In 1935, Stein and Leventhal reported a frame with signs and symptoms related to anovulation. In this context, we included women who had a history of infertility, menstrual disorder, hirsutism and obesity along with the demonstration of enlarged ovaries with cysts and hypertrophy of the stroma. Later known as polycystic ovary syndrome (PCOS) is now regarded as a complex hormonal disorder characterized by hyperandrogenic chronic anovulation that affecting 5 to 10% of women of reproductive age and affecting the reproductive sphere, aesthetics, metabolic and oncology.The key features of the syndrome consist of:i. Menstrual dysfunction (oligomenorrhea and, less often, amenorrhea or even a regular cycle, but anovulatory).ii. Hyperandrogenemia (increased concentration of total testosterone, free, and less constancy, dehydroepiandrosterone sulfate [DHEAS] and androstenedione).iii. Hyperandrogenism (hirsutism, acne, and androgenic alopecia).iv. Polycystic ovarian morphology identified by ultrasonography (presence of 12 or more follicles measuring between 2 mm and 9 mm in diameter or increased ovarian volume e 10 cm3).Hyperinsulinemia and insulin resistance (IR) are also described in patients with PCOS, regardless of body mass index (BMI), although such conditions are undoubtedly more prevalent in the presence of obesity. Descriptive study of College of Medicine, University of São Paulo (FMUSP) indicated that 36% of PCOS patients are obese. The IR may be the link between PCOS and obesity, since both frames are also characterized by decreased insulin sensitivity in both muscle and liver tissue. According to the College of Medicine, University of São Paulo (FMUSP), IR is present in 60% of patients with PCOS and, most likely, is heavily involved in the etiology of metabolic disorders often found in this population.It is known that in conditions of IR, high insulin levels stimulate ovarian androgen production. Excess androgens are known to be a contributing factor to the IR of patients with PCOS, thus generating a vicious circle in which hyperinsulinemia promotes increased production of androgen which, in turn, contribute to IR.A recent study showed that a high intensity exercise training program resulted in increased insulin sensitivity in obese patients with PCOS and obese volunteers without PCOS. However, exercise was not able to completely reverse the IR in PCOS patients, suggesting a suboptimal response to the stimulus of exercise training in this population. In fact, new research may elucidate the mechanisms by which exercise stimulates (or fails to stimulate) glucose uptake in PCOS.Therefore, understanding the molecular mechanisms associated with IR in patients with PCOS may be considered of vital importance for the development of therapeutic strategies (exercise or drugs) dedicated to the treatment of the syndrome. In this context, the acute physical exercise emerges as an excellent research model in order that the chronic adaptations to regular physical training appear to be the result of the sum of acute and repeated stimulation of several individual training sessions.
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