BackgroundTo evaluate the feasibility of executing a randomized controlled trial of progressive resistance training (PRT) in women with polycystic ovary syndrome (PCOS).MethodsWomen with PCOS were randomized to an experimental (PRT) group or a no-exercise (usual care) control group. The PRT group was prescribed two supervised and two unsupervised (home-based) training sessions per week for 12 weeks. Feasibility outcomes included recruitment and attrition, adherence, adverse events, and completion of assessments. Secondary outcomes, collected pre and post intervention, included a range of pertinent physiological, functional and psychological measures.ResultsFifteen participants were randomised into the PRT group (n = 8) or control group (n = 7); five women (n = 2 in PRT group and n = 3 in control group) withdrew from the study. The most successful recruitment sources were Facebook (40 %) and online advertisement (27 %), while least successful methods were referrals by clinicians, colleagues and flyers. In the PRT group, attendance to supervised sessions was higher (95 %; standard deviation ±6 %) compared to unsupervised sessions (51 %; standard deviation ±28 %). No adverse events were attributed to PRT. Change in menstrual cycle status was not significantly different between groups over time (p = 0.503). However, the PRT group significantly increased body weight (p = 0.01), BMI (p = 0.04), lean mass (p = 0.01), fat-free mass (p = 0.005) and lower body strength (p = 0.03), while reducing waist circumference (p = 0.03) and HbA1c (p = 0.033) versus the control group. The PRT group also significantly improved across several domains of disease-specific and general health-related quality of life, depression, anxiety and exercise self-efficacy.ConclusionA randomized controlled trial of PRT in PCOS would be feasible, and this mode of exercise may elicit a therapeutic effect on clinically important outcomes in this cohort. The success of a large-scale trial required to confirm these findings would be contingent on addressing the feasibility hurdles identified in this study with respect to recruitment, attrition, compliance, and collection of standardized clinical data.Trial registrationAustralia New Zealand Clinical Trials Registry; ACTRN12614000517673 Registered 15 May 2014.

Gonadal function is wholly reliant on the two pituitary-derived gonadotropins, FSH and LH. Identifying the specific effects of FSH has been difficult because of the intimate relationship between LH and FSH action and inherent limitations of classic research paradigms. We describe a novel transgenic model to characterize the definitive actions of FSH alone, distinct from LH effects, created by combining transgenic FSH expression with the gonadotropin-deficient background of the hypogonadal (hpg) mouse. A tandem transgene construct encoding each alpha- and beta-subunit of human FSH, under the rat insulin II promoter, expressed biologically active heterodimers at serum levels, by immunoassay, equivalent to circulating FSH concentrations in fertile humans (0.1-25 IU/liter). Transgenic mice were crossed into the hpg mouse genotype to obtain LH-deficient animals secreting FSH alone. Testis weights of adult FSHxhpg mice were increased up to 5-fold, relative to nontransgenic hpg controls (P < 0.001). However, only transgenic males with serum FSH levels more than 1 IU/liter showed testis weights increased relative to hpg controls, indicating a physiological FSH threshold for the testicular response. Histology of enlarged FSHxhpg testes revealed round spermatids and sparse numbers of elongated spermatids, demonstrating that the testosterone-independent FSH response targeting the Sertoli cell can facilitate completion of meiosis and minimal initiation, but not completion, of spermiogenesis. Transgenic FSH also induced inhibin B secretion in FSHxhpg mice, but showed a distinct sexual dimorphism with only females exhibiting a strong FSH dose-dependent increase in serum inhibin B levels (r(2) = 0.84). In addition, ovaries of FSHxhpg females were enlarged up to 10-fold (P < 0.001), characterized by increased follicular recruitment and development to type 7 antral follicles. Thus, these findings show that the transgenic FSHxhpg mouse provides a unique model for detailed investigations of the definitive in vivo actions of FSH alone.

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder and cause of subfertility in women. The etiology of PCOS has not been fully elucidated; however, insulin resistance has been shown to exacerbate the disease process due to its effect on androgen synthesis. Progressive resistance training (PRT) is an anabolic exercise modality that can improve skeletal muscle size and quality (metabolic capacity), and studies have consistently shown that PRT can increase insulin sensitivity in type 2 diabetes and other cohorts. However, PRT is not currently recommended or routinely prescribed in PCOS. The objective of this article was to provide a rationale for the application of PRT in the management and treatment of PCOS. This will be accomplished by (1) overviewing the pathophysiology of PCOS with emphasis on the etiological role of insulin resistance; (2) summarizing the effectiveness of PRT in treating insulin resistance; (3) presenting evidence that PRT is feasible to prescribe in women with PCOS; and (4) providing general recommendations for PRT to complement existing guidelines for aerobic training in this cohort. We also provide recommendations for future research.

In the "glucose-fatty acid" cycle (Randle, 1963), I overproduction and utilization of nonesterified fatty acids (NEFAs) inhibits glucose uptake and disposal. This may contribute to the insulin resistance seen in obesity and non-insulin-dependent diabetes mellitus (NIDDM).' Elevated plasma NEFA levels have been associated with body f a t n e s~,~.~ particularly in those with excess abdominal fat dep~sition,~ impaired glucose t~lerance,~ and decreased whole-body glucose uptake in NIDDM6 and in nondiabetic normal-weight Artificial reduction of NEFA availability improves glucose oxidation and decreases lipid utilization, while heparin-induced rises in serum NEFA enhance lipid oxidation and reduce glucose oxidation in healthy NIDDM subjects.IO In a recent study involving normal subjects, circulating NEFA levels were directly associated with rates of glucose and lipid oxidation and glycogen synthesis, suggesting a regulatory role for NEFA in both oxidative and nonoxidative pathways." As part of an ongoing study of metabolic changes in obesity, we studied the interrelationships between circulating levels of NEFAs and different parameters of glucose and lipid metabolism in obese subjects, both basally and following insulin stimulation.