Abstract 14182: Impact of Aortic Stiffness on Exercise Blood Pressure Response and Aerobic Fitness
Introduction: Exercise induced hypertension (EiH) defined as exercise SBP >210 mmHg, is associated with increased risk for cardiovascular morbidity even in normotensive individuals. The physiologic mediators contributing to this increased risk are unknown but may arise from increased central vascular stiffening, which may dampen rises in cardiac output (Qc) during exercise leading to decreased aerobic capacity. We hypothesized individuals with EiH would have increased aortic stiffening resulting in decreased aerobic fitness (VO2max).
Methods: This study included 134 (56% male) carefully screened seniors (≥60 yr) who were normotensive and had no evidence of inducible cardiac ischemia. VO2 (Douglas bags), Qc (acetylene rebreathe) and BP (ECG gated electrosphygmomanometry) were collected at rest and during exercise. Subjects performed incremental treadmill exercise to VO2max. Aortic pulse wave velocity (PWV) was measured by arterial tonometry. The Modelflow method was used to determine intrinsic structural aortic compliance, enumerated as biologic aortic age. Subjects were grouped into tertiles by peak exercise SBP response: <180, 180-210 and >210 mmHg.
Results: One third of subjects achieved peak exercise SBP >210 mmHg. There were no differences amongst tertiles in VO2max, max Qc or total peripheral resistance. The lowest BP tertile had the lowest aortic age (56 vs. 68 yrs; p<0.001), PWV and awake ambulatory BP (124 mmHg vs. 129 mmHg; p<0.05). Ambulatory BP and aortic age were the strongest predictors of peak exercise SBP (R2 = 0.2; p<0.001). Increased aortic age was associated with decreased VO2max but this relationship was seen in all exercise BP tertiles (Figure; 31 vs. 25 ml/min/kg, p<0.05).
Conclusion: EiH was not associated with a decrease in aerobic fitness. Rather increased aortic stiffness, irrespective of exercise BP response, predicted low aerobic fitness suggesting BP response alone during exercise may not be a mediator of increased CV morbidity.
- © 2013 by American Heart Association, Inc.