Renewed avenues through exercise muscle contractility and inflammatory status.

Physical inactivity leads to the accumulation of visceral fat and, consequently, to the activation of a network of inflammatory pathways which may promote development of insulin resistance, atherosclerosis, neurodegeneration, and tumour growth. These conditions belong to the "diseasome of physical inactivity". In contrast, the protective effect of regular exercise against diseases associated with chronic inflammation may to some extent be ascribed to an anti-inflammatory effect. The so called "acute exercise threshold", the complex mixture of several variables involved in exercise, such as type, volume, frequency, and intensity range is capable of inducing positive physiological adaptations and has been specifically addressed in the recent literature. The major concern is related to the level of the threshold: "exercise training shifts from a therapeutic adaptive intervention to one with potential pathological consequences". Nonetheless, if the mechanical stimulus is too weak to disrupt cellular homeostasis, training adaptations will not occur. Answering these questions could present practical applications, especially during inflammatory diseases associated with detrimental muscle effects and could theoretically constitute a "new" therapeutic approach to treat/improve an inflammatory state. This paper aims to describe specific data from the literature regarding the effects of exercise on inflammatory diseases in order to promote a more sophisticated perspective on the anti-inflammatory effects of exercise.

An experimental model for resistance exercise in rodents.

This study aimed to develop an equipment and system of resistance exercise (RE), based on squat-type exercise for rodents, with control of training variables. We developed an operant conditioning system composed of sound, light and feeding devices that allowed optimized RE performance by the animal. With this system, it is not necessary to impose fasting or electric shock for the animal to perform the task proposed (muscle contraction). Furthermore, it is possible to perform muscle function tests in vivo within the context of the exercise proposed and control variables such as intensity, volume (sets and repetitions), and exercise session length, rest interval between sets and repetitions, and concentric strength. Based on the experiments conducted, we demonstrated that the model proposed is able to perform more specific control of other RE variables, especially rest interval between sets and repetitions, and encourages the animal to exercise through short-term energy restriction and "disturbing" stimulus that do not promote alterations in body weight. Therefore, despite experimental limitations, we believe that this RE apparatus is closer to the physiological context observed in humans.

Does Branched-Chain Amino Acids Supplementation Modulate Skeletal Muscle Remodeling through Inflammation Modulation? Possible Mechanisms of Action.

Skeletal muscle protein turnover is modulated by intracellular signaling pathways involved in protein synthesis, degradation, and inflammation. The proinflammatory status of muscle cells, observed in pathological conditions such as cancer, aging, and sepsis, can directly modulate protein translation initiation and muscle proteolysis, contributing to negative protein turnover. In this context, branched-chain amino acids (BCAAs), especially leucine, have been described as a strong nutritional stimulus able to enhance protein translation initiation and attenuate proteolysis. Furthermore, under inflammatory conditions, BCAA can be transaminated to glutamate in order to increase glutamine synthesis, which is a substrate highly consumed by inflammatory cells such as macrophages. The present paper describes the role of inflammation on muscle remodeling and the possible metabolic and cellular effects of BCAA supplementation in the modulation of inflammatory status of skeletal muscle and the consequences on protein synthesis and degradation.

Effects of creatine supplementation on muscle wasting and glucose homeostasis in rats treated with dexamethasone.

We aimed to investigate the possible role of creatine (CR) supplementation in counteracting dexamethasone-induced muscle wasting and insulin resistance in rats. Also, we examined whether CR intake would modulate molecular pathways involved in muscle remodeling and insulin signaling. Animals were randomly divided into four groups: (1) dexamethasone (DEX); (2) control pair-fed (CON-PF); (3) dexamethasone plus CR (DEX-CR); and (4) CR pair-fed (CR-PF). Dexamethasone (5 mg/kg/day) and CR (5 g/kg/day) were given via drinking water for 7 days. Plantaris and extensor digitorum longus (EDL) muscles were removed for analysis. Plantaris and EDL muscle mass were significantly reduced in the DEX-CR and DEX groups when compared with the CON-PF and CR-PF groups (P<0.05). Dexamethasone significantly decreased phospho-Ser473-Akt protein levels compared to the CON-PF group (P<0.05) and CR supplementation aggravated this response (P<0.001). Serum glucose was significantly increased in the DEX group when compared with the CON-PF group (DEX 7.8±0.6 vs. CON-PF 5.2±0.5 mmol/l; P<0.05). CR supplementation significantly exacerbated hyperglycemia in the dexamethasone-treated animals (DEX-CR 15.1±2.4 mmol/l; P<0.05 vs. others). Dexamethasone reduced GLUT-4 translocation when compared with the CON-PF and CR-PF (P<0.05) groups and this response was aggravated by CR supplementation (P<0.05 vs. others). In conclusion, supplementation with CR resulted in increased insulin resistance and did not attenuate muscle wasting in rats treated with dexamethasone. Given the contrast with the results of human studies that have shown benefits of CR supplementation on muscle atrophy and insulin sensitivity, we suggest caution when extrapolating this animal data to human subjects.

An overview of the therapeutic effects of leucine supplementation on skeletal muscle under atrophic conditions.

The characterization of the mechanisms underlying skeletal muscle atrophy under different conditions has been a constant focus of research. Among anti-atrophic therapies, amino acid supplementation, particularly with leucine, has received a lot of attention. Supplementation has been shown to have remarkable effects on muscle remodeling through protein turnover modulation. This may then impact physiological parameters related to muscle function, and even quality of life. In light of this, leucine supplementation could be a useful therapy for mitigating the atrophic effects of catabolic conditions. The purpose of this review is to present the major results of human studies evaluating the effects of leucine supplementation on structure and function of skeletal muscle in atrophic conditions such as muscle disuse, sarcopenia, and cancer.

Tricuríase / Trichuriasis

A tricuríase é uma doença parasitária causada pelo Trichuris trichiura, com importante impacto universal. No presente artigo é apresentada uma revisão sobre os aspectos mais relevantes da tricuríase.

Botulismo: estudo clínico / Botulism: clinical studies

O botulismo é uma doença infecciosa, neuroparalítica, envolvendo a placa motora, causada pela toxina produzida pelo Clostridium botulinum. Apresenta impacto significativo quando de sua ocorrência, com relação à gravidade dos quadros produzidos. Os autores revisam os aspectos mais relevantes da doença.

The bolulism is a neuroparalitic disease caused by toxin produced by Clostridium botulinum with important impact in public health. In this article is presented a review with the most relevant aspects of the botulism.

Doença de Whipple / Whipple's disease

Os autores apresentam uma revisão sobre a doença de Whipple, uma rara enfermidade causada pelo bacilo Gram-positivo Tropheryma whipplei, que cursa, principalmente, com manifestações gastrintestinais - entre as quais síndrome de má absorção -, musculoesqueléticas, com artralgia, envolvimento do sistema nervoso central e febre baixa, podendo ser fatal se não tratada. O diagnóstico é confirmado pela biópsia do duodeno ou de outros órgãos envolvidos e(ou) pela detecção do agente pela utilização da reação de polimerase em cadeia (PCR). A terapia consiste em antibioticoterapia, devendo ser buscada a confirmação da cura com nova biópsia.

Ancilostomíase / Ancylostomiasis

A ancilostomíase é uma doença parasitária causada pelos helmintos Ancylostoma duodenale e Necator americanus, com importante.