Muscle Damage and Muscle Activity Induced by Strength Training Super-Sets in Physically Active Men.

Brentano, MA, Umpierre, D, Santos, LP, Lopes, AL, Radaelli, R, Pinto, RS, and Kruel, LFM. Muscle damage and muscle activity induced by strength training super-sets in physically active men. J Strength Cond Res 31(7): 1847-1858, 2017-In strength training, muscle activity is often analyzed by surface electromyography (EMG) and muscle damage through indirect markers, such as plasma concentrations of creatine kinase (CK) after exercise. However, there is little information about the influence of the strength exercises order on these parameters. The purpose of this study is to analyze the effect of strength exercises order (super-sets) in muscle activity and indirect markers of muscle damage. Twenty men were randomly assigned to one of the strength training sessions (TS). Each TS (5 sets × 8-10 repetition maximum) consisted of 2 exercises for the knee extensor muscles and 2 exercises for the horizontal shoulder flexors performed in a different order: exercises for the same muscle group grouped (grouped exercises [GE]: n = 10; 26.6 ± 3.4 years; 17.4 ± 3.4 body fat) or separated (separated exercises [SE]: n = 10; 24.9 ± 2.6 years; 15.4 ± 5.9 body fat). Muscle activity was analyzed by surface EMG (vastus lateralis [VL], vastus medialis [VM], rectus femoris [RF], pectoralis major [PM], and anterior deltoid [AD]), and the main indirect marker of muscle damage was the CK, evaluated immediately before and after the first 5 days of each TS. There was a higher EMG activity of GE in the RF (GE: 88.4% × SE: 73.6%) and AD (GE: 176.4% × SE: 100.0%), in addition to greater concentration of CK (GE: 632.4% × SE: 330.5%) after exercise. Our findings suggest that, in physically active men, implementing super-sets with GE promotes greater muscle effort and muscle damage, wherein 5 days are not enough to recover the trained muscle groups.

Gastroprotective activity and physicochemical analysis of carboxymethylated gum from Anadenanthera colubrina.

Biotechnological advancements require the physicochemical alteration of molecules to enhance their biological efficacy for the effective treatment of gastric ulcers. The study aimed to produce a polyelectrolytic compound from red angico gum (AG) by carboxymethylation, evaluate its physicochemical characteristics and investigate gastric protection against ethanol-induced ulcers. AG and carboxymethylated angico gum (CAG) were characterized by Fourier transform infrared spectroscopy, determination of the degree of substitution and gel permeation chromatography (GPC) and 13C NMR techniques. The results demonstrated that the modification of the polymer was satisfactory, presenting conformational changes e improving the interaction with the gastric mucosa. AG and CAG reduced macroscopic and microscopic damage such as edema, hemorrhage and cell loss caused by exposure of the mucosa to alcohol. Both demonstrated antioxidant activity in vitro, and in vivo, pretreatment with gums led to the restoration of superoxide dismutase and glutathione levels compared to the injured group. Concurrently, the levels of malondialdehyde and nitrite decreased. Atomic force microscopy showed that CAG presented better conformational properties of affinity and protection with the gastric mucosa compared to AG in the acidic pH. Based on our findings, it is suggested that this compound holds promise as a prospective product for future biotechnological applications.

Gaucher disease type I: assessment of basal metabolic rate in patients from southern Brazil.

INTRODUCTION: Gaucher disease (GD) is characterized by clinical heterogeneity and is associated with metabolic abnormalities such as increased resting energy expenditure. OBJECTIVES: To assess the basal metabolic rate (BMR) of patients with GD type I followed at the Gaucher Disease Reference Center of Rio Grande do Sul, Brazil. PATIENTS AND METHODS: Fourteen patients (male=6) and 14 healthy controls matched by gender, age and body mass index (BMI) were included in the study. The nutritional status of patients was assessed by BMI. The BMR was measured by indirect calorimetry. In two patients, it was possible to perform BMR in the pre- and the post-treatment periods. RESULTS: Mean age and BMI of patients and controls were, respectively, 32.8 ± 17.6 and 32.1 ± 16.6 years and 23.3 ± 3.1 and 22.4 ± 3.1 kg/m(2). Twelve patients were receiving enzyme replacement therapy (ERT) with imiglucerase (mean duration of treatment=5.2 ± 4.3 years; mean dosage of imiglucerase=24.2 ± 7.3 UI/kg/inf). Five patients (36%) were overweight, and nine (64%) were normal weight. Mean BMR of patients on ERT was 27.1% higher than that of controls (p=0.007). There was no difference between the BMR of patients on ERT and not on ERT (n=4) (p=0.92). Comparing the BMR of patients on ERT and their controls with the BMR estimated by the Harris-Benedict equation, the BMR of patients was 6.3% higher than the estimated (p = 0.1), while the BMR of their controls was 17.0% lower than the estimated (p = 0.001). CONCLUSION: Most treated GD type I patients were normal weight. The patients including those on ERT showed higher BMR when compared to controls. Imiglucerase is probably unable to normalize the hypermetabolism presented by GD type I patients. Additional studies should be performed to confirm our findings.

Mechanism of preservation of the intestinal mucosa architecture and NF-κB/PGE2 reduction by hydrogen sulfide on cholera toxin-induced diarrhea in mice.

AIMS: Investigate the involvement of Hydrogen sulfide (H2S) in inflammatory parameters and intestinal morphology caused by cholera toxin (CT) in mice. MAIN METHODS: Mice were subjected to the procedure of inducing diarrhea by CT in the isolated intestinal loop model. The intestinal loops were inoculated with H2S donor molecules (NaHS and GYY 4137) or saline and CT. To study the role of EP2 and EP4 prostaglandin E2 (PGE2) receptors in the H2S antisecretory effect, PAG (DL-propargylglycine - inhibitor of cystathionine-γ-lyase (CSE)), PF-04418948 (EP2 antagonist) and ONO-AE3-208 (EP4 antagonist) were used. The intestinal loops were evaluated for intestinal secretion, relation of the depth of villi and intestinal crypts, and real-time PCR for the mRNA of the CXCL2, IL-6, NOS-2, IL-17, NF-κB1, NF-κBIA, SLC6A4 and IFN-γ genes. KEY FINDINGS: H2S restored the villus/crypt depth ratio caused by CT. NaHS and GYY 4137 increased the expression of NF-κB1 and for the NF-κBIA gene, only GYY 4137 increased the expression of this gene. The increased expression of NF-κB inhibitors, NF-κB1 and NF-κBIA by H2S indicates a possible decrease in NF-κB activity. The pretreatment with PAG reversed the protective effect of PF-04418948 and ONO-AE3-208, indicating that H2S probably decreases PGE2 because in the presence of antagonists of this pathway, PAG promotes intestinal secretion. SIGNIFICANCE: Our results point to a protective activity of H2S against CT for promoting a protection of villus and crypt intestine morphology and also that its mechanism occurs at least in part due to decreasing the activity of NF-κB and PGE2.

Activation of transient receptor potential vanilloid channel 4 contributes to the development of ethanol-induced gastric injury in mice.

The transient receptor potential vanilloid channel 4 (TRPV4) is associated with the development of several pathologies, particularly gastric disorders. However, there are no studies associating this receptor with the pathophysiology of gastric erosions. The aim of this study was to investigate the role of TRPV4 in the development of ethanol-induced gastric damage in vivo. Gastric lesions were induced by ethanol in Swiss mice pretreated with TRPV4 antagonists, GSK2193874 (0.1; 0.3 and 0.9 mg/kg) or Ruthenium red (0.03; 0.1 or 0.3 mg/kg) or its agonist, GSK1016790A (0.9 mg/kg). Gastric mucosal samples were taken for histopathology, immunohistochemistry, atomic force microscopy and evaluation of antioxidant parameters. The gastric mucus content and TRPV4 mRNA expression were analyzed. Ethanol exposure induced upregulation of gastric mRNA and protein expression of TRPV4. TRPV4 blockade promoted gastroprotection against ethanol-induced injury on macro- and microscopic levels, leading to reduced hemorrhage, cell loss and edema and enhanced gastric mucosal integrity. Moreover, an increase in superoxide dismutase (SOD) and glutathione (GSH) activity was observed, followed by a decrease in malondialdehyde (MDA) levels. TRPV4 blockade during alcohol challenge reestablished gastric mucus content. The combination of TRPV4 agonist and ethanol revealed macroscopic exacerbation of gastric damage area. Our results confirmed the association of TRPV4 with the development of gastric injury, showing the importance of this receptor for further investigations in the field of gastrointestinal pathophysiology and pharmacology.

Alendronate-induced gastric damage in normoglycemic and hyperglycemic rats is reversed by metformin.

Alendronate is a bisphosphonate widely used for the treatment of osteoporosis; however, one of its main adverse reactions is gastric ulcer. Metformin is an oral antihyperglycemic agent that has several beneficial effects, including healing, gastroprotective and anti-tumoral action. This study aimed to evaluate the gastroprotective activity of metformin in alendronate-induced gastric damage in normoglycemic and hyperglycemic rats. The treatment with 100 mg/kg of metformin showed a significant gastroprotective effect in damage induced by alendronate (50 mg/kg) in macroscopic analysis and the analysis of light microscopy and atomic force microscopy. The results suggested metformin decreased the inflammatory response by reducing the expression of proinflammatory cytokines (TNF-α, IL-1ß and IL-6), myeloperoxidase activity, and malondialdehyde levels. Also, the results suggested that metformin induces the maintenance of basal levels of collagen and increase the production of mucus. Interestingly, with the presence of the AMPK inhibitor (Compound C), metformin presented impairment of its gastroprotective action. The gastroprotective effect of metformin might be related to the activation of the AMPK pathway. These findings revealed that metformin has a gastroprotective action and may be considered a therapeutic potential for the prevention and treatment of gastric lesions induced by alendronate.

Ghrelin, leptin and adiponectin levels in Gaucher disease type I patients on enzyme replacement therapy.

BACKGROUND: Gaucher disease type I (GD type I) is characterized by clinical heterogeneity and is associated with metabolic abnormalities such as increased basal metabolic rate. OBJECTIVE: To evaluate ghrelin, leptin and adiponectin levels in patients with GD type I on enzyme replacement therapy (ERT). SUBJECTS AND METHODS: A cross-sectional study of patients with GD type I (n = 15), matched for sex, age and BMI with healthy controls. The levels of glucose, insulin, ghrelin, leptin and adiponectin were assessed in both groups. Insulin resistance was defined by the index HOMA-IR. RESULTS: Eight patients had adequate weight, seven were overweight (4 preobese, 3 obese class I). Eight patients presented metabolic syndrome, five of whom with insulin resistance. The median levels of ghrelin, leptin and adiponectin of the patients did not differ from those of the controls. Ghrelin and adiponectin levels were correlated with each other; inversely correlated with BMI, waist circumference and triglyceride levels; and directly correlated with HDL-cholesterol. Leptin levels were inversely correlated with LDL-cholesterol and directly correlated with BMI, waist circumference, enzyme dosage, triglycerides, insulin, and HOMA-IR. CONCLUSIONS: Metabolic syndrome and overweight appear to be common in patients with GD type I on ERT. As leptin was strongly associated with insulin and HOMA index, it could become a biomarker to assess early evidence of insulin resistance in patients with GD. Further studies are needed to investigate the associations found.

Assessment of Basal Metabolic Rate and Nutritional Status in Patients with Gaucher Disease Type III.

UNLABELLED: Gaucher disease type III (GD III) is a rare form of GD characterized by neurological involvement and severe systemic disease. The objective of this study was to assess the nutritional status and energy metabolism of patients with GD III. METHODS: The basal metabolic rate (BMR, measured by indirect calorimetry) and anthropometric parameters (height, weight, body mass index (BMI), and arm circumference) of three patients with GD III (p.L444P/L444P genotype) were assessed at different time points. The clinical severity of GD was assessed by means of physical examination, laboratory tests, imaging findings, and the severity scores proposed by Zimran (SSI) and Davies (SSNI). RESULTS: The measured BMR of patients 1 (age 14 years, not on enzyme replacement therapy (ERT), SSI score 33, SSNI score 14.5), 2 (age 17 years, on ERT, SSI score 33, SSNI score 16), and 3 (age 20 years, on ERT, SSI score 33, SSNI score 7.5) was, respectively, 47%, 72%, and 15% higher than that estimated by the Harris-Benedict equation. Patients with a more severe phenotype had more marked hypermetabolism. Patients 1 and 2 had BMI-for-age z scores of -1.09 and -1.39, respectively, and height-for-age z scores of -4.27 and -3.02, respectively; patient 3 had a BMI of 24.7 kg/m(2). CONCLUSION: All three patients showed hypermetabolism; however, the two patients with the highest BMR had more severe GD and were malnourished. Additional studies are warranted to assess whether hypermetabolism may be a biomarker of disease severity in GD.

Six-minute walk distance and work relationship with incremental treadmill cardiopulmonary exercise test in COPD.

INTRODUCTION: Cardiopulmonary exercise testing (CPET) is increasingly used to evaluate the overall impact of the illness on patients with chronic obstructive pulmonary disease (COPD). While laboratory tests of exercise performance are costly, the 6-min walk test (6-MWT) can be more easily performed. Although the main outcome commonly used in this field test is the distance walked in 6 min (6-MWD), this measure does not account for differences in body weight. Previous studies showed a good correlation between the work performed during the 6-MWT with incremental cycling CPET, an exercise modality more associated with quadriceps fatigability and with lower peak oxygen consumption than incremental walking tests. OBJECTIVE: Evaluate the correlation between the 6-MWD and its derivative body weight-walking distance product, an estimation of the work performed during the 6-MWT, with peak from a treadmill CPET. METHODS: Thirty COPD patients [forced expiratory volume in 1 s (FEV1) = 39 ± 13%; peak predicted] performed CPET to the limit of tolerance on a treadmill and 6-MWT, 48 h apart.6-MWD and work were correlated to resting and exercise functional variables. RESULTS: The work of walking during the 6-MWT provided greater associations with peak than observed with 6-MWD. This was the case for FEV1, forced vital capacity, inspiratory capacity, lung diffusion capacity for carbon monoxide, peak , carbon dioxide output, minute ventilation and double product (r = 0.57, r = 0.57, r = 0.73, r = 0.7, r = 0.75, r = 0.65, r = 0.51 and r = 0.4, respectively; all P < 0.05). CONCLUSION: A better association was found between the work estimated from the 6-MWT and peak achieved during CPET, in this case with a treadmill, than the 6-MWD alone.

The effects of diet- and diet plus exercise-induced weight loss on basal metabolic rate and acylated ghrelin in grade 1 obese subjects.

BACKGROUND: Diet and exercise are often prescribed as primary intervention regarding obesity-related disorders. Additionally, recent studies have shown beneficial effects of weight loss through diet and exercise in ghrelin concentrations in obese subjects. The aim of this study was to evaluate the effects of a 5% weight loss on lipid profile, resting metabolic rate (RMR), and acylated ghrelin (AG) using two different methods of intervention (diet or diet plus exercise). MATERIALS AND METHODS: Eighteen subjects (twelve women and six men) aged 20-40 years with a body mass index of 30-34.9 kg/m(2) (grade 1 obesity) were randomized into two intervention groups: diet (n=9) or diet plus exercise (n=9). Both groups underwent treatment until 5% of the initial body weight was lost. At baseline and upon completion, RMR and AG were analyzed. RESULTS: Both groups showed a significant decrease in body fat percentage and fat mass. The diet-plus-exercise group showed a decrease in AG (pre: 54.4±25.3 pg/mL and post: 33.2±19.1 pg/mL) and an increase in RMR (pre: 1,363±379 kcal/day, post: 1,633±223 kcal/day). CONCLUSION: These data suggest that diet plus exercise induced weight loss and had beneficial effects on AG concentration and RMR, essential factors to ensure the benefits of a weight-loss program.

Intensive practical lifestyle intervention improves endothelial function in metabolic syndrome independent of weight loss: a randomized controlled trial.

The objective was to evaluate the metabolic and vascular effects of lifestyle interventions involving a healthy diet and either a moderate- or a high-intensity exercise regimen in nondiabetic subjects with metabolic syndrome. The effects of these interventions on flow-mediated vasodilation (FMD) and risk profiles were compared with a standard low-fat diet and engaging in daily walking (standard of care). Seventy-five healthy adults with metabolic syndrome (30-55 years old) were randomized to a 10,000-steps-a-day exercise program, a 3-times-a-week fitness (>75% peak VO(2)) program, or a 1-hour-walking-a-day program for 12 weeks. The first 2 interventions were combined with an accessible healthy, no-sugar diet; and the third was combined with a tailored low-fat diet. The outcomes, including FMD and risk factors, were examined at 12 weeks and at 1-year reassessment. Significant increase in FMD (mean difference = 1.51%, 95% confidence interval = 1.05%-3.017%, P = .0007) and decrease in arterial pressure (mean difference = 19.3 ± 2.3/-12.6 ± 1.8 mm Hg, P = .0001) were observed in all groups. However, the FMD changed most favorably in the high-intensity, low-sugar group (mean difference = 1.56%, 95% confidence interval = 0.1%-3.02%, P = .036). Significant improvements in body mass index, waist, insulin-like growth factor-1, homeostasis model assessment of insulin resistance, insulin, glucose, urinary albumin excretion, and lipid profiles occurred in all groups. Metabolic syndrome was resolved in 64%. One year later, weight loss (-9.1 ± 2.3 kg, P = .0001) and arterial pressure decrease (-18.5 ± 2.3/-12.3 ± 2.1 mm Hg, P = .0001) were maintained. Practical, health-centered diet combined with high-intensity exercise is associated with enhanced vascular protection. These data suggest that more intense exercise combined with a low-sugar diet modulates endothelium-dependent vasodilation.