Search

While chemotherapy treatment can be lifesaving, it also has adverse effects that negatively impact the quality of life. To investigate the effects of doxorubicin chemotherapy on body weight loss, strength and muscle mass loss, and physical function impairments, all key markers of cachexia, sarcopenia, and frailty. Seventeen C57/BL/6 mice were allocated into groups. 1) Control (n = 7): mice were exposed to intraperitoneal (i.p.) injections of saline solution. 2) Dox (n = 10): mice were exposed to doxorubicin chemotherapy cycles (total dose of 18 mg/kg divided over 15 days). The body weight loss and decreased food intake were monitored to assess cachexia. To assess sarcopenia, we measured muscle strength loss using a traction method and evaluated muscle atrophy through histology of the gastrocnemius muscle. To evaluate physical function impairments and assess frailty, we employed the open field test to measure exploratory capacity. Doxorubicin administration led to the development of cachexia, as evidenced by a significant body weight loss (13%) and a substantial decrease in food intake (34%) over a 15-day period. Furthermore, 90% of the mice treated with doxorubicin exhibited sarcopenia, characterized by a 20% reduction in traction strength (p

Abstract Statins are cholesterol-lowering drugs commonly used among people with HIV, associated with an increased risk of myopathies. Considering that cardiovascular disease, statin therapy, and sarcopenia are independently prevalent in people with HIV, clarity on the potential benefits or harms of statin therapy on muscle health is useful to provide insight into ways to maximize skeletal muscle health and minimize CVD risk in this population. We aimed to study the effects of statin therapy on strength, muscle mass, and physical function parameters in people with HIV. This was a pilot cross-sectional study. People with HIV on continuous statin therapy (n = 52) were paired 1:1 according to age (people with HIV 53.9 ± 8.2 and people with HIV on statins 53.9 ± 8.4 years), sex, body mass index (Body mass index, people with HIV 28.6 ± 5.3 and people with HIV on statins 28.8 ± 6.3 kg/m2), and race with people with HIV not using statin (n = 52). Participants were evaluated for muscle strength (i.e. handgrip strength), lean and fat body mass (using bioelectric impedance analysis), and physical function (i.e. Short Physical Performance Battery—SPPB). Isokinetic strength and appendicular lean mass (using dual-energy X-ray absorptiometry), more accurate strength and body composition measures, were determined in 38% of the participants. Overall, statin usage does not exacerbated loss of muscle strength (32.2 ± 11.5 vs. 30.3 ± 9.6 kg, p > 0.05) muscle mass (7.6 ± 1.8 vs. 7.7 ± 1.1 kg/m2, p > 0.05), and impaired physical performance (10.1 ± 1.8 vs. 9.7 ± 2.1 points, p > 0.05) of PLWH. When analyzed by sex, men living with HIV on statins usage presented higher appendicular muscle mass (28.4 ± 3.1 vs. 26.2 ± 4.9 kg, p

ABSTRACT Exercise is a relevant tool in the oncology rehabilitation program due to restoring functional capacity, improving quality of life, and preventing early cancer mortality, mainly in unfit cancer patients. According to a systematic physical evaluation and risk stratification model, exercise physiologists (or equivalent) and physiotherapists with additional cancer exercise training are candidates to provide and supervise exercise to cancer survivors. However, the referral pathways are unclear, and a few cancer survivors are educated about personalized exercise oncology programs. This article aims to engage and stimulate additional training of Exercise physiologists and Physiotherapists in a collaborative exercise oncology program and proposes a dynamic and supervised model to attend to the emerging multidisciplinary scenario of cancer.

ABSTRACT People living with HIV (PLH), who use antiretroviral therapy (ART), are more susceptible to changes in the inflammatory profile and oxidative stress, and women have greater access to ART. Although physical exercise is a complementary strategy to treatment due to its antioxidant and anti-inflammatory effects, it is not clear whether acute responses to exercise can be harmful to PLH. The aim of the study was to investigate the acute effect of resistance exercise (RE) on inflammatory and oxidative stress markers in PLH. Ten women, using ART, performed RE session consisting of seven exercises for the whole body. For biochemical evaluation, blood samples were collected before (pre), 1 hour (1h) and 2 hours (2h) after the RE session. One-way ANOVA followed by Bonferroni's post hoc test was used to compare results between time points. There was an increase only in markers, GSSG of 160% (pre: 0.40 ± 0.11; 1h: 1.18 ± 0.36; 2h: 1.04 ± 0.25 mmol/g), TNF-α of 98 % (pre: 4.60 ± 0.55; 1h: 6.95 ± 0.77; 2h: 9.10 ± 1.03 pg/ml) and 52% IL-6 (pre: 2.47 ± 0 .67; 1h: 3.63 ± 1.26; 2h: 5.38 ± 2.15 pg/ml). The other variables remained unchanged (P > 0.05). It is concluded that a RE session increased the levels of inflammatory markers and oxidative stress in PLH in a non-exacerbated way.

BackgroundThe purpose of this review was to analyze the acute effects of low-load resistance exercise with blood flow restriction (LLE-BFR) on oxidative stress markers in healthy individuals in comparison with LLE or high-load resistance exercise (HLRE) without BFR.Materials and methodsA systematic review was performed in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. These searches were performed in CENTRAL, SPORTDiscus, EMBASE, PubMed, CINAHL and Virtual Health Library- VHL, which includes Lilacs, Medline and SciELO. The risk of bias and quality of evidence were assessed through the PEDro scale and GRADE system, respectively.ResultsThirteen randomized clinical trials were included in this review (total n = 158 subjects). Results showed lower post-exercise damage to lipids (SMD = -0.95 CI 95%: -1.49 to -0. 40, I2 = 0%, p = 0.0007), proteins (SMD = -1.39 CI 95%: -2.11 to -0.68, I2 = 51%, p = 0.0001) and redox imbalance (SMD = -0.96 CI 95%: -1.65 to -0.28, I2 = 0%, p = 0.006) in favor of LLRE-BFR compared to HLRE. HLRE presents higher post-exercise superoxide dismutase activity but in the other biomarkers and time points, no significant differences between conditions were observed. For LLRE-BFR and LLRE, we found no difference between the comparisons performed at any time point.ConclusionsBased on the available evidence from randomized trials, providing very low or low certainty of evidence, this review demonstrates that LLRE-BFR promotes less oxidative stress when compared to HLRE but no difference in levels of oxidative damage biomarkers and endogenous antioxidants between LLRE.Trial registrationRegister number: PROSPERO number: CRD42020183204.

Objective: This article describes the development process and summarizes the results of the Brazilian physical activity recommendations for cancer prevention and control, which was prepared to support health-care professionals. Material and Methods: These recommendations were elaborated considering: (i) the effect of physical activity on cancer prevention in the general healthy population; and (ii) on all-cause and cancer-specific mortality in cancer survivors. The process of preparing the recommendations was systematized, transparent and reproducible, following the recommendations of the appraisal of guidelines for research and evaluation (AGREE-II). We appraised the certainty of evidence for breast, prostate, colorectal and lung cancers, which are among the most frequent in Brazil, using the grading of recommendations, assessment, development and evaluations (GRADE) approach. Results: Regarding the risk of cancer, we found high certainty of evidence supporting the association between moderate-to-vigorous physical activity and lower risk of breast and colon cancer, moderate certainty of evidence for lung cancer and low certainty of evidence for prostate and rectal cancer. We found moderate certainty of evidence supporting the association between moderate-to-vigorous physical activity and reduction of all-cause and cancer-specific mortality from breast, colon and rectal cancer, and cancer-specific mortality from prostate cancer, when physical activity was performed after the disease diagnosis. We found low certainty of evidence for the association between physical activity and lung cancer mortality. Based on our findings, physical activity recommendations were proposed, including a step-by-step guide to support health-care professionals when recommending physical activity for all adults (including elderly people), with or without a diagnosis of cancer. Conclusion: Our recommentations may be useful to support health-care professionals counselling for physical activity, which contribute to reductions in physical inactivity in the general population and in the growing population of cancer survivors.

Endurance exercise training promotes a protective phenotype in skeletal muscle known as exercise preconditioning. Exercise preconditioning protects muscle fibers against a variety of threats including inactivity-induced muscle atrophy. The mechanism(s) responsible for exercise preconditioning remain unknown and are explored in these experiments. Specifically, we investigated the impact of endurance exercise training on key components of the renin-angiotensin system (RAS). The RAS was targeted because activation of the classical axis of the RAS pathway via angiotensin II type I receptors (AT1Rs) promotes muscle atrophy whereas activation of the non-classical RAS axis via Mas receptors (MasRs) inhibits the atrophic signaling of the classical RAS pathway. Guided by prior studies, we hypothesized that an exercise-induced decrease in AT1Rs and/or increases in MasRs in skeletal muscle fibers is a potential mechanism responsible for exercise preconditioning. Following endurance exercise training in rats, we examined the abundance of AT1Rs and MasRs in both locomotor and respiratory muscles. Our results indicate that endurance exercise training does not alter the protein abundance of AT1Rs or MasRs in muscle fibers from the diaphragm, plantaris, and soleus muscles compared to sedentary controls (p ​> ​0.05). Furthermore, fluorescent angiotensin II (AngII) binding analyses confirm our results that exercise preconditioning does not alter the protein abundance of AT1Rs in the diaphragm, plantaris, and soleus (p ​> ​0.05). This study confirms that exercise-induced changes in RAS receptors are not a key mechanism that contributes to the beneficial effects of exercise preconditioning in skeletal muscle fibers.

Abstract Mechanical ventilation (MV) is a life‐saving instrument used to provide ventilatory support for critically ill patients and patients undergoing surgery. Unfortunately, an unintended consequence of prolonged MV is the development of inspiratory weakness due to both diaphragmatic atrophy and contractile dysfunction; this syndrome is labeled ventilator‐induced diaphragm dysfunction (VIDD). VIDD is clinically important because diaphragmatic weakness is an important contributor to problems in weaning patients from MV. Investigations into the pathogenesis of VIDD reveal that oxidative stress is essential for the rapid development of VIDD as redox disturbances in diaphragm fibers promote accelerated proteolysis. Currently, no standard treatment exists to prevent VIDD and, therefore, developing a strategy to avert VIDD is vital. Guided by evidence indicating that activation of the classical axis of the renin‐angiotensin system (RAS) in diaphragm fibers promotes oxidative stress and VIDD, we hypothesized that activation of the nonclassical RAS signaling pathway via angiotensin 1‐7 (Ang1‐7) will protect against VIDD. Using an established animal model of prolonged MV, our results disclose that infusion of Ang1‐7 protects the diaphragm against MV‐induced contractile dysfunction and fiber atrophy in both fast and slow muscle fibers. Further, Ang1‐7 shielded diaphragm fibers against MV‐induced mitochondrial damage, oxidative stress, and protease activation. Collectively, these results reveal that treatment with Ang1‐7 protects against VIDD, in part, due to diminishing oxidative stress and protease activation. These important findings provide robust evidence that Ang1‐7 has the therapeutic potential to protect against VIDD by preventing MV‐induced contractile dysfunction and atrophy of both slow and fast muscle fibers.

PurposeAlthough the role of signal transducers and activators of transcription (STAT3) in cachexia due to the association of circulating IL-6 and muscle wasting has been extensively demonstrated, the effect of resistance training on STAT3 in mediating muscle atrophy in tumor-bearing mice is unknown. The aim of this study is to investigate the effects of resistance exercise training on inflammatory cytokines and oxidative-mediated STAT3 activation and muscle loss prevention in tumor-bearing mice.MethodsMale Swiss mice were inoculated with Ehrlich tumor cells and exposed or not exposed to resistance exercise protocol of ladder climbing. Skeletal muscle STAT3 protein content was measured, compared between groups, and tested for possible association with plasma interleukins and local oxidative stress markers. Components of the ubiquitin-proteasome and autophagy pathways were assessed by real-time PCR or immunoblotting.ResultsResistance training prevented STAT3 excessive activation in skeletal muscle mediated by the overabundance of plasma IL-6 and muscle oxidative stress. These mechanisms contributed to preventing the increased key genes and proteins of ubiquitin-proteasome and autophagy pathways in tumor-bearing mice, such as Atrogin-1, LC3B-II, and Beclin-1. Beyond preventing muscle atrophy, RT also prevented strength loss and impaired locomotor capacity, hallmarks of sarcopenia.ConclusionOur results suggest that STAT3 inhibition is central in resistance exercise protective effects against cancer-induced muscle atrophy and strength loss.

ABSTRACT It is now well-known that physical activity and exercise are both able to prevent the appearance of different types of cancer, increase survival, improve quality of life and attenuate the adverse effects caused by cancer and its treatment. Therefore, the current recommendation is that every cancer survivor must be encouraged to stay active, begin or keep exercising after the cancer diagnosis, contrary to the recommendation of 20 years ago to “rest and avoid physical efforts”. In fact, physical exercise is now recognized as a reliable, inexpensive, adverse effect-free, safe and relatively simple tool to be incorporated into the context of cancer treatment. However, Brazil has not contributed and is not part of the agenda to make exercise as a standard in cancer care. This literature review aims to present the scientific evidence of the use of physical exercise in the different stages of cancer treatment and the most recent contributions to the development of exercise prescription for people with cancer. In addition, I will discuss the main challenges and future perspectives for the area of exercise oncology, considering the Brazilian context.

Abstract Investigations of plasma amino acids in early psychosis and their unaffected siblings are rare. We measured plasma amino acids involved in the co-activation of dopaminergic, GABAergic, glutamatergic, and serotoninergic neurotransmitters in first-episode psychosis (FEP) patients (n = 166), unaffected siblings (n = 76), and community-based controls (n = 166) included in a cross-sectional study. Plasma levels of glutamic acid (GLU), glutamine, glycine, proline (PRO), tryptophan (TRP), tyrosine, serine and GABA were quantified by gas-chromatography-mass spectrometry. We used the generalized linear model adjusted by sex, age, and body mass index for group comparison and paired t-test for FEP-Sibling pairs. FEP had reduced GABA plasma levels compared to siblings and controls (p

The first report demonstrating that prolonged endurance exercise promotes oxidative stress in humans was published more than 4 decades ago. Since this discovery, many ensuing investigations have corroborated the fact that muscular exercise increases the production of reactive oxygen species (ROS) and results in oxidative stress in numerous tissues including blood and skeletal muscles. Although several tissues may contribute to exercise-induced ROS production, it is predicted that muscular contractions stimulate ROS production in active muscle fibers and that skeletal muscle is a primary source of ROS production during exercise. This contraction-induced ROS generation is associated with (1) oxidant damage in several tissues (e.g., increased protein oxidation and lipid peroxidation), (2) accelerated muscle fatigue, and (3) activation of biochemical signaling pathways that contribute to exercise-induced adaptation in the contracting muscle fibers. While our understanding of exercise and oxidative stress has advanced rapidly during the last decades, questions remain about whether exercise-induced increases in ROS production are beneficial or harmful to health. This review addresses this issue by discussing the site(s) of oxidant production during exercise and detailing the health consequences of exercise-induced ROS production.

We tested the hypothesis that creatine supplementation may potentiate exercise’s protective effects against doxorubicin-induced hepatotoxicity. Thirty-eight Swiss mice were randomly allocated into five groups: control (C, n = 7), exercised (Ex, n = 7), treated with doxorubicin (Dox, n = 8), treated with doxorubicin and exercised (DoxEx, n = 8), and treated with doxorubicin, exercised, and supplemented with creatine (DoxExCr, n = 8). Doxorubicin was administered weekly (i.p.) for a total dose of 12 mg/kg. Creatine supplementation (2% added to the diet) and strength training (climbing stairs, 3 times a week) were performed for a total of 5 weeks. The results demonstrated that doxorubicin caused hepatotoxicity, which was evidenced by increased (p < 0.05) hepatic markers of inflammation (i.e., TNF-α and IL-6) and oxidative damage, while the redox status (GSH/GSSG) was reduced. The plasma concentrations of liver transaminases were also significantly (p < 0.05) elevated. Furthermore, doxorubicin-treated animals presented hepatic fibrosis and histopathological alterations such as cellular degeneration and the infiltration of interstitial inflammatory cells. Exercise alone partly prevented doxorubicin-induced hepatotoxicity; thus, when combined with creatine supplementation, exercise was able to attenuate inflammation and oxidative stress, morphological alterations, and fibrosis. In conclusion, creatine supplementation potentiates the protective effects of exercise against doxorubicin-induced hepatotoxicity in mice.

Introdução: A sarcopenia é definida como uma desordem muscular esquelética progressiva e generalizada que está associada a maior probabilidade de complicações de saúde, incluindo quedas, fraturas, incapacidade física e mortalidade. Esta desordem, anteriormente entendida como uma condição inerente à idade, apresenta causas diferentes e afeta muitos indivíduos independentemente da idade. A sarcopenia é atualmente reconhecida como uma condição patológica e foi incluída na Classificação Internacional de Doenças (CID-10-CM – M62.84). Objetivo: Apresentar uma revisão literária sobre as causas da sarcopenia, epidemiologia e forma e métodos de diagnóstico atualmente utilizados. Fontes de dados: MEDLINE/PubMed, Embase e SciELO (pesquisa inicial) e referências bibliográficas dos artigos selecionados da pesquisa primária (pesquisa em cascata). Métodos de revisão: Utilizou-se uma combinação dos seguintes termos: sarcopenia, diagnóstico, definição operacional, prevalência, consequências. Foram considerados artigos originais, artigos de revisão, diretrizes clínicas e consensos em inglês e português publicados desde 1989 (ano da proposta do termo sarcopenia) até maio de 2020. Resultados: As principais referências selecionadas foram os artigos que tratavam da definição de sarcopenia. Foram também selecionados os artigos relacionados com testes e avaliações utilizados para o diagnóstico da sarcopenia e artigos que descrevem a prevalência da sarcopenia em diferentes populações. Conclusões: Considerando a evolução histórica do diagnóstico da doença, é notório tentar aproximar o conhecimento científico da prática clínica com a sugestão de métodos e pontos de corte que facilitam a identificação imediata da sarcopenia. No entanto, há um elevado número de diferentes posições e definições operacionais de sarcopenia, o que dificulta a determinação da prevalência real. Apesar dos recentes desenvolvimentos na compreensão da sarcopenia, uma definição operacional definitiva e a melhor forma de diagnosticar a sarcopenia ainda são motivo de debate. Assim, acredita-se que a atual definição operacional não é definitiva e pode sofrer alterações consideráveis à medida que o conhecimento sobre a sarcopenia se desenvolve.

Mechanical ventilation (MV) is a life-saving intervention for many critically ill patients. Unfortunately, an unintended consequence of prolonged MV is the rapid development of diaphragmatic atrophy and contractile dysfunction, known as ventilator-induced diaphragm dysfunction (VIDD). Although the mechanism(s) responsible for VIDD are not fully understood, abundant evidence reveals that oxidative stress leading to the activation of the major proteolytic systems (i.e., autophagy, ubiquitin-proteasome, caspase, and calpain) plays a dominant role. Of the proteolytic systems involved in VIDD, calpain has received limited experimental attention due to the longstanding dogma that calpain plays a minor role in inactivity-induced muscle atrophy. Guided by preliminary experiments, we tested the hypothesis that activation of calpains play an essential role in MV-induced oxidative stress and the development of VIDD. This premise was rigorously tested by transgene overexpression of calpastatin, an endogenous inhibitor of calpains. Animals with/without transfection of the calpastatin gene in diaphragm muscle fibers were exposed to 12 h of MV. Results confirmed that overexpression of calpastatin barred MV-induced activation of calpain in diaphragm fibers. Importantly, deterrence of calpain activation protected the diaphragm against MV-induced oxidative stress, fiber atrophy, and contractile dysfunction. Moreover, prevention of calpain activation in the diaphragm forstalled MV-induced mitochondrial dysfunction and prevented MV-induced activation of caspase-3 along with the transcription of muscle specific E3 ligases. Collectively, these results support the hypothesis that calpain activation plays an essential role in the early development of VIDD. Further, these findings provide the first direct evidence that calpain plays an important function in inactivity-induced mitochondrial dysfunction and oxidative stress in skeletal muscle fibers.

High-intensity exercise increases reactive oxygen species formation, which in excess may cause oxidative stress. We assessed nutritional status and exercise-induced oxidative stress in 20 adolescent male soccer players (age: 15-17). Participants were divided into two teams for a 60-minute friendly match and evaluated immediately before (Pre-match), 30 minutes after (Post-match I) and 24 hours after (Post-match II) the game. All players recorded a 3-day dietary intake. Biochemical tests were performed for lipid profile, muscle damage (creatinine and creatinine kinase [CK]) and oxidative stress (thiobarbituric acid-reactive substances [TBARS], protein carbonyls [PC], reduced glutathione [GSH], and vitamins E, C, and A). CK and creatinine were significantly elevated at Post-match I (p < 0.01), returning to baseline at Post-match II. Vitamins E, C and A were significantly elevated at Post-match I (p < 0.01), but only vitamins E and A remained high at Post-match II. TBARS showed no significant changes. GSH showed a significant decrease (p < 0.01) and PC showed a slight but significant increase (p < 0.01) at Post-match II. The recruitment of non-enzymatic antioxidants prevented lipid peroxidation, but dietary and especially endogenous defence responses were insufficient to prevent protein oxidation. Proper nutrition is essential to improve the activity of the antioxidant defence system, preventing exercise-induced oxidative stress.

Abstract Aim: Determine the relationship between changes in oxidative stress markers, muscle damage, DOMS, and their relationship with performance in response to a session of football training during a 1-week recovery period of young football players. Methods: Nineteen young football players aged 16.7±1.0 years were included in the study. After initial evaluation for basal levels of oxidative stress and muscle damage markers, DOMS, and performance testing (Vertical Jump, Agility T-test, and RAST potency test), the athletes were submitted to a routine training session composed of squatting exercises, followed by a simulated football match of 45 minutes. Athletes were reevaluated for 3 consecutive days (24h, 48h, and 72h after the training session) during the recovery week. Results: An elevated DOMS score in the quadriceps and posterior thigh (P

Background: Increasing evidence has shown that an elevated a level of homocysteine (Hcy) in the blood is related to several diseases. Over the last few years, studies have demonstrated creatine (Cr) synthesis and Hcy formation are metabolically connected; and Cr supplementation can decrease Hcy blood levels in different situations. This data however is inconsistent and still controversial. Objective: The aim of this critical review with meta-analysis was to discuss and ascertain the effects of Cr supplementation on blood Hcy levels. Method: A review was conducted according to the PRISMA guidelines using PubMed Discuss and Scielo online databases to identify relevant studies through November 2015. RevMan was used to calculate the effect size of the change in Hcy plasma/serum concentration from baseline to post-supplementation with Cr vs. placebo groups. Weighted mean differences were calculated using random effect models. Results: Cr supplemented trials were divided into two subgroups according to whether the experimental design included animals or humans participants. Overall, 14 studies were included in the meta-analysis. The six rodent included studies reported decreased plasma Hcy concentration after Cr supplementation with a mean effect size equal to −2.43 μmol/l (95% CI: 3.60, −1.26, P

Abundant evidence reveals that activation of the renin-angiotensin system promotes skeletal muscle atrophy in several conditions including congestive heart failure, chronic kidney disease, and prolonged mechanical ventilation. However, controversy exists about whether circulating angiotensin II (AngII) promotes skeletal muscle atrophy by direct or indirect effects; the centerpiece of this debate is the issue of whether skeletal muscle fibers express AngII type 1 receptors (AT1Rs). While some investigators assert that skeletal muscle expresses AT1Rs, others argue that skeletal muscle fibers do not contain AT1Rs. These discordant findings in the literature are likely the result of study design flaws and additional research using a rigorous experimental approach is required to resolve this issue. We tested the hypothesis that AT1Rs are expressed in both human and rat skeletal muscle fibers. Our premise was tested using a rigorous, multi-technique experimental design. First, we established both the location and abundance of AT1Rs on human and rat skeletal muscle fibers by means of an AngII ligand-binding assay. Second, using a new and highly selective AT1R antibody, we carried out Western blotting and determined the abundance of AT1R protein within isolated single muscle fibers from humans and rats. Finally, we confirmed the presence of AT1R mRNA in isolated single muscle fibers from rats. Our results support the hypothesis that AT1Rs are present in both human and rat skeletal muscle fibers. Moreover, our experiments provide the first evidence that AT1Rs are more abundant in fast, type II muscle fibers as compared with slow, type I fibers. Together, these discoveries provide the foundation for an improved understanding of the mechanism(s) responsible for AngII-induced skeletal muscle atrophy.

Meta-analyses have shown that supervised isometric handgrip training reduces blood pressure in hypertensives. However, the mechanism(s) underlying these effects in medicated hypertensive patients, as well as the effects from home-based exercise training, is uncertain. The purpose of this study was to compare the effects of supervised and home-based isometric handgrip training on cardiovascular parameters in medicated hypertensives. In this randomized controlled trial, 72 hypertensive individuals (38–79 years old, 70% female) were randomly assigned to three groups: home-based, supervised isometric handgrip training or control groups. Home-based and supervised isometric handgrip training was completed thrice weekly (4 × 2 min at 30% of maximal voluntary contraction, with 1-min rest between bouts, alternating the hands). Before and after 12 weeks brachial, central and ambulatory blood pressures (BP), arterial stiffness, heart rate variability, vascular function, oxidative stress and inflammation markers were obtained. No significant (p > 0.05) effect was observed for ambulatory BP, arterial stiffness, heart rate variability, vascular function and oxidative stress and inflammatory markers in all three groups. Brachial BP decreased in the supervised group (Systolic: 132 ± 4 vs. 120 ± 3 mmHg; Diastolic: 71 ± 2 vs. 66 ± 2 mmHg, p < 0.05), whereas no significant differences were observed in the home-based (Systolic: 130 ± 4 vs. 126 ± 3 mmHg; diastolic: 73 ± 3 vs. 71 ± 3 mmHg) and control groups (p > 0.05). Supervised handgrip exercise also reduced central BP systolic (120 ± 5 vs. 109 ± 5 mmHg), diastolic (73 ± 2 vs. 67 ± 2 mmHg); and mean BP (93 ± 3 vs. 84 ± 3 mmHg), whereas no significant effects were found in the home-based (Systolic: 119 ± 4 vs. 115 ± 3 mmHg; Diastolic: 74 ± 3 vs. 71 ± 3 mmHg) and control groups (p > 0.05). In conclusion, supervised, but not home-based, isometric training lowered brachial and central BP in hypertensives.

BACKGROUND:Capillary rather than venipuncture may be a simpler and less invasive blood collection protocol that would increase the number of potential sampling tests. However, if capillary sampling can be used as an alternative to venipuncture to determine changes in plasma, total creatine kinase (CK) activity in response to a football training session is poorly known. OBJECTIVE:This study aims to determine whether capillary blood sampling would provide representative measures of total CK activity compared to venipuncture in response to a football training session-induced elevated CK plasma levels. METHODS:Twenty-two players from an under-19 football team performed a simulated football match with 11 players on each team for 90 minutes total duration (two halves of 45 minutes with 15 minutes rest between). Venous and ear lobe capillary blood samples were collected before and after (24h and 48h) the training session. Athletes retested for three consecutive days after exercise during the recovery week. RESULTS:The simulated match significantly increased (P< 0.05) total CK activity as determined in both venous (1.7-fold) and capillary (1.9-fold) blood sampling. Total CK activity determined using capillary samples demonstrated significant correlation (r = 0.85; P < 0.01) and an elevated concordance Lin index (pc = 0.80) when compared to venous sampling total CK. The Bland-Altman plot showed capillary sampling CK overestimated venous CK levels by 130 U/L (61%), with moderated variance and low bias. CONCLUSIONS:Our results demonstrated that capillary sampling for total CK activity assay may be considered a reliable alternative to venipuncture to determine changes in plasma total CK activity in response to a football training session.

Introduction: In order to examine the effectiveness of vitamin C (ascorbic acid) in combating the oxidative insult caused by Trypanosoma cruzi during the development of the chronic phase of Chagas disease, Swiss mice were infected intraperitoneally with 5.0 × 104 trypomastigotes of T. cruzi QM1strain. Methods: Mice were given supplements of two different doses of vitamin C for 180 days. Levels of lipid oxidation (as indicated by thiobarbituric acid reactive substances-TBARS), total peroxide, vitamin C, and reduced glutathione were measured in the plasma, TBARS, total peroxide and vitamin C were measured in the myocardium and histopathologic analysis was undertaken in heart, colon and skeletal muscle. Results: Animals that received a dose equivalent to 500 mg of vitamin C daily showed increased production of ROS in plasma and myocardium and a greater degree of inflammation and necrosis in skeletal muscles than those that received a lower dose or no vitamin C whatsoever. Conclusion: Although some research has shown the antioxidant effect of vitamin C, the results showed that animals subject to a 500 mg dose of vitamin C showed greater tissue damage in the chronic phase of Chagas disease, probably due to the paradoxical actions of the substance, which in this pathology, will have acted as a pro-oxidant or pro-inflammatory.

This study aimed to examine the benefits of different amounts of omega-3 (n-3) polyunsaturated fatty acids from fish oil (FO) on lipid metabolism, insulin resistance and gene expression in rats fed a high-fructose diet. Male Wistar rats were separated into two groups: Control (C, n = 6) and Fructose (Fr, n = 32), the latter receiving a diet containing 63% by weight fructose for 60 days. After this period, 24 animals from Fr group were allocated to three groups: FrFO2 (n = 8) receiving 63% fructose and 2% FO plus 5% soybean oil; FrFO5 (n = 8) receiving 63% fructose and 5% FO plus 2% soybean oil; and FrFO7 (n = 8) receiving 63% fructose and 7% FO. Animals were fed these diets for 30 days. Fructose led to an increase in liver weight, hepatic and serum triacylglycerol, serum alanine aminotransferase and HOMA1-IR index. These alterations were reversed by 5% and 7% FO. FO had a dose-dependent effect on expression of genes related to hepatic β-oxidation (increased) and hepatic lipogenesis (decreased). The group receiving the highest FO amount had increased markers of oxidative stress. It is concluded that n-3 fatty acids may be able to reverse the adverse metabolic effects induced by a high fructose diet.

Muscle wasting has been emerging as one of the principal components of cancer cachexia, leading to progressive impairment of work capacity. Despite early stages melanomas rarely promotes weight loss, the appearance of metastatic and/or solid tumor melanoma can leads to cachexia development. Here, we investigated the B16F10 tumor-induced cachexia and its contribution to muscle strength and locomotor-like activity impairment. C57BL/6 mice were subcutaneously injected with 5 × 104 B16F10 melanoma cells or PBS as a Sham negative control. Tumor growth was monitored during a period of 28 days. Compared to Sham mice, tumor group depicts a loss of skeletal muscle, as well as significantly reduced muscle grip strength and epididymal fat mass. This data are in agreement with mild to severe catabolic host response promoted by elevated serum tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and lactate dehydrogenase (LDH) activity. Tumor implantation has also compromised general locomotor activity and decreased exploratory behavior. Likewise, muscle loss, and elevated inflammatory interleukin were associated to muscle strength loss and locomotor activity impairment. In conclusion, our data demonstrated that subcutaneous B16F10 melanoma tumor-driven catabolic state in response to a pro-inflammatory environment that is associated with impaired skeletal muscle strength and decreased locomotor activity in tumor-bearing mice.

OBJECTIVE: The objective of this study was to assess the effects of resistance training on oxidative stress markers in the livers of ovariectomized rats. METHOD: Adult Sprague-Dawley rats were divided into the following four groups (n = 8 per group): sham-operated sedentary, ovariectomized sedentary, sham-operated resistance training, and ovariectomized resistance training. During the resistance training period, the animals climbed a 1.1-m vertical ladder with weights attached to their tails; the sessions were conducted 3 times per week, with 4-9 climbs and 8-12 dynamic movements per climb. The oxidative stress was assessed by measuring the levels of reduced glutathione and oxidized glutathione, the enzymatic activity of catalase and superoxide dismutase, lipid peroxidation, vitamin E concentrations, and the gene expression of glutathione peroxidase. RESULTS: The results showed significant reductions in the reduced glutathione/oxidized glutathione ratio (4.11±0.65 nmol/g tec), vitamin E concentration (55.36±11.11 nmol/g), and gene expression of glutathione peroxidase (0.49±0.16 arbitrary units) in the livers of ovariectomized rats compared with the livers of unovariectomized animals (5.71±0.71 nmol/g tec, 100.14±10.99 nmol/g, and 1.09±0.54 arbitrary units, respectively). Moreover, resistance training for 10 weeks was not able to reduce the oxidative stress in the livers of ovariectomized rats and induced negative changes in the hepatic anti-oxidative/oxidative balance. CONCLUSION: Our findings indicate that the resistance training program used in this study was not able to attenuate the hepatic oxidative damage caused by ovariectomy and increased the hepatic oxidative stress.

BACKGROUND:Although studies have demonstrated that physical exercise alters homocysteine levels in the blood, meta-analyses of the effects of acute exercise and exercise training on homocysteine blood concentration have not been performed, especially regarding the duration and intensity of exercise, which could affect homocysteine levels differently. OBJECTIVE:The aim of this meta-analysis was to ascertain the effects of acute exercise and exercise training on homocysteine levels in the blood. METHOD:A review was conducted according to the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses using the online databases PubMed, SPORTDiscus, and SciELO to identify relevant studies published through June 2015. Review Manager was used to calculate the effect size of acute exercise and exercise training using the change in Hcy plasmaserum concentration from baseline to post-acute exercise and trained vs. sedentary control groups, respectively. Weighted mean differences were calculated using random effect models. RESULTS:Given the abundance of studies, acute exercise trials were divided into two subgroups according to exercise volume and intensity, whereas the effects of exercise training were analyzed together. Overall, 22 studies with a total of 520 participants indicated increased plasma homocysteine concentration after acute exercise (1.18 μmol/L, 95% CI: 0.71 to 1.65, p < .01). Results of a subgroup analysis indicated that either long-term exercise of low-to-moderate intensity (1.39 μmol/L, 95% CI: 0.9 to 1.89, p < .01) or short-term exercise of high intensity (0.83 μmol/L, 95% CI: 0.19 to 1.40, p < .01) elevated homocysteine levels in the blood. Increased homocysteine induced by exercise was significantly associated with volume of exercise, but not intensity. By contrast, resistance training reduced plasma homocysteine concentration (-1.53 μmol/L, 95% CI: -2.77 to -0.28, p = .02), though aerobic training did not. The cumulative results of the seven studies with a total of 230 participants in exercise training analysis did not demonstrate a significant impact on homocysteine levels in the blood (-0.56 μmol/L, 95% CI: -1.61 to 0.50, p = .23). CONCLUSIONS:Current evidence demonstrates that acute exercise increases homocysteine levels in the blood independent of exercise duration and intensity. Resistance, but not aerobic training decreases plasma homocysteine levels.

The tissue changes that occur in Chagas disease are related to the degree of oxidative stress and antioxidant capacity of affected tissue. Studies with vitamin C supplementation did not develop oxidative damage caused by Chagas disease in the host, but other studies cite the use of peroxiredoxins ascorbate - dependent on T. cruzi to offer protection against immune reaction. Based on these propositions, thirty "Swiss" mice were infected with T. cruzi QM1 strain and treated with two different vitamin C doses in order to study the parasitemia evolution, histopathological changes and lipid peroxidation biomarkers during the acute phase of Chagas disease. The results showed that the parasite clearance was greater in animals fed with vitamin C overdose. There were no significant differences regarding the biomarkers of lipid peroxidation and inflammatory process or the increase of myocardium in animals treated with the recommended dosage. The largest amount of parasite growth towards the end of the acute phase suggests the benefit of high doses of vitamin C for trypomastigotes. The supplementation doesn't influence the production of free radicals or the number of amastigote nests in the acute phase of Chagas disease.

Body composition is a determinant factor for performance in different sports modalities. Safe, practical and validated instruments are necessary for the measurement of body composition and for the identification of alterations that occur during the training period. A critical review was performed comparing studies that apply skinfold thickness (SKF) and bioelectrical impedance (BIA) for the estimation of body composition in athletes. Studies published between 1990 and 2007 available online in the Pubmed, SportDiscus and Scielo databases were reviewed. Seven critical points were evaluated to rate the studies: number of subjects, performance level of the athletes studied, statistical methods applied, number of equations tested, test control, sample control, and gold standard used to compare the data. SKF and BIA present advantages for the assessment of body composition in athletes compared to other methods, such as their easy application, non-invasiveness and relatively low cost. The accuracy and reliability of the results obtained with these methods depend on test conditions, equations selected for data analysis and characteristics of the particular group (sports modality, gender, age and performance level). SKF seems to be a better method to estimate body composition in athletes because of the availability of specific equations for different sports modalities and because of the low sensitivity of BIA in detecting minimal alterations that occur during the training period.

A creatina é uma substância popular entre atletas devido a sua possível propriedade ergogênica. Tal popularidade incentivou autores a estudar e explorar o possível potencial terapêutico desta substância. A síntese de creatina é responsável pela maioria das transferências de grupos metila no metabolismo hepático normal. Como a homocisteína é um aminoácido formado exclusivamente a partir da desmetilação da metionina, acredita-se que a creatina e homocisteína estejam metabolicamente conectadas. Estudos têm mostrado que a hiperhomocisteinemia está diretamente ligada à formação de espécies reativas de oxigênio pela autooxida ção da homocisteína e/ou da cisteína e que tal auto-oxidação pode provocar danos celulares. O objetivo desta revisão é discutir aspectos da suplementação com creatina relacionados aos níveis de homocisteína e o estresse oxidativo.

Abstract Introduction: Recent studies have pointing creatine supplementation as a promising therapeutic alterna- tive in several diseases, especially myopathies and neurodegenerative disorder. Objective: elucidate the role of creatine supplementation on deleterious effect caused by limb immobilization in humans and rats. Methods: Analyzed articles were searched by three online databases, PubMed, SportDicus e Scielo. After a review and analysis, the studies were included in this review articles on effect of creatine supplementation on skeletal muscle in humans and rat, before, during and after a period of limb immobilization. Results: Studies analyzed demonstrated positive points in use of creatine supplementation as a therapeutic tool to mitigating the deleterious effects of limb immobilization, in humans and rat. Conclusion: The dataset of this literature review allows us to conclude that creatine supplementation may reduce muscle loss and/or assist in the recovery of muscle atrophy caused by immobilization and disuse in rats and humans. Also, we note that further research with better methodological rigor is needed to clarify the mechanisms by which creatine support the recovery of muscle atrophy. Moreover, these effects are positive and promising in the field of muscle rehabilitation, especially after member’s immobilization.