Circuit resistance training in women with normal weight obesity syndrome: body composition, cardiometabolic and echocardiographic parameters, and cardiovascular and skeletal muscle fitness.

BACKGROUND: Normal weight obesity (NWO) syndrome has been characterized in subjects with normal Body Mass Index (BMI) and high body fat mass percentage (BF%>30 for women) being a risk factor for cardiometabolic dysregulation and cardiovascular mortality. This study evaluated whether circuit resistance training (CRT) improves body composition, heart size and function, cardiometabolic parameters, and cardiorespiratory, cardiovascular and skeletal muscle fitness in women with NWO. METHODS: Data are means (95% Confidence Interval). Twenty-three women participated: 10 NWO-CRT (baseline: BMI=22.4 [21.4-23.3] kg/m2; BF%=44.5 [41.0-48.0]%) performed CRT; and 13 untrained NWO-control (baseline: BMI=21.7 [20.8-22.7] kg/m2; BF%=37.8 [34.6-41.1]%). At baseline and after 10 weeks were performed/measured dual-energy X-ray absorptiometry, echocardiography, blood tests, arterial pressure, exercise testing, and total-overload-by-training-session (TOL). RESULTS: At baseline, the NWO-CRT exhibited larger BF (27.28 [23.9-30.6] kg) than NWO-control (22.41 [19.5-25.3] kg) (P=0.0227). After training, NWO-CRT: reduced 8 kg of BF (P=0.000002); became BF% lower than NWO-control (33.1 [30.1-36.0] <37.0 [34.3-39.6]%, P=0.0423), with 30% of NWO-CRT subjects becoming without-obesity; reduced 3 kg in trunk fat mass (P=0.000005); showed fasting glucose (72.8 [69.4-76.2] mg/dL) smaller than NWO-control (81.7 [78.6-84.8] mg/dL) (P=0.004); increased TOL (5087.5 [4142.5-6032.5] to 6963.3 [6226.4-7700.2] rep.kg, P=0.0004); increased load at VO2peak (122.5 [106.8-138.2] to 137.5 [118.18-156.82] W, P=0.0051); reduced double product/load at VO2peak ratio (277.4 [222.1-332.8] to 237.7 [194.2-281.2] mmHg.bpm/W, P=0.0015); and increased left ventricular mass/body surface area ratio (84.29 [78.98-89.6] to 90.29 [81.45-99.12] g/m2, P=0.0215). CONCLUSIONS: CRT reduced BF% and generated cardiometabolic, cardiac, skeletal muscle and cardiovascular benefits, being a useful strategy to combat the normal weight obesity syndrome in women.

Resistance training and hormone replacement increase MMP-2 activity, quality and quantity of bone in ovariectomized rats

AIMS: The aim of the present study was to investigate the influence of resistance training (RT) and hormone replacement (HR) on MMP-2 activity, biomechanical and physical properties bone of ovariectomized (OVX) rats. METHODS: Sprague-Dawley female rats were grouped into six experimental groups (n = 11 per group): sham-operated sedentary (SHAM Sed), ovariectomized sedentary (OVX Sed), sham-operated resistance training (SHAM RT), ovariectomized resistance training (OVX RT), ovariectomized sedentary hormone replacement (OVX Sed-HR), and ovariectomized resistance training hormone replacement (OVX RT-HR). HR groups received implanted silastic capsules with a 5% solution of 17ß-estradiol (50 mg 17ß-estradiol/ml of sunflower oil). In a 12-week RT period (27 sessions; 4-9 climbs) the animals climbed a 1.1 m vertical ladder with weights attached to their tails. Biomechanical and physical bone analyses were performed using a universal testing machine, and MMP-2 activity analysis was done by zymography. RESULTS: Bone density and bone mineral content was higher in the RT and HR groups. The MMP-2 activity was higher in the RT and HR groups. The biomechanical analysis (stiffness, fracture load and maximum load) demonstrated better bone tissue quality in the RT associated with HR. CONCLUSION: The RT alone as well as when it is associated with HR was efficient in increasing MMP-2 activity, biomechanical and biophysical properties bone of ovariectomized rats.(AU)

GLUT2 proteins and PPARγ transcripts levels are increased in liver of ovariectomized rats: reversal effects of resistance training.

PURPOSE: This study investigated the effects of ovariectomy (Ovx) and 12 weeks of resistance training (RT) on gene expression of GLUT2, the main glucose transporter in the liver, and on PPARγ, a transcription factor known to target GLUT2 expression. METHODS: Forty Holtzman rats were divided into 5 groups: Sham-sedentary (Sed), Sham- RT, Ovx-Sed, Ovx-RT, and Ovx-Sed with hormone replacement (E2). The RT protocol consisted of sessions held every 72 h for 12 weeks, during which the animals performed 4 to 9 vertical climbs (1.1 m) at 2 min intervals with progressively heavier weights (30 g after the fourth climb) tied to the tail. The E2 silastic capsule was inserted into the rats' backs 48 hours before the first RT session. RESULTS: In addition to liver fat, GLUT2 protein levels and PPARγ transcripts were increased (P < 0.05) in Ovx compared to Sham-Sed animals, suggesting increased hepatic glucose uptake under estrogen deficient conditions. RT and E2 in Ovx rats decreased liver fat accumulation as well as GLUT2 and PPARγ gene expression to the level of Sham- Sed animals. CONCLUSION: The results of this study suggest that liver GLUT2 as well as PPARγ expression in Ovx rats are accompanied by increased fat accumulation and glucose uptake, thus providing a substrate for increased de novo lipogenesis. RT appears to be an appropriate exercise model to circumvent these effects.

Hydrogen peroxide production regulates the mitochondrial function in insulin resistant muscle cells: effect of catalase overexpression.

The mitochondrial redox state plays a central role in the link between mitochondrial overloading and insulin resistance. However, the mechanism by which the ROS induce insulin resistance in skeletal muscle cells is not completely understood. We examined the association between mitochondrial function and H2O2 production in insulin resistant cells. Our hypothesis is that the low mitochondrial oxygen consumption leads to elevated ROS production by a mechanism associated with reduced PGC1α transcription and low content of phosphorylated CREB. The cells were transfected with either the encoded sequence for catalase overexpression or the specific siRNA for catalase inhibition. After transfection, myotubes were incubated with palmitic acid (500µM) and the insulin response, as well as mitochondrial function and fatty acid metabolism, was determined. The low mitochondrial oxygen consumption led to elevated ROS production by a mechanism associated with ß-oxidation of fatty acids. Rotenone was observed to reduce the ratio of ROS production. The elevated H2O2 production markedly decreased the PGC1α transcription, an effect that was accompanied by a reduced phosphorylation of Akt and CREB. The catalase transfection prevented the reduction in the phosphorylated level of Akt and upregulated the levels of phosphorylated CREB. The mitochondrial function was elevated and H2O2 production reduced, thus increasing the insulin sensitivity. The catalase overexpression improved mitochondrial respiration protecting the cells from fatty acid-induced, insulin resistance. This effect indicates that control of hydrogen peroxide production regulates the mitochondrial respiration preventing the insulin resistance in skeletal muscle cells by a mechanism associated with CREB phosphorylation and ß-oxidation of fatty acids.

[Regulation of glucose and fatty acid metabolism in skeletal muscle during contraction]. / Regulação do metabolismo de glicose e ácido graxo no músculo esquelético durante exercício físico.

The glucose-fatty acid cycle explains the preference for fatty acid during moderate and long duration physical exercise. In contrast, there is a high glucose availability and oxidation rate in response to intense physical exercise. The reactive oxygen species (ROS) production during physical exercise suggests that the redox balance is important to regulate of lipids/carbohydrate metabolism. ROS reduces the activity of the Krebs cycle, and increases the activity of mitochondrial uncoupling proteins. The opposite effects happen during moderate physical activity. Thus, some issues is highlighted in the present review: Why does skeletal muscle prefer lipids in the basal and during moderate physical activity? Why does glucose-fatty acid fail to carry out their effects during intense physical exercise? How skeletal muscles regulate the lipids and carbohydrate metabolism during the contraction-relaxation cycle?

Regulação do metabolismo de glicose e ácido graxo no músculo esquelético durante exercício físico / Regulation of glucose and fatty acid metabolism in skeletal muscle during contraction

O ciclo glicose-ácido graxo explica a preferência do tecido muscular pelos ácidos graxos durante atividade moderada de longa duração. Em contraste, durante o exercício de alta intensidade, há aumento na disponibilidade e na taxa de oxidação de glicose. A produção de espécies reativas de oxigênio (EROs) durante a atividade muscular sugere que o balanço redox intracelular é importante na regulação do metabolismo de lipídios/carboidratos. As EROs diminuem a atividade do ciclo de Krebs e aumentam a atividade da proteína desacopladora mitocondrial. O efeito oposto é esperado durante a atividade moderada. Assim, as questões levantadas nesta revisão são: Por que o músculo esquelético utiliza preferencialmente os lipídios no estado basal e de atividade moderada? Por que o ciclo glicose-ácido graxo falha em exercer seus efeitos durante o exercício intenso? Como o músculo esquelético regula o metabolismo de lipídios e carboidratos em regime envolvendo o ciclo contração-relaxamento.

The glucose-fatty acid cycle explains the preference for fatty acid during moderate and long duration physical exercise. In contrast, there is a high glucose availability and oxidation rate in response to intense physical exercise. The reactive oxygen species (ROS) production during physical exercise suggests that the redox balance is important to regulate of lipids/carbohydrate metabolism. ROS reduces the activity of the Krebs cycle, and increases the activity of mitochondrial uncoupling proteins. The opposite effects happen during moderate physical activity. Thus, some issues is highlighted in the present review: Why does skeletal muscle prefer lipids in the basal and during moderate physical activity? Why does glucose-fatty acid fail to carry out their effects during intense physical exercise? How skeletal muscles regulate the lipids and carbohydrate metabolism during the contraction-relaxation cycle?.