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A session of resistance exercise increases vasodilation in intermittent claudication patients
Lima A, Ritti-Dias R, Forjaz CLM, Correia M, Miranda A, Brasileiro-Santos M, Santos A, Sobral Filho D, Silva A
Physiologie Appliquee Nutrition et Metabolisme [Applied Physiology, Nutrition, & Metabolism] 2015 Jan;40(1):59-64
clinical trial
4/10 [Eligibility criteria: Yes; Random allocation: Yes; Concealed allocation: No; Baseline comparability: Yes; Blind subjects: No; Blind therapists: No; Blind assessors: No; Adequate follow-up: No; Intention-to-treat analysis: No; Between-group comparisons: Yes; Point estimates and variability: Yes. Note: Eligibility criteria item does not contribute to total score] *This score has been confirmed*

No study has shown the effects of acute resistance exercise on vasodilatory capacity of patients with peripheral artery disease. The aim of this study was to analyse the effects of a single session of resistance exercise on blood flow, reactive hyperemia, plasma nitrite, and plasma malondialdehyde in patients with peripheral artery disease. Fourteen peripheral artery disease patients underwent, in a random order, 2 experimental sessions: control (rest for 30 min) and resistance exercise (8 exercises, 2 sets of 10 repetitions at an intensity of 5 to 7 in the OMNI Resistance Exercise Scale). Blood flow, reactive hyperemia, plasma nitrite, and malondialdehyde were measured before and 40 min after the interventions in both sessions. Data were compared between sessions by analysis of covariance, using pre-intervention values as covariates. The increases in blood flow, reactive hyperemia, and log plasma nitrite were greater (p < 0.05) after resistance exercise than the control session (3.2 +/- 0.1 versus 2.7 +/- 0.1 mL/100 mL tissue/min, 8.0 +/- 0.1 versus 5.7 +/- 0.1 AU, and 1.36 +/- 0.01 versus 1.26 +/- 0.01 mumol/L, respectively). On the other hand, malondialdehyde was similar between sessions (p > 0.05). In peripheral arterial disease patients, a single session of resistance exercise increases blood flow and reactive hyperemia, which seems to be mediated, in part, by increases in nitric oxide release.

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