title: Vascular and Haemorheological Responses following Acute Exercise in Lean and Active women with Polycystic Ovary Syndrome
Creators: name: Brotherton, Emily J
Publisher: name: Griffith University
Year: 2019
Subjects: subject: Polycystic Ovary Syndrome
subject: PCOS
subject: cardiovascular disease
subject: CVD
subject: Endothelial dysfunction

description: Polycystic Ovary Syndrome (PCOS) is associated with an increased risk of cardiovascular disease (CVD), which is suggested to be largely due to vascular endothelial dysfunction. Endothelial dysfunction is typically represented as an impaired vasodilatory response to an appropriate shear stimulus which is dictated by the flow of blood and its components as well as vessel diameter. Notably, both vascular and haemorheological parameters have been well-documented to improve following long-term exercise in many disease states that share similar characteristics to PCOS. As such, high levels of cardiorespiratory fitness have been associated with healthy vascular function and blood characteristics in various populations. In contrast to long-term exercise, vascular and haemorheological responses to acute exercise would provide insight into the mechanisms that may stimulate beneficial long-term exercise-induced adaptions. Therefore, the current study aimed to examine the vascular and haemorheological responses in PCOS to two acute exercise bouts (moderate and heavy-intensity) compared to controls matched for cardiorespiratory fitness. The findings of the present study may provide an understanding to the influence of exercise training on vascular function and haemorheology in women with PCOS and whether prolonged adaptations or impairments to these variables are observed in this population. Methods: Endothelial function and haemorheological measurements were performed at baseline and following moderate and heavy-intensity exercise in eight women with PCOS (age: 26 ± 4 years) and ten controls (age: 28 ± 6 years), matched for BMI (23.8 ± 3.1; 21.2 ± 3.1 kg·m-2) and cardiorespiratory fitness (V̇O2max: 39.33 ± 6.07; 40.70 ± 5.74 mL·kg-1·min-1). Endothelial function was assessed by flow-mediated dilation (FMD), and normalised for the shear stimulus (FMD:SRAUC). FMD variables measured at baseline and following exercise were expressed as absolute and magnitude in change values. Haemorheology was assessed by measurement of blood viscosity (at native and standardised haematocrit), red blood cell (RBC) aggregation (at native and standardised haematocrit), plasma viscosity and RBC deformability. Cardiorespiratory fitness and metabolic, hormone and cardiovascular profiles were also assessed. Results: At baseline, there were no significant differences in FMD variables between groups, however RBC aggregation indices in both native and standardised haematocrit (p = 0.001) and plasma viscosity (p = 0.026) were elevated in PCOS women compared to controls. FMD and haemorheological parameters were not different between groups following moderate-intensity exercise (p &gt; 0.05). Following heavy-intensity exercise, the baseline to post-exercise change in SRAUC (p = 0.04) and SR max (p = 0.009) were significantly greater in women with PCOS compared to controls. In contrast, women with PCOS demonstrated a significantly lower baseline to post exercise change in FMD:SRAUC (p = 0.021) following heavy-intensity exercise in comparison to controls. Conclusion: The findings of the present study demonstrated that at rest, women with PCOS exhibited preserved vascular function, however haemorheology (as demonstrated by elevations in RBC aggregation and plasma viscosity) was altered despite being young, healthy weight and fit. Furthermore, vascular reactivity was similar between groups following moderate-intensity exercise. In contrast, women with PCOS demonstrated an altered vasodilatory response in comparison to controls following heavy-intensity exercise. These findings provide new evidence that despite being young, lean and fit, women with PCOS exhibit altered baseline haemorheology parameters and an altered vasodilatory response to heavy-intensity exercise ─ factors that can further exacerbate endothelial dysfunction, potentially increasing the risk of CVD.