Efeitos do exercício aeróbio e de força nas respostas hemodinâmicas, autonômicas e de função endotelial em indivíduos pré-hipertensos com sobrepeso

Abstract

Although physical exercise may result in lowering blood pressure (BP), the mechanisms underlying this effect are still controversial. The aim of this study was to evaluate the acute effect of aerobic (AE) and strength exercise (SE) on hemodynamic, autonomic and endothelial function in pre-hypertensive overweight individuals. Fifteen men (34.7 ± 9.7 years) performed AE (30 minutes on a cycle ergometer at heart rate (HR) of ventilatory threshold 1), SE (10 sets of 12-15 repetitions with 70% of 15 repetitions maximum - RM) and control (CTL) session in a counterbalanced order. Prior to the experimental protocol, the individuals carried out the evaluation of habitual level of physical activity and endothelial function at rest; the 15 RM workload in the leg extension exercise and the maximal cardiopulmonary exercise test on a cycle ergometer. In all sessions, continuous record of BP, cardiac output (CO), systemic vascular resistance (SVR, by photoplethysmography with Finometer Pro), evaluation of pulse wave reflection (by applanation tonometry with SphygmoCor), heart rate variability (by Polar® RS800 heart rate monitor), and endothelial function assessment (by the peripheral arterial tonometry with Endo-PAT2000®) were obtained. Both exercises increased systolic BP in the recovery time in relation to the pre-exercise period. This phenomenon occurred from 20 minutes onwards for the SE (+4.0±0.4 mmHg) and from 40 minutes onwards for the AE (+5.0±0.3 mmHg) with concomitant increase in HR since beginning of recovery (SE: +21.5±0.1 bpm; AE: +11.5±0.2 bpm) and in CO (SE: +2.2±0.0 l/min; AE: +0.9±0.1 l/min) for both types of exercise. However, only CO recovered in the end of 60 minutes after the AE (-0.4±0.1 l/min). Although SVR reduced initially after both types of exercise (SE: 0.18±0.1 mmHg.l/min; AE: -0.08±0.1 mmHg.l/min), it was not enough to override the increment imposed by CO. In addition, both exercises significantly reduced parameters of pulse wave reflection (SE: aortic pulse pressure: 6.5±0.2 mmHg; AE: aortic pulse pressure: -4.0±0.5 mmHg; augmentation pressure: -2.4±0.0 mmHg; augmentation index: -5.1±0.5 %), but without effects on endothelial function. The sympathovagal balance (LF/HF) showed higher values in the beginning and at the end of AE recovery (0.9±0.2 vs 0.7±0.2), and during the whole period of SE recovery (1.1±0.2). In conclusion, in these pre-hypertensive overweight individuals, none of the protocols was able to cause post-exercise hypotension, nor changes in endothelial function. In addition, the SE had greater influence on LF/HF in relation to the AE, with different blood pressure responses in post-exercise period. Finally, both types of exercise reduced the variables related to the pulse wave reflection.