Effects of plaster therapy on thigh fat

Background: Thigh fat is associated with high cardiometabolic risks, attenuate risk for dyslipidemia, and glucose intolerance. Aerobic exercise has been linked to fat metabolization due to the increase of free fatty acid oxidation and the preservation of muscle glycogen. Plaster therapy, a beauty treatment that allows the quick elimination or reduction of cellulite, flaccid skin, and localized fat, eliminating liquid from the body, producing improvements that are not only aesthetic but also health-wise, may be used to maximize fat loss in the thigh area and complement exercise. The aim of this study was to analyze the effect of plaster therapy in combination with aerobic exercise on thigh fat. Methods: Six female volunteers were randomly divided into an intervention group (TG; n = 3) performing an aerobic exercise with plaster therapy and a control group (CG; n = 3) performing only aerobic exercise. Subcutaneous fat was estimated by the analysis of skinfolds and thigh perimeters. Results: The treatment group demonstrated a significant decrease (p ≤ 0.05) in subcutaneous fat at the left and right perimeters and thigh skinfold measurements at the end of the 10-session protocol. Conclusion: Comparing skinfold measurements, both groups revealed a statistically significant decrease in the perimeter of both left and right thighs. Furthermore, skinfold measurements showed, for the treatment groups, significant statistical results in the thigh area. Exercise is indeed one of the most critical components for the metabolism of fat. Plaster therapy in combination with aerobic exercise seems to be effective for thigh fat reduction.

Physical Exercise and Myokines: Relationships with Sarcopenia and Cardiovascular Complications

Skeletal muscle is capable of secreting different factors in order to communicate with other tissues. These mediators, the myokines, show potentially far-reaching effects on non-muscle tissues and can provide a molecular interaction between muscle and body physiology. Sarcopenia is a chronic degenerative neuromuscular disease closely related to cardiomyopathy and chronic heart failure, which influences the production and release of myokines. Our objective was to explore the relationship between myokines, sarcopenia, and cardiovascular diseases (CVD). The autocrine, paracrine, and endocrine actions of myokines include regulation of energy expenditure, insulin sensitivity, lipolysis, free fatty acid oxidation, adipocyte browning, glycogenolysis, glycogenesis, and general metabolism. A sedentary lifestyle accelerates the aging process and is a risk factor for developing sarcopenia, metabolic syndrome, and CVD. Increased adipose tissue resulting from the decrease in muscle mass in patients with sarcopenia may also be involved in the pathology of CVD. Myokines are protagonists in the complex condition of sarcopenia, which is associated with adverse clinical outcomes in patients with CVD. The discovery of new pathways and the link between myokines and CVD remain a cornerstone toward multifaceted interventions and perhaps the minimization of the damage resulting from muscle loss induced by factors such as atherosclerosis.

Modulation of Cardiac Metabolism in Heart Failure

Heart failure is associated with altered cardiac metabolism, in part, due to maladaptive mechanisms, in part secondary to comorbidities such as diabetes and ischaemic heart disease. The metabolic derangements taking place in heart failure are not limited to the cardiac myocytes, but extend to skeletal muscles and the vasculature causing changes that contribute to the worsening of exercise capacity. Modulation of cardiac metabolism with partial inhibition of free fatty acid oxidation has been shown to be beneficial in patients with heart failure. At the present, the bulk of evidence for this class of drugs comes from Trimetazidine. Newer compounds partially inhibiting free fatty acid oxidation or facilitating the electron transport on the mitochondrial cristae are in early phase of their clinical development.

Impact of anaerobic glycolysis and oxidative substrate selection on contractile function and mechanical efficiency during moderate severity ischemia

The role of anaerobic glycolysis and oxidative substrate selection on contractile function and mechanical efficiency during moderate severity myocardial ischemia is unclear. We hypothesize that 1) preventing anaerobic glycolysis worsens contractile function and mechanical efficiency and 2) increasing glycolysis and glucose oxidation while inhibiting free fatty acid oxidation improves contractile function during ischemia. Experiments were performed in anesthetized pigs, with regional ischemia induced by a 60% decrease in left anterior descending coronary artery blood flow for 40 min. Three groups were studied: 1) no treatment, 2) inhibition of glycolysis with iodoacetate (IAA), or 3) hyperinsulinemia and hyperglycemia (HI + HG). Glucose and free fatty acid oxidation were measured using radioisotopes and anaerobic glycolysis from net lactate efflux and myocardial lactate content. Regional contractile power was assessed from left ventricular pressure and segment length in the anterior wall. We found that preventing anaerobic glycolysis with IAA during ischemia in the absence of alterations in free fatty acid and glucose oxidation did not adversely affect contractile function or mechanical efficiency during myocardial ischemia, suggesting that anaerobic glycolysis is not essential for maintaining residual contractile function. Increasing glycolysis and glucose oxidation with HI + HG inhibited free fatty acid oxidation and improved contractile function and mechanical efficiency. In conclusion, these results show a dissociation between myocardial function and anaerobic glycolysis during moderate severity ischemia in vivo, suggesting that metabolic therapies should not be aimed at inhibiting anaerobic glycolysis per se, but rather activating insulin signaling and/or enhancing carbohydrate oxidation and/or decreasing fatty acid oxidation.