Cardiovascular disease and diabetes are major health burdens. Diabetes is a primary risk factor of cardiovascular disease, and there is a strong link between obesity and risk of developing diabetes. With the prevalence of prediabetes highest among overweight/obese individuals, investigation into preventative strategies are needed. Aerobic exercise is a potent stimulus for both insulin and non-insulin dependent glucose uptake into the skeletal muscle. A single exercise session can improve insulin sensitivity within hours after exercise. The effects of intensity, type, and volume of exercise on glucose homeostasis have been studied extensively; however, controlling for muscle contraction frequency with a constant exercise intensity and workload has not been examined. The purpose of this study was to compare muscle contraction frequency during aerobic exercise by altering cycling cadence on insulin sensitivity and vascular health. Eleven obese males (age=28yr, BMI=35kg/m2) completed three conditions in random order: 1) control-no exercise; 2) 45-min cycling at 45 revolutions per minute (45RPM) at 65-75%VO2max; 3) 45-min cycling at 90RPM at 65-75%VO2max. Glucose control and insulin sensitivity were assessed with oral glucose tolerance tests (OGTT) 4 hours post-exercise. Vascular health was assessed via flow-mediated dilation (FMD) pre-exercise, 1-hr and 2-hr post exercise and ambulatory blood pressure was assessed pre-exercise, and continually every 15 min post-exercise. Linear mixed models were used to compare the mean differences in outcome variables. There were no significant differences found between control and both exercise conditions for all OGTT outcomes and no differences were found between control and exercise in FMD (all, p>0.05). Significant effects for exercise were found for both brachial and central blood pressure measures. Brachial systolic blood pressures were lower at 2- and 4-hr post-exercise by approximately -10 and -8mmHg, respectively (p<0.001 and p=0.004) versus control. Central systolic blood pressures were lower at 2-, 3-, and 4-hr post-exercise by approximately -8, -9 and -6mmHg, respectively (p<0.001, p=0.021 and p=0.004) versus control. In conclusion, aerobic exercise, regardless of muscle contraction frequency, were unable to effect glucose control and insulin sensitivity. Similarly, there was no effect on vascular function. However, there was a significant effect of aerobic exercise on reducing post-exercise blood pressure.

Birds have plasma glucose levels that are 1.5-2 times greater than mammals of similar body mass in addition to higher free fatty acid concentrations, both of which would typically impair endothelium-dependent vasodilation if observed in mammals. Endothelium-dependent vasodilation can be stimulated in mammals through the use of acetylcholine (ACh), which primarily acts through nitric oxide (NO) and cyclooxygenase (COX)-mediated pathways, with varying reliance on endothelial-derived hyperpolarizing factors (EDHFs). Very few studies have been conducted on small resistance systemic arteries from birds. The hypothesis was that because birds have naturally high glucose and free fatty acid concentrations, ACh-induced vasodilation of isolated arteries from mourning doves (Zenaida macroura) would be independent of endothelial-derived factors and resistant to high glucose-mediated vascular dysfunction. Small resistance mesenteric and cranial tibial (c. tibial) arteries were pre-constricted to 50% of resting inner diameter with phenyleprine then exposed to increasing doses of ACh (10-9 to 10-5 μM) or the NO donor, sodium nitroprusside (SNP; 10-12 to 10-3 μM). For both vessel beds, ACh-induced vasodilation occurred mainly through the activation of potassium channels, whereas vasodilation of mesenteric arteries additionally occurred through COX. Although arteries from both vessel beds fully dilated with exposure to sodium nitroprusside, ACh-mediated vasodilation was independent of NO. To examine the effect of high glucose on endothelium-dependent vasodilation, ACh dose response curves were conducted following exposure of isolated c. tibial arteries to either a control solution (20mM glucose) or high glucose (30mM). ACh-induced vasodilation was significantly impaired (p = 0.013) when exposed to high glucose, but normalized in subsequent vessels with pre-exposure to the superoxide dismutase mimetic tiron (10 mM). Superoxide concentrations were likewise significantly increased (p = 0.0072) following exposure to high glucose. These findings indicate that dove arteries do not appear to have endogenous mechanisms to counteract the deleterious effects of oxidative stress. Additional studies are required to assess whether endogenous mechanisms exist to protect avian vascular reactivity from systemic hyperglycemia.