Physical Activity Patterns in Normal-Weight and Overweight/Obese Pregnant Women.

The aims of the present study were to assess the volume of physical activity (PA) throughout pregnancy in normal-weight vs overweight/obese women, and to investigate which factors may predict compliance to PA recommendations in these women throughout gestation. In 236 pregnant women, 177 normal-weight and 59 overweight/obese (median[IQR] BMI 21.2[19.9-22.8] vs 26.5[25.5-29.0] kg/m2, respectively), medical history, anthropometry and clinical data, including glucose tolerance, were recorded. In addition, pre-pregnancy PA was estimated by the Kaiser questionnaire, while total, walking and fitness/sport PA during pregnancy were assessed by the Physical Activity Scale for the Elderly (PASE) modified questionnaire, at 14-16, 24-28 and 30-32 weeks of gestation. PA volume was very low in the first trimester of pregnancy in both groups of women. However, it increased in the second and third trimester in normal-weight, but not in overweight/obese subjects. Higher pre-pregnancy PA was a statistically significant predictor of being physically active (>150 minutes of PA per week) during all trimesters of gestation. In conclusion, physical activity volume is low in pregnant women, especially in overweight/obese subjects. PA volume increases during pregnancy only in normal-weight women. Pre-pregnancy PA is an independent predictor of achieving a PA volume of at least 150 min per week during pregnancy.

Serum testosterone predicts cardiorespiratory fitness impairment in normal-weight women with polycystic ovary syndrome.

OBJECTIVE: Limited literature has shown that maximal oxygen consumption (V'O2max), that is the maximal capacity of an individual to perform aerobic work, may be lowered in overweight/obese women with polycystic ovary syndrome (PCOS). However, it remains unclear whether this impairment is associated with PCOS per se or is entirely due to body fat excess. Our objective was to assess whether cardiorespiratory fitness is altered in normal-weight PCOS women and to investigate which factors are associated with this phenomenon. SUBJECTS: Fifteen normal-weight PCOS women and 15 age- and BMI-matched healthy controls. Fourteen subjects in each group completed the protocol. MEASUREMENTS: V'O2max and ventilatory thresholds (maximal incremental cycle ergometer test with breath-by-breath analysis of gas exchange), insulin sensitivity (hyperinsulinaemic euglycaemic clamp) and androgenaemia (serum total and free testosterone, measured by liquid chromatography mass spectrometry and equilibrium dialysis) were accurately assessed. RESULTS: Maximal V'O2 and power were strikingly impaired in normal-weight PCOS individuals, as compared with healthy controls (29·4 ± 1·5 vs 35·8 ± 1·6 ml O2/kg/min, P = 0·008; 138 ± 6 vs 170 ± 10 W, P = 0·011, respectively). Similarly, oxygen consumption and power at both the first and second ventilatory thresholds were significantly lower in PCOS subjects than in healthy women. In multiple regression analysis, V'O2max was negatively predicted by serum-free testosterone levels, but not by body fat mass and glucose disposal rate (R(2) = 0·45 P = 0·013). CONCLUSIONS: Cardiorespiratory fitness is impaired in normal-weight PCOS women. Androgen excess but not insulin sensitivity is associated with this alteration.

Total body fat and central fat mass independently predict insulin resistance but not hyperandrogenemia in women with polycystic ovary syndrome.

CONTEXT/OBJECTIVE: Obesity is a common feature of women with polycystic ovary syndrome (PCOS). The aim of this study was to assess the role of body fat on insulin resistance and androgen excess in these subjects. PATIENTS/DESIGN: One hundred sixteen consecutive Caucasian women with PCOS, diagnosed by the Rotterdam criteria, underwent accurate assessment of clinical, anthropometric, hormonal, and metabolic features. In particular, total fat mass and fat distribution were assessed by dual-energy x-ray absorptiometry, serum-free T by liquid chromatography mass spectrometry and equilibrium dialysis and insulin sensitivity by the glucose clamp technique. RESULTS: Total fat mass and truncal fat were significantly higher in insulin-resistant than in insulin-sensitive PCOS subjects (+89% and +127%, respectively, both P < .001), and both tended to be higher in hyperandrogenemic than in normoandrogenemic women (+22% and +28%, respectively, P = .087 and P = .090). All parameters of adiposity correlated inversely with insulin sensitivity (P < .001) and directly with serum-free T (P ≤ .001). A statistically significant inverse relationship was observed between insulin sensitivity and serum-free T concentrations (r = -0.527, P < .001). In a multiple regression analysis, either total fat mass or truncal fat, in addition to serum-free T and age, were independent predictors of insulin sensitivity. However, insulin sensitivity, but not total fat mass or truncal fat, was an independent predictor of free T concentrations. CONCLUSIONS: These data suggest that body fat contributes to determining insulin resistance in PCOS women. However, the association between body fat and hyperandrogenism seems to be to a large extent explained by insulin resistance.

Plasma levels of pentraxin-3, an inflammatory protein involved in fertility, are reduced in women with polycystic ovary syndrome.

OBJECTIVE: Pentraxin-3 (PTX3), like C-reactive protein (CRP), is an acute-phase protein that belongs to the pentraxin superfamily. Moreover, it is expressed in the cumulus oophorus and appears to be involved in female fertility. The aim of the present study was to assess whether PTX3 levels are altered in polycystic ovary syndrome (PCOS) women and whether they show any relationship with the main features of these subjects. DESIGN: A cross-sectional study was conducted at the outpatient clinic of an academic centre. METHODS: A total of 66 women affected with PCOS and 51 healthy controls were studied. Plasma PTX3 and serum CRP were measured by ELISA. Androgens were measured by liquid chromatography-mass spectrometry and free testosterone was measured by equilibrium dialysis. In PCOS women, insulin sensitivity was assessed by the glucose clamp technique. RESULTS: Adjusting for age and BMI, plasma PTX3 was reduced in PCOS women (P=0.036), in contrast with serum CRP, which was increased (P=0.004). In multiple regression analysis, serum androgens and other endocrine and ovarian features of PCOS were predictors of PTX3 levels, whereas body fat was the main independent predictor of CRP concentrations. CONCLUSIONS: Plasma PTX3 levels were reduced in PCOS women and independently associated with hyperandrogenism and other endocrine and ovarian features of PCOS.

Metabolic inflexibility is a feature of women with polycystic ovary syndrome and is associated with both insulin resistance and hyperandrogenism.

CONTEXT: Metabolic inflexibility, ie, the impaired ability of the body to switch from fat to carbohydrate oxidation under insulin-stimulated conditions, is associated with insulin resistance. This alteration in metabolic plasticity can lead to organ dysfunction and is considered a key issue among the abnormalities of the metabolic syndrome. It is still unknown whether this phenomenon occurs in women with polycystic ovary syndrome (PCOS). OBJECTIVE: Our objective was to examine whether metabolic inflexibility is a feature of PCOS women and whether hyperandrogenism may contribute to this phenomenon. DESIGN AND PATIENTS: Eighty-nine Caucasian women with PCOS were submitted to hyperinsulinemic-euglycemic clamp. Respiratory exchange ratios were evaluated at baseline and during hyperinsulinemia by indirect calorimetry to quantify substrate oxidative metabolism. Total testosterone was measured by liquid chromatography mass spectrometry and free testosterone by equilibrium dialysis. SETTING: Outpatients were seen in a tertiary care academic center. MAIN OUTCOME MEASURE: Metabolic flexibility was assessed by the change in respiratory quotient upon insulin stimulation. RESULTS: Sixty-five of the 89 PCOS women (73%) had increased serum free testosterone, 68 (76%) were insulin resistant, and 62 (70%) had an impaired metabolic flexibility. Comparison of hyperandrogenemic and normoandrogenemic women showed that the 2 subgroups were of similar age but differed in terms of several anthropometric and metabolic features. In particular, hyperandrogenemic women had greater body mass index (32.9 ± 1.0 vs 24.7 ± 0.9 kg/m(2), P < .001) and lower glucose utilization during the clamp (9.2 ± 0.4 vs 10.9 ± 0.7 mg/kg fat-free mass · min, P = .023) and metabolic flexibility (0.09 ± 0.06 vs 0.12 ± 0.01, P = .014). In univariate analysis, metabolic flexibility was associated with several anthropometric, endocrine, and metabolic features. In multivariate analysis, this feature was directly associated with baseline respiratory quotient and insulin sensitivity and inversely with free testosterone and free fatty acids concentrations under insulin suppression (R(2) = 0.634, P < .001). CONCLUSIONS: Metabolic inflexibility is a feature of PCOS women. Both insulin resistance and androgen excess might contribute to this abnormality.

Divergences in insulin resistance between the different phenotypes of the polycystic ovary syndrome.

CONTEXT/OBJECTIVE: Current diagnostic criteria for polycystic ovary syndrome (PCOS) have generated distinct PCOS phenotypes, based on the different combinations of diagnostic features found in each patient. Our aim was to assess whether either each single diagnostic feature or their combinations into the PCOS phenotypes may predict insulin resistance in these women. PATIENTS/DESIGN: A total of 137 consecutive Caucasian women with PCOS, diagnosed by the Rotterdam criteria, underwent accurate assessment of diagnostic and metabolic features. Insulin sensitivity was measured by the glucose clamp technique. RESULTS: Among women with PCOS, 84.7% had hyperandrogenism, 84.7% had chronic oligoanovulation, and 89% had polycystic ovaries. According to the individual combinations of these features, 69.4% of women had the classic phenotype, 15.3% had the ovulatory phenotype, and 15.3% had the normoandrogenic phenotype. Most subjects (71.4%) were insulin resistant. However, insulin resistance frequency differed among phenotypes, being 80.4%, 65.0%, and 38.1%, respectively, in the 3 subgroups (P < .001). Although none of the PCOS diagnostic features per se was associated with the impairment in insulin action, after adjustment for covariates, the classic phenotype and, to a lesser extent, the ovulatory phenotype were independently associated with insulin resistance, whereas the normoandrogenic phenotype was not. Metabolic syndrome frequency was also different among phenotypes (P = .030). CONCLUSIONS: There is a scale of metabolic risk among women with PCOS. Although no single diagnostic features of PCOS are independently associated with insulin resistance, their combinations, which define PCOS phenotypes, may allow physicians to establish which women should undergo metabolic screening. In metabolic terms, women belonging to the normoandrogenic phenotype behave as a separate group.