NOS3 Polymorphisms Can Influence the Effect of Multicomponent Training on Blood Pressure, Nitrite Concentration and Physical Fitness in Prehypertensive and Hypertensive Older Adult Women.

Associations of endothelial nitric oxide synthase (NOS3) polymorphisms with hypertension and response to exercise training in prehypertensive and hypertensive older adult women remain unclear. This study used a multicomponent program (various capacities and motor skills) in the physical training intervention. It analyzed the influence of NOS3 polymorphisms [-786T > C, 894G > T (Glu298Asp), and intron 4b/a] on the response of blood pressure (BP), nitrite concentration, and physical fitness in older adult women. Fifty-two participants aged between 50 and 80 underwent body mass index, BP, 6-min walk, elbow flexion, and sit and stand-up tests to assess physical fitness. The intervention duration was 12 weeks, twice a week, on non-consecutive days. Each session lasted 90 min, maintaining an intensity between 13 (moderate) and 15 (intense), controlled by the Subjective Effort Perception Scale. Plasma/blood samples were collected to assess nitrite concentration and genotyping. The statistical analysis included Fisher's exact test and linear mixed-effects models. The multicomponent training's positive effect was observed with a similar response in both prehypertensive and hypertensive groups. However, carriers of different genotypes demonstrated different responses to training: the decreases in systolic and diastolic BP and increases in nitrite expected from the physical training were smaller in variant genotype than ancestral genotype carriers, especially in the hypertensive group. At positions -786T > C and Glu298Asp, only the ancestral genotypes showed a decrease in diastolic BP (Δ% = -8.1, and Δ% = -6.5, respectively) and an increase on nitrite (Δ% = 19.1, and Δ% = 24.1, respectively) in the hypertensive group. Our results show that the benefits of a multicomponent training intervention seem to be genotype-dependent. It should be possible to consider genetic variants when selecting an exercise treatment intervention.

Taurine supplementation associated with exercise increases mitochondrial activity and fatty acid oxidation gene expression in the subcutaneous white adipose tissue of obese women.

PURPOSE: To evaluate the effects of taurine supplementation associated or not with chronic exercise on body composition, mitochondrial function, and expression of genes related to mitochondrial activity and lipid oxidation in the subcutaneous white adipose tissue (scWAT) of obese women. METHODS: A randomized and double-blind trial was developed with 24 obese women (BMI 33.1 ± 2.9 kg/m2, 32.9 ± 6.3 y) randomized into three groups: Taurine supplementation group (Tau, n = 8); Exercise group (Ex, n = 8); Taurine supplementation + exercise group (TauEx, n = 8). The intervention was composed of 3 g of taurine or placebo supplementation and exercise training for eight weeks. Anthropometry, body fat composition, indirect calorimetry, scWAT biopsy for mitochondrial respiration, and gene expression related to mitochondrial activity and lipid oxidation were assessed before and after the intervention. RESULTS: No changes were observed for the anthropometric characteristics. The Ex group presented an increased resting energy expenditure rate, and the TauEx and Ex groups presented increased lipid oxidation and a decreased respiratory quotient. Both trained groups (TauEx and Ex) demonstrated improved scWAT mitochondrial respiratory capacity. Regarding mitochondrial markers, no changes were observed for the Tau group. The TauEx group had higher expression of CIDEA, PGC1a, PRDM16, UCP1, and UCP2. The genes related to fat oxidation (ACO2 and ACOX1) were increased in the Tau and Ex groups, while only the TauEx group presented increased expression of CPT1, PPARa, PPARγ, LPL, ACO1, ACO2, HSL, ACOX1, and CD36 genes. CONCLUSION: Taurine supplementation associated with exercise improved lipid metabolism through the modulation of genes related to mitochondrial activity and fatty acid oxidation, suggesting a browning effect in the scWAT of obese women.

One-Week High-Intensity Interval Training Increases Hippocampal Plasticity and Mitochondrial Content without Changes in Redox State.

Evidence suggests that physical exercise has effects on neuronal plasticity as well as overall brain health. This effect has been linked to exercise capacity in modulating the antioxidant status, when the oxidative stress is usually linked to the neuronal damage. Although high-intensity interval training (HIIT) is the training-trend worldwide, its effect on brain function is still unclear. Thus, we aimed to assess the neuroplasticity, mitochondrial, and redox status after one-week HIIT training. Male (C57Bl/6) mice were assigned to non-trained or HIIT groups. The HIIT protocol consisted of three days with short bouts at 130% of maximum speed (Vmax), intercalated with moderate-intensity continuous exercise sessions of 30 min at 60% Vmax. The mass spectrometry analyses showed that one-week of HIIT increased minichromosome maintenance complex component 2 (MCM2), brain derived neutrophic factor (BDNF), doublecortin (DCX) and voltage-dependent anion-selective channel protein 2 (VDAC), and decreased mitochondrial superoxide dismutase 2 (SOD 2) in the hippocampus. In addition, one-week of HIIT promoted no changes in H2O2 production and carbonylated protein concentration in the hippocampus as well as in superoxide anion production in the dentate gyrus. In conclusion, our one-week HIIT protocol increased neuroplasticity and mitochondrial content regardless of changes in redox status, adding new insights into the neuronal modulation induced by new training models.

RANKL induces beige adipocyte differentiation in preadipocytes.

The receptor activator of nuclear factor-κB (NF-κB) (RANK), its ligand (RANKL), and the decoy receptor osteoprotegerin (OPG) are a triad of proteins that regulate bone metabolism, and serum OPG is considered a biomarker for cardiovascular diseases and Type 2 diabetes; however, the implications of OPG in adipose tissue metabolism remains elusive. In this study, we investigate RANK-RANKL-OPG signaling in white adipose tissue browning. Histological analysis of osteoprotegerin knockout (OPG-/-) mice showed subcutaneous white adipose tissue (sWAT) browning, resistance for high-fat diet-induced weight gain, and preserved glucose metabolism compared with wild-type (WT) mice. Stromal vascular fraction (SVF) cells from sWAT of OPG-/- mice showed multilocular morphology and higher expression of brown adipocyte marker genes compared with those from the WT group. Infusion of RANKL induced browning and elevated respiratory rates in sWAT, along with increased whole body oxygen consumption in mice measured by indirect calorimetry. Subcutaneous WAT-derived SVF and 3T3-L1 cells, but not mature white adipocytes, differentiated into beige adipose tissue in the presence of RANKL. Moreover, SVF cells, even under white adipocyte differentiation, showed multilocular lipid droplet, lower lipid content, and increased expression of beige adipocyte markers with RANKL stimulation. In this study, we show for the first time the contribution of RANKL to increase energy expenditure by inducing beige adipocyte differentiation in preadipocytes.

Cellular and molecular effects of silymarin on the transdifferentiation processes of LX-2 cells and its connection with lipid metabolism.

Fibrosis process in the liver is a clinical condition established in response to chronic lesions and may be reversible in many situations. In this process, hepatic stellate cells (HSCs) activate and produce extracellular matrix compounds. During fibrosis, the lipid metabolism is also altered and contributes to the transdifferentiation of the HSCs. Thus, controlling lipid metabolism in HSCs is suggested as a method to control or reverse the fibrotic condition. In the search for therapies that modulate lipid metabolism and treat liver diseases, silymarin has been identified as a relevant natural compound to treat liver pathologies. The present study aimed to evaluate the cellular and molecular effects of silymarin in the transdifferentiation process of HSCs (LX-2) from activated phenotype to a more quiesced-like cells , also focusing on understanding the modulatory effects of silymarin on lipid metabolism of HSCs. In our analyses, 100 µM of silymarin reduced the synthesis of actin filaments in activated cells, the synthesis of the protein level of α-SMA, and other pro-fibrotic factors such as CTGF and PFGF. The concentration of 150 µM silymarin did not reverse the activation aspects of LX-2 cells. However, both evaluated concentrations of the natural compound protected the cells from the negative effects of dimethyl sulfoxide (DMSO). Furthermore, we evaluated lipid-related molecules correlated to the transdifferentiation process of LX-2, and 100 µM of silymarin demonstrated to control molecules associated with lipid metabolism such as FASN, MLYCD, ACSL4, CPTs, among others. In contrast, cellular incubation with 150 µM of silymarin increased the synthesis of long-chain fatty acids and triglycerides, regarding the higher presence of DMSO (v/v) in the solvent. In conclusion, silymarin acts as a hepatoprotective agent and modulates the pro-fibrogenic stimuli of LX-2 cells, whose effects depend on stress levels in the cellular environment.

Physical exercise protects against mitochondria alterations in the 6-hidroxydopamine rat model of Parkinson's disease.

Parkinson's disease (PD) is typicaly caractherized by loss of dopaminergic neurons, as well as the presence of mitochondrial impairments. Although physical exercise is known to promote many beneficial effects in healthy subjects, such as enhancing mitocondrial biogenesis and function, it is not clear if these effects are evident after exercise in individuals with PD. The aim of this study was to investigate the effects of two different protocol durations on motor behavior (aphomorphine and gait tests), mitochondrial biogenesis signaling (PGC-1α, NRF-1 and TFAM), structure (oxidative phosphorylation system protein levels) and respiratory chain activity (complex I) in a unilateral PD rat model. For this, male Wistar rats were injected with 6-hydroxydopamine unilaterally into the striatum and submitted to an intermitent moderate treadmill exercise for one or four weeks. In the gait test, only stride width data revealed an improvement after one week of exercise. On the other hand, after 4 weeks of the exercise protocol all gait parameters analyzed and the aphomorphine test demonstrated a recovery. Analysis of protein revealed that one week of exercise was able to prevent PGC-1α and NRF-1 expression decrease in PD animals. In addition, after four weeks of physical exercise, besides PGC-1α and NRF-1, reduction in TFAM and complex I protein levels and increased complex I activity were also prevented in PD animals. Thus, our results suggest a neuroprotective and progressive effect of intermittent treadmill exercise, which could be related to its benefits on mitochondrial biogenesis signaling and respiratory chain modulation of the dopaminergic system in PD.

Moderate Exercise Modulates Tumor Metabolism of Triple-Negative Breast Cancer.

Triple-negative breast cancer (TNBC) stands out for its aggressiveness and accelerated rate of proliferation. Evidence shows that exercise may exert antitumorigenic effects, but the biochemical mechanisms underlying them remain unclear. Our objective was to evaluate the ability of exercise to modulate tumor growth and energy metabolism in an experimental TNBC model. Female BALB/c mice were sedentary or trained for 12 weeks and inoculated with 1 × 104 4T1 cells in the eighth week. Analyzes of macronutrient oxidation, mitochondrial respiration, and expression of genes related to cell metabolism were performed. The results showed that the trained group had a smaller tumor mass and the mitochondria in the tumors presented lower respiratory rates in the state of maximum electron transport capacity. Additionally, the tumors of the exercised group showed a higher expression of genes related to tumor suppressors, while the genes linked with cellular growth were similar between groups. Furthermore, the training modulated the corporal macronutrient oxidation to almost exclusive carbohydrate oxidation, while the sedentary condition metabolized both carbohydrate and lipids. Therefore, the exercise reduced tumor growth, with an impact on mitochondrial and macronutrient metabolism. Our results shed light on the understanding of the antitumorigenic effects of physical exercise, particularly regarding the metabolic transformations in TNBC.

Impairment of PGC-1α-mediated mitochondrial biogenesis precedes mitochondrial dysfunction and Alzheimer's pathology in the 3xTg mouse model of Alzheimer's disease.

Impairment of mitochondrial biogenesis and mitochondrial dysfunction is a prominent feature of Alzheimer's disease (AD). However, the extent to which the impairment of mitochondrial biogenesis influences mitochondrial dysfunction at the onset and during progression of AD is still unclear. Our study demonstrated that the protein expression pattern of the transcription factor pCREB/CREB, together with the protein expression of PGC-1α, NRF1 and TFAM are all significantly reduced in early ages of 3xTg-AD mice. We also found reduced mRNA expression levels of PKAC-α, CREB, PGC-1α, NRF1, NRF2 and TFAM as early as 1 month-of-age, an age at which there was no significant Aß oligomer deposition, suggesting that mitochondrial biogenesis is likely impaired in ages preceding the development of the AD pathology. In addition, there was a decrease in VDAC2 expression, which is related to mitochondrial content and mitochondrial function, as demonstrated by protein expression of complex IV, as well as complex II + III, and complex IV activities, at later ages in 3xTg-AD mice. These results suggest that the impairment in mitochondrial biogenesis signaling mediated by PGC-1α at early ages of the AD mice model likely resulted in mitochondrial dysfunction and manifestation of the AD pathology at later ages. Taken together, enhancing mitochondrial biogenesis may represent a potential pharmacological approach for the treatment of AD.

ß2 adrenergic interaction and cardiac autonomic function: effects of aerobic training in overweight/obese individuals.

PURPOSE: To verify the influence of different volumes and intensities of aerobic exercise on cardiac autonomic function (CAF) through heart rate variability (HRV) analysis as well the influence of ß2 adrenergic receptor (ADRB2) variants in overweight/obese individuals. METHODS: 70 physically inactive adults were randomly allocated into the following 16-week training: 1-high-intensity interval training (HIIT) (n = 25, 1 × 4 min bout at 85-95%HR peak, 3×/week), 4-HIIT (n = 26, 4 × 4 min bouts at 85-95%HR peak, interspersed with 3 min of recovery at 50-70%HR peak, 3×/week), and moderate continuous training (MCT) (n = 19, 30 min at 60-70%HR peak, 5×/week). Before and after the exercise training, anthropometric, BP, cardiorespiratory fitness, and HRV measures were evaluated. R-R intervals recorded for 10 min in a supine position at pre- and post-intervention were used to analyze HRV in the plot-Poincare indexes (SD1, SD2), and frequency-domain (LF, HF, LF/HF). Full blood samples were used for genotyping. RESULTS: 4-HIIT and MCT showed positive outcomes for almost all variables while 1-HIIT had a positive influence only on SBP and SD2 index. No associations were observed between isolated ADRB2 variants and changes in HRV. In the analysis of the interaction genotypes, all groups responded positively for the SD1 index of HRV and only the H1 (GG and CC) and H2 (GG and CG + GG) groups presented increases in the RMSSD index. Furthermore, there was an increase in the LF index only in the H3 (CC and AA + AG) and H4 (AA + AG and CG + GG) groups. CONCLUSIONS: ADRB2 variants and aerobic exercise training are important interacting variables to improve autonomic function and other health variables outcomes in overweight or obese individuals.

Energy Metabolism and Redox State in Brains of Wistar Audiogenic Rats, a Genetic Model of Epilepsy.

The Wistar Audiogenic Rat (WAR) strain is a genetic model of epilepsy, specifically brainstem-dependent tonic-clonic seizures, triggered by acute auditory stimulation. Chronic audiogenic seizures (audiogenic kindling) mimic temporal lobe epilepsy, with significant participation of the hippocampus, amygdala, and cortex. The objective of the present study was to characterize the mitochondrial energy metabolism in hippocampus and cortex of WAR and verify its relationship with seizure severity. Hippocampus of WAR naïve (no seizures) presented higher oxygen consumption in respiratory states related to the maximum capacities of phosphorylation and electron transfer system, elevated mitochondrial density, lower GSH/GSSG and catalase activity, and higher protein carbonyl and lactate contents, compared with their Wistar counterparts. Audiogenic kindling had no adding functional effect in WAR, but in Wistar, it induced the same alterations observed in the audiogenic strain. In the cortex, WAR naïve presented elevated mitochondrial density, lower GSH/GSSG and catalase activity, and higher protein carbonyl levels. Chronic acoustic stimulation in Wistar induced the same alterations in cortex and hippocampus. Mainly in the hippocampus, WAR naïve presented elevated mRNA expression of glucose, lactate and excitatory amino acids transporters, several glycolytic enzymes, lactate dehydrogenase, and Na+/K+ ATPase in neurons and in astrocytes. In vivo treatment with mitochondrial uncoupler 2,4-dinitrophenol (DNP) or N-acetylcysteine (NAC) in WAR had no effect on mitochondrial metabolism, but lowered oxidative stress. Unlike DNP, NAC downregulated all enzyme genes involved in glucose and lactate uptake, and metabolism in neurons and astrocytes. Additionally, it was able to reduce brainstem seizure severity in WAR. In conclusion, in WAR naïve animals, both cerebral cortex and hippocampus display elevated mitochondrial density and/or activity associated with oxidative damage, glucose and lactate metabolism pathways upregulation, and increased Na+/K+ ATPase mRNA expression. Only in vivo treatment with NAC was able to reduce seizure severity of kindled WARs, possibly via down regulation of glucose/lactate metabolism. Taken together, our results are a clear contribution to the field of mitochondrial metabolism associated to epileptic seizures.

Effects of intermittent dietary supplementation with conjugated linoleic acid and fish oil (EPA/DHA) on body metabolism and mitochondrial energetics in mice.

Understanding the mitochondrial processes that contribute to body energy metabolism may provide an attractive therapeutic target for obesity and co-morbidities. Here we investigated whether intermittent dietary supplementation with conjugated linoleic (CLA, 18:2n-6), docosahexaenoic (22:6n-3, DHA) and eicosapentaenoic (20:5n-3, EPA) acids, either alone or in combination, changes body metabolism associated with mitochondrial functions in the brain, liver, skeletal muscle and brown adipose tissue (BAT). Male C57Bl/6 mice were divided into groups: CLA (50% cis-9, trans-11; 50% trans-10, cis-12), EPA/DHA (64% EPA; 28% DHA), CLA plus EPA/DHA or control (linoleic acid). Each mouse received 3 g/kg b.w. of the stated oil by gavage on alternating days for 60 days. Dietary supplementation with CLA or EPA/DHA increased body VO2 consumption, VCO2 production and energy expenditure, being fish oil (FO) the most potent even in combination with CLA. Individually, both oils reduced mitochondrial density in BAT. CLA supplementation alone also a) elevated the expression of uncoupling proteins in soleus, liver and hippocampus and the uncoupling activity in the last two, ad this effect was associated with reduced hydrogen peroxide production in hippocampus; b) increased proteins related to mitochondrial fission in liver. EPA/DHA supplementation alone also a) induced mitochondrial biogenesis in liver, soleus and hippocampus associated with increased expression of PGC1-α; b) induced proteins related to mitochondrial fusion in the liver, and fission and fusion in the hippocampus. Therefore, this study shows changes on mitochondrial mechanisms induced by CLA and/or EPA/DHA that can be associated with elevated body energy expenditure.

Caracterização da variabilidade da frequência cardíaca em indivíduos com síndrome metabólica / Characterization of the heart rate variability in individuals with metabolic syndrome / Caracterización de la variabilidad de la frecuencia cardiaco en pacientes con síndrome metabólico

RESUMO Introdução: A variabilidade da frequência cardíaca (VFC) tem sido considerada um mecanismo de modulação do sistema nervoso autônomo. A diminuição da VFC pode estar associada à síndrome metabólica (SM). Objetivo: Comparar a VFC e variáveis de saúde em indivíduos com e sem SM. Métodos: Cento e dezenove participantes foram divididos em dois grupos: sem SM (SSM, n = 68) e com SM (CSM, n = 51). Foi avaliada a análise espectral da VFC em repouso, durante teste cardiopulmonar de exercício (TCPE) e na recuperação em bandas de baixa frequência (LF = 0,04-0,15 Hz), alta frequência (HF = 0,15-0,4 Hz) e razão LF/HF. Adicionalmente, a frequência cardíaca (FC) de repouso (FCrep), FC máxima (FCmáx), pressão arterial sistólica (PAS) e diastólica (PAD), glicemia, perfil lipídico, consumo de oxigênio pico (VO2pico) e composição corporal foram avaliados. Resultados: A FCrep e o VO2pico não apresentaram diferenças entre o CSM e o SSM (73,3 ± 9,1 vs. 70,1 ± 11,0 bpm) (26,8 ± 4,6 vs. 28,1 ± 6,6 ml.kg-1.min-1), respectivamente. A VFC foi similar entre os grupos nos diferentes momentos analisados. A glicemia (99,8 ± 22,5 vs. 87,6 ± 8,6 mg/dl) foi superior no CSM comparado ao SSM. Os valores de triglicérides (159,5 ± 68,8 vs. 89,2 ± 34,3 mg/dl) e VLDL-c (31,9 ± 13,8 vs. 17,8 ± 6,9 mg/dl) foram superiores no CSM comparado ao SSM. O HDL-c (40,7 ± 11,5 vs. 49,3 ± 9,8 mg/dl) foi menor no CSM comparado ao SSM. O IMC (33,1 ± 4,7 vs. 30,8 ± 3,8 Kg/m²) foi superior no CSM comparado ao SSM. A PAS (128,6 ± 12,9 vs. 119,5 ± 11,3 mmHg) e a PAD (77,2 ± 10,5 vs. 72,9 ± 8,1 mmHg) foram superiores no CSM comparado ao SSM, p < 0,05. Conclusão: Os resultados sugerem que a presença de SM não é suficiente para provocar alterações nos índices de VFC em repouso, durante teste cardiopulmonar de exercício (TCPE) e na recuperação quando os pacientes são comparados a indivíduos sem a doença.

ABSTRACT Introduction: Heart rate variability (HRV) has been considered a modulation mechanism of the autonomic nervous system. The reduction of HRV may be associated with metabolic syndrome (MS). Objective: To compare the HRV and health variables in individuals with and without MS. Methods: One hundred and nineteen participants were divided into two groups: without MS (WOMS, n=68) and with MS (WMS, n=51). We evaluated the spectral analysis of HRV at rest, during cardiopulmo-nary exercise testing (CPET) and recovery in low frequency bands (LF = 0.04-0.15 Hz), high frequency (HF = 0.15-0.4 Hz) and LF/HF ratio. Resting heart rate (HRres), maximum heart rate (HRmax), systolic blood pressure (SBP) and diastolic (DBP), blood glucose, lipid profile, peak oxygen consumption (VO2peak) and body composition were also evaluated. Results: There were no differences between HRres and VO2peak between the WMS and WOMS groups (73.3±9.1 vs. 70.1±11.0 bpm), (26.8±4.6 vs. 28.1±6.6 ml.kg-1.min-1), respectively. HRV was similar between the groups at the different moments analyzed. The blood glucose levels (99.8±22.5 vs. 87.6±8.6 mg/dl) were higher in WMS compared to WOMS. Triglyceride values (159.5±68.8 vs. 89.2±34.3 mg/dl) and VLDL-c (31.9±13.8 vs. 17.8±6.9 mg/dl) were higher in WMS compared to WOMS. HDL-c (40.7±11.5 vs. 49.3±9.8 mg/dl) was lower in WMS compared to WOMS. BMI (33.1±4.7 vs. 30.8±3.8 kg/m²) was higher in WMS compared to WOMS. The SBP (128.6±12.9 vs. 119.5±11.3 mmHg) and DBP (77.2±10.5 vs. 72.9± 8.1mmHg) were higher in WMS com-pared to WOMS, p<0.05. Conclusion: The results suggest that the presence of MS is not sufficient to induce changes in HRV at rest, during cardiopulmonary exercise test (CPET), and in recovery when patients are compared to healthy individuals.

RESUMEN Introducción: La variabilidad de la frecuencia cardiaca (VFC) ha sido considerada como un mecanismo de modulación del sistema nervioso autónomo. La disminución de VFC puede estar asociada con el síndrome metabólico (SM). Objetivo: Comparar la VFC y variables de salud en individuos con y sin SM. Métodos: Ciento diecinueve sujetos se dividieron en dos grupos: sin SM (SSM, n = 68) y con SM (CSM, n = 51). Se evaluó el análisis espectral de la VFC en reposo durante las pruebas de ejercicio cardiopulmonar (PECP) y la recuperación en banda de baja frecuencia (LF = 0,04-0,15 Hz), alta frecuencia (HF = 0,15-0,4 Hz) y la relación LF/HF. Además, se evaluaron la frecuencia cardiaca en reposo (FCrep), FC máxima (FCmáx), presión arterial sistólica (PAS) y diastólica (PAD), glicemia, perfil lipídico, consumo pico de oxígeno (VO2pico) y composición corporal. Resultados: FCrep y VO2pico no mostraron diferencias entre CSM y SSM (73,3 ± 9,1 vs. 70,1 ± 11,0 bpm) (26,8 ± 4,6 vs. 28,1 ± 6,6 ml.kg-1.min-1), respectivamente. La VFC fue similar entre los grupos en diferentes momentos analizados. La glicemia (99,8 ± 22,5 vs. 87,6 ± 8,6 mg/dl) fue mayor en CSM en comparación con SSM. Los valores de triglicéridos (159,5 ± 68,8 vs. 89,2 ± 34,3 mg/dl) y VLDL-C (31,9 ± 13,8 vs. 17,8 ± 6,9 mg/dl) fueron más altos en CSM en comparación con SSM. HDL-C (40,7 ± 11,5 vs. 49,3 ± 9,8 mg/dl) fue menor en CSM en comparación con el SSM. El IMC (33,1 ± 4,7 vs. 30,8 ± 3,8 kg/m²) fue mayor en CSM en comparación con SSM. La PAS (128,6 ± 12,9 vs. 119,5 ± 11,3 mmHg) y la PAD (77,2 ± 10,5 vs. 72,9 ± 8,1 mmHg) fueron más altas en CSM en comparación con SSM, p < 0,05. Conclusión: Los resultados sugieren que la presencia de SM no es suficiente para provocar cambios en los índices de VFC en reposo durante las pruebas de ejercicio cardiopulmonar (PECP) y en la recuperación cuando se comparan los pacientes y los individuos saludables.

A multidisciplinary weight-loss program: the importance of psychological group therapy

Abstract In addition to dietary factors and sedentary habits, there is a relationship between obesity and psychological variables, even without a clear distinction between cause, effect, and correlation. Despite this relationship, weight-loss programs are limited to a combination of nutrition and physical education, leaving psychological intervention out of the treatment plan. Self-esteem issues, depression, and anxiety are just some of the emotional conditions related to obesity. However, there is no information in the literature about the importance of psychological counseling in a multidisciplinary program for weight-loss in adults. In this context, the main objective of this study was to analyze the effect of cognitive-behavioral therapy in groups (CBTG) combined with nutrition and physical education within a multidisciplinary approach to treat obesity. 46 individuals (7 men and 39 women) were divided into two groups: control (GC) and psychology (GP). Baseline and intervention measures were obtained prior to intervention and before the final meeting, including physical capacity tests and the administering the International Physical Activities Questionnaire (IPAQ). Both groups attended weekly lectures given by a nutritionist and two physical education professionals for 12 weeks. In addition, the GP participated in weekly sessions of CBTG for the same period. After the program, there were significant changes in body mass index, waist circumference, body fat percentage, and strength of the lower limbs in both groups. In addition to these changes, the GP also showed improvements in diastolic blood pressure and IPAQ scores, being the only one that increased its time of weekly physical activity. Thus, it was concluded that the psychological treatment might play an important role in a multidisciplinary weight-loss program.(AU)

Efeito de treinamentos de flexibilidade sobre a força e o torque muscular: uma revisão crítica / Effect of flexibility trainings on strength and muscle torque: a critical review

A flexibilidade é uma capacidade física de vital importância tanto para atletas como para os demais indivíduos. O presente artigo analisou estudos que observaram as possíveis influências do treino de flexibilidade nos níveis de força e torque muscular. Para isso, foi realizada uma busca na base de dados Google Scholar, com as palavras chave “Flexibility training, range of motion, strength and torque”, no período entre 2004 e 2010. Dos 23 estudos incluídos na análise, 15 observaram o efeito agudo de uma sessão de alongamento, sendo que destes, 8 não mostraram efeito do treinamento de flexibilidade nos níveis de força e torque e 7 verificaram efeito negativo no ganho de força. Ainda, 8 dos estudos analisados eram longitudinais, apresentando rotinas de treinamento de no mínimo 4 semanas de alongamento. Entre os estudos longitudinais, 7 observaram uma melhora nos níveis de força e torque e apenas um relatou influência negativa. Os estudos analisados apresentavam diferentes metodologias e protocolos de treinamento, o que dificultou a obtenção de resultados conclusivos. Entretanto, parece que o músculo avaliado tem grande importância para o resultado, isso devido às diferenças estruturais e da capacidade elástica específica dos componentes musculares. Ainda, a frequência de treinamento se mostrou mais importante que o volume de cada sessão para causar mudanças nas variáveis analisadas. Aparentemente, o treinamento de flexibilidade tem efeito agudo deletério ou neutro nos níveis de força e torque, devendo ser evitado antes de uma sessão de treinamento de força. Por outro lado, seu efeito crônico parece ser benéfico, devendo ser mantida a recomendação para a inclusão de rotinas de exercícios de flexibilidade paralelamente ao treinamento de força, como forma de se obter melhores ganhos na força e no torque muscular.

Flexibility is a paramount physical capacity for athletes and others as well. This paper has analyzed studies which had observed possible influences in flexibility training of muscle strength and muscle torque levels. In order to accomplish that we searched the Google Scholar database the following key-words: “flexibility training, range of motion, strength and torque” looking up 2004 through 2010. Of the twenty-three studies we included in this analysis, fifteen observe acute effect from a stretching session; of those, eight did not sport any strength and torque flexibility training effect and seven show a negative strength gain. Moreover, a total of eight studies we have reviewed were longitudinal, exhibiting training routines of at least four weeks of stretching. Amongst those longitudinal studies, seven depict improvement of strength and torque levels and just one mentions negative results. All surveyed results use distinct methodologies and training protocols, which made our gathering of conclusive data rather difficult. Nevertheless, it appears that the evaluated muscle is of great importance for the result due to structural discrepancies and elastic capacity specific to each muscle component. Moreover, training frequency has been revealed to be more important than the volume of each session in causing changes in the investigated variables. Apparently flexibility training has harmful to neutral acute effect of strength and torque levels and should be avoided before strength training sessions. On the other hand, its chronic impact seems to be beneficial, henceforth we recommend it should be maintained in exercise routines parallel to strength training as a means of obtaining better muscle strength and torque gain.