trauma muscle repair, we used an experimental murine model of crush injury muscle. The animals were divided into four groups, (i) control (CO), (ii) sham trauma, (iii) trauma and (iv) trauma+l-NAME. The animals received a single dose of 100mg/kg of the l-NAME, an inhibitor of nitric oxide synthase, 2h after lesion, and the muscle tissue was analyzed in two time-points: 24h and 7 days. Twenty-four hours after injury, the crushed muscle was characterized by an intense inflammatory cell infiltrate and edema demonstrated by histological analysis. These changes were accompanied by increased iNOS, MMP-2 and HGF mRNA transcription and protein expression of the iNOS and MMP-2 in the gastrocnemius muscle. Crushing injury also promoted cell proliferation and increase number satellite cell, responsible for the regeneration of the muscle fiber. Treatment with l-NAME blocking local NO production, greatly attenuated these histological and molecular findings at 24h. On the 7th day the molecular findings of both groups were comparable to the control (sham trauma) group. However, the l-NAME group showed increase deposition of collagen and decrease of SC expression. These findings demonstrate that activation of NO during muscle crush is critical in the early phases of the skeletal muscle repair process and indicate its possible role as a regulator of the balance between fibrosis and muscle regeneration.

The role of nitric oxide during healing of trauma to the skeletal muscle.

INTRODUCTION: The role of NO in muscle injury is not clear. METHODS: We examined the involvement of the NO system in the development of muscle damage in an experimental model of crush injury. The animals were divided into four groups: (1) control (CO), (2) sham trauma, (3) trauma, (4) trauma + L -NAME, in two experimental phases, 24 h and 7 days after injury. RESULTS: Twenty-four hours post-trauma, the crushed muscle was characterized by an intense inflammatory reaction. These changes were accompanied by increased oxidative damage, increased cytokine mRNA transcription, NF-κB binding ability and TGF-ß growth factor expression in the gastrocnemius muscle. Treatment with L: -NAME markedly decreased these histological and molecular abnormalities at 24 h. However, at 7 days post-trauma, increased collagen formation was observed in the L: -NAME group. DISCUSSION: These findings indicate that NO is involved in the balance between fibrosis and healing with regeneration.

S-nitroso-N-acetylcysteine attenuates liver fibrosis in cirrhotic rats.

This study was aimed to investigate the molecular mechanisms underlying prevention of hepatic fibrosis by S-nitroso-N-acetylcysteine (SNAC), a nitric oxide donor that inhibits lipid peroxidation. Secondary biliary cirrhosis was induced by 4 weeks of common bile duct ligation (CBDL). Both sham-operated and CBDL animals received SNAC (6.0 micromol/kg/day) starting 2 weeks after surgery. SNAC treatment reduced the increase in blood enzyme activities (alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase), induced by CBDL. Histological changes were attenuated and there was a significant decrease in the area of liver fibrosis and in the activation of stellate cells measured by alpha-smooth muscle actin (alpha-SMA) immunostaining. The increase in TBARS concentration and hydroperoxide-induced chemiluminescence were also reduced by SNAC treatment. SNAC down-regulated expression of collagen 1 alpha, alpha-SMA, tumor necrosis factor-alpha, tumor growth factor-beta, metalloproteinase-2, metalloproteinase inhibitor 1, platelet-derived growth factor (PDGF), and PDGF receptor in CBDL rats. These effects were accompanied by inhibited activation of extracellular signal-regulated kinases, Jun amino-terminal kinases, p38 and Akt. Antifibrotic effects were more efficient than those of the free thiol NAC administered at a dose of 60 mumol/kg. In conclusion, results obtained indicate that SNAC, beyond its antioxidant capacity, exerts antifibrotic effects in rats with secondary biliary cirrhosis by down-regulating increased expression of genes and modulating intracellular signaling pathways that contribute to the accumulation of matrix proteins. Thus, SNAC may be an interesting candidate for the treatment of human fibrosis and cirrhosis.