Insulin resistance (IR) is an endocrine disease [1], [2], characterized by diminished response to insulin, whereby the target tissues cannot store sufficient blood glucose; in case of compensatory response, insulin secretion rises, causing hyperinsulinemia [3]. IR plays a key role in the pathogenesis of polycystic ovary syndrome (PCOS) as well as nonalcoholic fatty liver disease (NAFLD). It involves a biological reaction from tissues such as liver, muscles, and adipose tissue to insulin stimulation [4]. One of the earliest theories presented for explaining the muscular IR mechanisms was propounded by Ranell et al. in the 1960s. They concluded that dramatic increase in fatty acid oxidation of muscles leads to citrate accumulation, causing inhibition of phosphofructokinase (the axial enzyme in glycolysis), resulting in impaired glucose uptake [3].

Prevalence of obesity and chronic diseases in recent years worldwide has grown dramatically. Low physical activity, high caloric intake, or both lead to positive energy balance and weight gain [5]. Also, PCOS is often characterized by a wide range of dysglycemia conditions such as IR and type 2 diabetes (T2D), which occur more frequently in comparison to healthy women with the same body mass index [6]. Insulin plays a key role in regulating the adipose tissue functioning including, regulation of glucose uptake in insulin-sensitive tissues such as adipose cells, skeletal muscle cells, and liver cells, which are the main factors in PCOS [7]. Impaired insulin messaging, which involves INSR, IRS1, PI3K, and Akt pathways in IR leads to diminished glucose uptake by insulin [3]. IR also plays a fundamental role in PCOS [8], causing impaired ovulation and development of endometrial dysfunction, both resulting in infertility. Meanwhile, IR has long-term and harmful effects on the metabolism of patients with PCOS [9]. Excessive insulin production can stimulate the pituitary gland's insulin receptor, whereby LH is released, and androgen secretion is elevated by the ovaries as well as adrenal gland along with free testosterone level. Excessive androgen secretion may lead to hirsutism, acne, as well as alopecia symptoms, and prevent the growth and development of ovarian follicles. It is considered the most common reason of secondary infertility in ovulation dysfunction [9], [10]. In addition, insulin can directly regulate the ovary's follicle growth and hormone secretion through insulin receptors’ system in follicle membrane cells. Further, insulin can increase the activity of the insulin-like growth factor (IGF-1) receptor in the ovary, causing its elevated free IGF level. It also promotes androgen production; changes in the endometrial function may be a considerable reason in low fertility in PCOS patients [10]. Meanwhile, one of the main contributing factors underlying the pathogenesis of IR is the effect of lipotoxicity. Lipotoxicity is a kind of cellular stress, which occurs due to accumulation of lipid mediators such as diacyl glycerols (DAGs), ceramides, and triglycerides, causing elevated IR in muscles, liver, and adipose tissue [3].

According to studies, the prevalence of obesity has doubled in developed countries over the past two decades [11]. Obesity is associated with inflammatory and pro-inflammatory factors [12]. In the liver, accumulation of triglyceride is involved in the pathogenesis of hepatic IR, where the high levels of fatty acid mediators impair the insulin messaging through reducing carriage of GLUT4 across the myocyte surface. These factors cause extrauterine lipid accumulation in both old and young individuals, which is reversible through weight loss, exercise, and proper diet [3]. Some studies have shown that general weight loss and loss of considerable portions of abdominal fat are important therapeutic strategies in this regard [11]. According to studies, exercise develops positive clinical outcomes for women with PCOS; lifestyle factors such as suitable diet and exercise can be key factors in improving the metabolic state [8]. Exercise is characterized as an effective measure for reducing development of T2D, IR, and PCOS as well as related diseases in the long run [13]. Ramanjaneya et al. (2022) investigated how moderate aerobic exercise influences insulin sensitivity and complement system dysregulation in women with PCOS. Their findings suggest that complement-related proteins may play a role in modulating exercise response, which could be a novel target for future therapies [14]. Aye et al. (2018) demonstrated that while endurance exercise improves insulin sensitivity in women with PCOS, it does not alter the fundamental mechanisms of lipid-induced insulin resistance. This highlights the transient nature of exercise-induced improvements and suggests that underlying metabolic defects remain unchanged [15]. However, vigorous-intensity aerobic exercise and resistance training yield significant improvements in insulin resistance measures like HOMA-IR [16], [17]. Recent systematic reviews, including those by Patten et al. (2020) [16] and Alesi et al. (2022) [18], have demonstrated the efficacy of exercise interventions and nutritional supplements in improving insulin sensitivity and metabolic health outcomes in women with PCOS. However, gaps remain regarding the comparative effectiveness of different exercise modalities, intensities, and durations. The present study aimed to review the findings of recent studies regarding the effect of exercise on IR in PCOS.