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Medicine & Science in Sports & Exercise:
doi: 10.1249/MSS.0000000000000450
Original Investigation: PDF Only

Post-Walking Exercise Hypotension in Patients with Intermittent Claudication.

Cucato, Gabriel Grizzo; da Rocha Chehuen, Marcel; Ritti-Dias, Raphael Mendes; Carvalho, Celso Ricardo Fernades; Wolosker, Nelson; Saxton, John Michael; de Moraes Forjaz, Cláudia Lúcia

Published Ahead-of-Print
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Abstract

Porpose: To investigate the acute effect of intermittent walking exercise (WE) on blood pressure (BP) responses in patients with intermittent claudication (IC). Secondly, to gain an improved insight into the physiological mechanisms controlling BP regulation following intermittent WE in this patient group.

Methods: Twenty patients with IC participated in two experimental sessions in random order: 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 heart rate (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 mmHg 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/min, P<0.05) vs pre-intervention 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 over the subsequent 24 hours was similar between experimental conditions.

Conclusion: In patients with IC, WE induced post-exercise hypotension (PEH) response that had a significant magnitude versus control but was not maintained over the next 24 h of daily activities. The acute PEH 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.

(C) 2014 American College of Sports Medicine

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