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Effects of short-term exercise-training on aortic systolic pressure augmentation in overweight and obese individuals
Aletta M E Millen1, Gavin R Norton, Ingrid Avidon
1Cardiovascular Pathophysiology and Genomics Research Unit, and the Exercise Physiology Laboratory, School of Physiology, Faculty of Health Sciences, University of Witwatersrand Medical School, Johannesburg, South Africa.
Abstract:
To determine whether exercise training-induced decreases in blood pressure (BP) can be explained by decreases in aortic systolic pressure augmentation in overweight or obese individuals. Thirty-five sedentary or recreationally active men and women (30-57 years) who were either overweight (40 %) or obese (60 %) completed 6 weeks of exercise training (≥3 days/week; stationary bike and/or treadmill) either preceded (n = 19) or followed (n = 16) by a 6-week control period of no exercise. Aortic augmentation pressure (AP), aortic and peripheral augmentation indices (AIx), and central aortic BP (SphygmoCor) were determined before and after exercise training and a control period. Peak oxygen consumption increased (p = 0.0001) from 27.0 ± 5.1 to 28.8 ± 5.8 mL/(kg min) after 6 weeks of exercise. Exercise training decreased brachial systolic (SBP) and diastolic BP from 142 ± 8/94 ± 8 to 134 ± 11/86 ± 11 mmHg (p < 0.005/p < 0.005); whereas no changes were observed after the control period (141 ± 11/91 ± 9 mmHg, p = 0.81/p = 0.34). Neither AP (baseline: 9.2 ± 4.2 mmHg; after 6 weeks training: 8.7 ± 6.1 mmHg), aortic AIx (baseline: 24.6 ± 11.0 %; after 6 weeks training: 22.7 ± 11.1 %), nor peripheral AIx (baseline: 81.4 ± 16.7 mmHg; after 6 weeks training: 76.4 ± 16.5 mmHg) were modified by exercise training. Although aortic SBP decreased after exercise (132 ± 8 to 124 ± 12 mmHg, p < 0.002), these changes were accounted for by decreases in mean arterial pressure. In overweight or obese individuals, although short-term aerobic exercise training, which improved cardiorespiratory fitness, may produce marked decreases in aortic and brachial BP; these effects are not attributed to alterations in aortic systolic pressure augmentation.
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