Post-Walking Exercise Hypotension in Patients with Intermittent Claudication.

• Autores: Gabriel Grizzo Cucato, John Michael Saxton, Marcel da Rocha Chehuen, Raphael Mendes Ritti-Dias, Cláudia Lucía de Moraes Forjaz, Celso Ricardo Fernandes Carvalho, Nelson Wolosker
• Localización: Medicine & Science in Sports & exercise: Official Journal of the American College of Sports Medicine, ISSN 0195-9131, Vol. 47, Nº. 3, 2015, págs. 460-467
• Idioma: inglés
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• Resumen

  • AB Purpose: This study aimed to investigate the acute effect of intermittent walking exercise (WE) on blood pressure (BP) responses in patients with intermittent claudication (IC). Secondly, this study aimed to gain improved insight into the physiological mechanisms controlling BP regulation after intermittent WE in this patient group. Methods: Twenty patients with IC participated in two experimental sessions in a random order, as follows: WE (15 x 2-min bouts of WE interpolated with 2-min rest intervals) and control (standing rest on a treadmill for 60 min). BP, cardiac output (CO: CO2 rebreathing), and cardiovascular autonomic modulation (spectral analysis of HR variability) were assessed before and after both experimental sessions during supine rest, and stroke volume (SV) and systemic vascular resistance (SVR) were calculated. Data were analyzed using two-way ANOVA. Results: WE decreased systolic, diastolic, and mean BP, with net effects of -13 +/- 2, -5 +/- 2, and -7 +/- 2 mm Hg versus control, respectively (all P < 0.05). WE also decreased SV (-5.62 +/- 1.97 mL, P < 0.05) and CO (-0.05 +/- 0.13 L[middle dot]min-1, P < 0.05) versus preintervention and prevented the observed increase in SVR in the control condition (+4.2 +/- 1.4 U, P < 0.05). HR showed a decrease (P < 0.05), consistent with evidence of increased vagal modulation, in the control condition. BP measurements over the subsequent 24 h were similar between experimental conditions. Conclusions: In patients with IC, WE induced a postexercise hypotension response that had a significant magnitude versus control but was not maintained over the next 24 h of daily activities. The acute postexercise hypotension response was mediated by a decrease in CO and SV, which was not compensated by an augmentation of SVR, as observed in the control arm of the study