Abstract

BACKGROUNDObesity is a complex inflammatory disease characterized by an accumulation of abdominal visceral fat that increases cardiovascular risk factors. Chronic exposure to inflammation leads to endothelial dysfunction where response to sheer stress is inadequate to promote smooth muscle relaxation and thus healthy arterial dilation. When combined with a decline in estrogen, the obese, postmenopausal population is at a higher risk of developing cardiovascular disease than younger women with a lower body mass index. Exercise training can improve endothelial function regardless of aging. Acute exercise temporarily increases nitric oxide (NO) bioavailability in response to sheer stress to prevent further vascular damage. Chronic exposure to sheer stress through exercise leads to adaptations in NO bioavailability and overall endothelial function. Flow‐mediated dilation (FMD) is a mechanical measure of endothelial function. FMD is expressed as a percent change from baseline to maximal dilation after reactive hyperemia in brachial artery diameter in response to blood flow occlusion. Minimal work has been done on the influence of aerobic and resistance training on FMD in obese, postmenopausal women.PURPOSETo determine the influence of acute and chronic resistance and aerobic exercise on FMD in obese, postmenopausal women.METHODSOverweight to obese (BMI 33.01 ± 4.60 kg·m2), postmenopausal women (64.3 ± 5.3 yr) were randomized into either an exercise (EX, n = 20) or education control (ED, n = 18) group for a 12‐week intervention where EX underwent moderate intensity aerobic and resistance exercise training (treadmill walking 70–80% VO2max; 8 whole‐body resistance exercises, 2 sets @ 8–12RM, respectively) 3 days per week and ED attended education sessions (talks on health, CPR certification, etc.) twice per week. Before (BT) and after (AT) the 12‐week intervention, both groups underwent an experimental trial day where FMD was performed before exercise (PRE) and two hours after exercise completion (2HR) for EX and at the same time points for resting ED. FMD was analyzed blinded using Brachial Analyzer for Research (Medical Imaging Applications, LLC; Coralville, IA).RESULTSAcute exercise increased % FMD at 2HR where EX was greater than ED (EX: PRE 9.72 ± 0.48, 2HR 11.2 ± 0.51%; ED: PRE 9.46 ± 0.51, 2HR: 8.83 ± 0.53%; p = 0.04). There was no significant effect of exercise training in EX (BT PRE 9.54 ± 3.19, 2HR 11.33 ± 3.46; AT PRE 9.89 ± 2.82, 2HR 11.08 ± 3.08%) or education sessions in ED (BT PRE 9.88 ± 3.01, 2HR 9.53 ± 2.96; AT PRE 9.04 ± 3.56, 2HR 8.14 ± 3.15%; p = 0.33).CONCLUSIONAcute exercise increased FMD 2 hours after exercise suggesting that there is a residual effect of exercise on FMD up to at least 2 hours in our population. Resting FMD did not increase in response to a 12‐week aerobic and resistance exercise training program. The duration of the program may not have been adequate to observe significant changes in endothelial function. In addition, the intensity of the exercise may not have been high enough to promote improvements in endothelial function.Support or Funding InformationTCU Invests in Scholarship Grant, TCU Research and Creative Activities GrantThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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