Effects Of Exercise Training On Endothelial Function And Vascular Responses During Stress In Female Smokers

Abstract

There is longitudinal evidence that increased physical activity and/or exercise reduces the risk of morbidity and mortality associated with cardiovascular disease in female smokers. It is plausible that the mechanism responsible for the reduced risk is improved vascular health and reduced hyper-reactivity to a neurovascular stressor. PURPOSE: To determine the benefits of 3 weeks of aerobic exercise training on endothelial function, measured by flow-mediated dilation (FMD), and cardiovascular responses to neurovascular stress among sedentary female smokers and non-smokers. METHODS: Thirty-five participants were recruited. Non-smokers were randomly assigned into the exercise training (n=12) or to the passive rest group (n=12). All regular smokers underwent (n=11) the exercise training protocol. FMD and stress responses were measured before and after a 3 week moderate intensity (∼50%VO2max) aerobic exercise training program. FMD was determined by brachial arterial velocity, arterial diameter, and blood flow measured by Doppler Ultrasonography. Those measures and beat-to-beat finger blood pressure (BP), and heart rate (HR) were assessed in responses to 2 min of forehead cold and 4 min of the Stroop Color-Word conflict test (CWT) (separated by 8 min of rest) at baseline and three weeks later. RESULTS: Compared to non-smokers, FMD was impaired (5.98 ± 3.27 vs. 4.55 ± 4.18, p=0.04) and decreases in arterial diameter (-0.10 ± 0.08 vs. -0.04 ± 0.07; p=.03) and blood flow (-81.69 ± 49.51 vs. -45.12 ± 27.46; p=.05) responses during forehead cold were augmented at baseline among female smokers. Three weeks of cycle exercise training at a moderate intensity did not improve endothelial function measured by FMD or alter stress reactivity during neurovascular stress in smokers or non-smokers. CONCLUSIONS: Based on these results, the impact of 3 weeks of moderate intensity exercise training was insufficient to observe a measurable change in endothelial function or cardiovascular responses during stress.