Vanessa Neves de Oliveira

The effects of aerobic, resistance, and combined exercise on metabolic control, inflammatory markers, adipocytokines, and muscle insulin signaling in patients with type 2 diabetes mellitus

The purpose of this study was to compare the effects of 3 different modalities of exercise on metabolic control, insulin resistance, inflammatory markers, adipocytokines, and tissue expression of insulin receptor substrate (IRS)-1 after 12 weeks of training among patients with type 2 diabetes mellitus. Forty-eight patients with type 2 diabetes mellitus were randomly assigned to 4 groups of training (3 times a week, 60 minutes per session): aerobic group (n = 12), resistance group (n = 12), combined (aerobic and resistance) group (n = 12), and control group (n = 12). Fasting and postprandial blood glucose, glycated hemoglobin, lipid profile, insulin resistance index (homeostasis model assessment of insulin resistance), adipocytokines (adiponectin, visfatin, and resistin), tumor necrosis factor, interleukin, and high-sensitivity C-reactive protein (hs-CRP) were measured at baseline and at the end of the study. Patients also underwent a muscle microbiopsy before and after training to quantify IRS-1 expression. All 4 groups displayed decreases in blood pressure, fasting plasma glucose, postprandial plasma glucose, lipid profile, and hs-CRP (P < .05); and there was no difference across the groups. After training, the IRS-1 expression increased by 65% in the resistance group (P < .05) and by 90% in the combined group (P < .01). Exercise training favorably affects glycemic parameters, lipid profile, blood pressure, and hs-CRP. In addition, resistance and combined training can increase IRS-1 expression.

The effect of different training programs on antioxidant status, oxidative stress, and metabolic control in type 2 diabetes

We compared the effects of 12 weeks of 3 different exercise types on type 2 diabetic (T2DM) male and female human subjects, randomly divided into 4 groups: aerobic training (AT; n = 11), strength training (ST; n = 10), combined training (CBT; n = 10), and no training (NT; n = 12). Metabolic control, anthropometric parameters, lipid and hematological profiles, kidney and liver function markers, hormones, antioxidant enzymes, and oxidative stress markers were assessed prior to and after the training programs. At baseline, fasting blood glucose and hemoglobin A(1c) in the ST group were higher than in the NT group; after the training, we no longer observed differences in these groups, suggesting an improvement on these parameters. In the AT group, catalase and superoxide dismutase activity, nitrite concentration, levels of sulfhydryl groups, and peak rate of oxygen consumption were elevated after the training (p < 0.05). No changes were observed in antioxidant enzymes or oxidative stress markers in the ST group. The levels of sulfhydryl groups diminished in the NT group (p < 0.01) and increased in the CBT group (p < 0.05). These data demonstrate that the AT program for the T2DM subjects provided important upregulation in antioxidant enzymes and increased nitric oxide bioavailability, which may help minimize oxidative stress and the development of the chronic complications of diabetes. We propose that the beneficial effects observed in the metabolic parameters of the ST group occurred in response to the poor baseline metabolic health n this group, and not necessarily in response to the training itself.

The higher exercise intensity and the presence of allele I of ACE gene elicit a higher post-exercise blood pressure reduction and nitric oxide release in elderly women: an experimental study

BackgroundThe absence of the I allele of the angiotensin converting enzyme (ACE) gene has been associated with higher levels of circulating ACE, lower nitric oxide (NO) release and hypertension. The purposes of this study were to analyze the post-exercise salivary nitrite (NO2-) and blood pressure (BP) responses to different exercise intensities in elderly women divided according to their ACE genotype.MethodsParticipants (n = 30; II/ID = 20 and DD = 10) underwent three experimental sessions: incremental test - IT (15 watts workload increase/3 min) until exhaustion; 20 min exercise 90% anaerobic threshold (90% AT); and 20 min control session without exercise. Volunteers had their BP and NO2- measured before and after experimental sessions.ResultsDespite both intensities showed protective effect on preventing the increase of BP during post-exercise recovery compared to control, post-exercise hypotension and increased NO2- release was observed only for carriers of the I allele (p < 0.05).ConclusionGenotypes of the ACE gene may exert a role in post-exercise NO release and BP response.

Exercise Intensity and Recovery: Biomarkers of Injury, Inflammation, and Oxidative Stress

Abstract Bessa, AL, Oliveira, VN, Agostini, GG, Oliveira, RJS, Oliveira, ACS, White, GE, Wells, GD, Teixeira, DNS, and Espindola, FS. Exercise intensity and recovery: Biomarkers of injury, inflammation, and oxidative stress. J Strength Cond Res 30(2): 311–319, 2016—Biomarkers of inflammation, muscle damage, and oxidative stress after high-intensity exercise have been described previously; however, further understanding of their role in the postexercise recovery period is necessary. Because these markers have been implicated in cell signaling, they may be specifically related to the training adaptations induced by high-intensity exercise. Thus, a clear model showing their responses to exercise may be useful in characterizing the relative recovery status of an athlete. The purpose of this study was twofold: (a) to investigate the time course of markers of muscle damage and inflammation in the blood from 3 to 72 hours after combined training exercises and (b) to investigate indicators of oxidative stress and damage associated with increased reactive oxygen species production during high-intensity exercise in elite athletes. Nineteen male athletes performed a combination of high-intensity aerobic and anaerobic training exercises. Samples were acquired immediately before and at 3, 6, 12, 24, 48, and 72 hours after exercise. The appearance and clearance of creatine kinase and lactate dehydrogenase in the blood occurred faster than previous studies have reported. The neutrophil/lymphocyte ratio summarizes the mobilization of 2 leukocyte subpopulations in a single marker and may be used to predict the end of the postexercise recovery period. Further analysis of the immune response using serum cytokines indicated that high-intensity exercise performed by highly trained athletes only generated inflammation that was localized to the skeletal muscle. Biomarkers are not a replacement for performance tests, but when used in conjunction, they may offer a better indication of metabolic recovery status. Therefore, the use of biomarkers can improve a coachs ability to assess the recovery period after an exercise session and to establish the intensity of subsequent training sessions.

Alterations of antioxidant biomarkers and type I collagen deposition in the parotid gland of streptozotocin-induced diabetic rats

BACKGROUND AND OBJECTIVE Acarbose is a competitive inhibitor of intestinal alpha-glycosidases that slows the breakdown of sucrose and starch, thereby reducing glucose and fructose absorption. The aim of this study was to evaluate the effect of acarbose treatment on antioxidant parameters and deposition of type I collagen in the parotid glands of diabetic rats. METHODS Diabetes mellitus was induced by intravenous injection of streptozotocin, and rats were divided into four groups: non-diabetic (NDM), diabetic (DM), diabetic treated with 25mg/kg acarbose (DMA) and non-diabetic treated with acarbose (NDMA). Changes in enzymatic antioxidant systems, such as the activity of SOD and GPx enzymes, were evaluated, and the specific staining pattern of the type I collagen fibres was investigated in the rat parotid glands. RESULTS The DM group presented high levels of SOD and GPx enzymes, which were reduced by acarbose treatment. Tissue damage, which was indicated by an increased MDA concentration in the parotid glands of rats in the DM group, was also reversed in the DMA group. Moreover, type I collagen fibres from DM rats were more intensely stained than those of NDM rats. Acarbose treatment was effective in decreasing collagen deposition, which was shown by a decrease in staining intensity of approximately 25%. CONCLUSIONS These results suggest that the diabetic state influences the type I collagen concentration in the parotid glands of rats. In addition, acarbose treatment was helpful in preventing the deposition of such fibres, as well the increase in oxidative stress induced by hyperglycemia.

Neuroprotective effects of Pouteria ramiflora (Mart.) Radlk (Sapotaceae) extract on the brains of rats with streptozotocin-induced diabetes.

Diabetes mellitus is a chronic disease involving persistent hyperglycemia, which causes an imbalance between reactive oxygen species and antioxidant enzymes and results in damage to various tissues, including the brain. Many societies have traditionally employed medicinal plants to control the hyperglycemia. Pouteria ramiflora, a species occurring in the savanna biome of the Cerrado (Brazil) has been studied because of its possible ability to inhibit carbohydrate digestion. Rats with streptozotocin-induced diabetes treated with an alcoholic extract of Pouteria ramiflora show an improved glycemic level, increased glutathione peroxidase activity, decreased superoxide dismutase activity, and reduced lipid peroxidation and antioxidant status. The extract also restored myosin-Va expression and the nuclear diameters of pyramidal neurons of the CA3 subregion and that of the polymorphic cells of the hilus. We conclude that Pouteria ramiflora extract exerts a neuroprotective effect against oxidative damage and myosin-Va expression and is able to prevent hippocampal neuronal loss in the CA3 and hilus subfields of diabetic rats. However, future studies are needed to understand the mechanism of action of Pouteria ramiflora extract in acute and chronic diabetes.

Phaseolamin treatment prevents oxidative stress and collagen deposition in the hearts of streptozotocin-induced diabetic rats

The development of cardiovascular complications in patients with diabetes is often associated with an imbalance between reactive oxygen species and antioxidant systems. This imbalance can contribute to high cardiac collagen content, which increases cross-linking and the stiffness of the myocardium. In this study, the protective effect of phaseolamin against damage under oxidative stress and collagen deposition in the cardiac tissue in association with diabetes was evaluated. Non-diabetic and diabetic animals were distributed into groups and treated for 20 days with commercial phaseolamin. The phaseolamin treatment increased total antioxidant activity but reduced the following in diabetic rats: (a) hyperglycaemic state, (b) catalase and superoxide dismutase activity and (c) tissue damage caused by lipid peroxidation. Additionally, the phaseolamin treatment attenuated the collagen levels compared to non-treated diabetic rats. Thus, the short-term anti-hyperglycaemic effect of the phaseolamin treatment may prevent the initial changes caused by oxidative stress and the deposition of collagen, as well as reduce the incidence of heart complications.

Myosins Are Differentially Expressed under Oxidative Stress in Chronic Streptozotocin-Induced Diabetic Rat Brains

Diabetes mellitus is a disease characterized by persistent hyperglycemia, which may lead to brain tissue damage due to oxidative stress and also contributes to neuronal death and changes in synaptic transmission. This study evaluated the effect of oxidative stress and the use of antioxidants supplementation on myosins expression levels in the brains of chronic diabetic rats induced by streptozotocin. Lipid peroxidation, antioxidant enzymes activities, and myosins-IIB and -Va expressions at transcriptional and translational levels were examined after 90 days induction. The chronic effect of the diabetes led to the upregulation of superoxide dismutase (SOD) and catalase (CAT) activities, and the downregulation of glutathione peroxidase (GPx), but there was no statistically significant increase in the malondialdehyde (MDA) levels. These alterations were accompanied by high myosin-IIB and low myosin-Va expressions. Although the antioxidant supplementation did not interfere on MDA levels, the oxidative stress caused by chronic hyperglycemia was reduced by increasing SOD and restoring CAT and GPx activities. Interestingly, after supplementation, diabetic rats recovered only myosin-Va protein levels, without interfering on myosins mRNA levels expressed in diabetic rat brains. Our results suggest that antioxidant supplementation reduces oxidative stress and also regulates the myosins protein expression, which should be beneficial to individuals with diabetes/chronic hyperglycemia.