Eficácia do treinamento aeróbicoem medidas biológicas e funcionais em indivíduos pós-AVE crônico: um ensaio clínico randomizado

Abstract

INTRODUCTION: The stroke process triggers an inflammatory reaction that, if exacerbated, may last up to several months, causing an increase in inflammatory cytokines. This increase has a negative effect on the brain-derived neurotrophic fator (BDNF) function, an important mediator of the neuroplasticitiy process, which is associated with motor learning after stroke. Aerobic exercise has the potential to change the concentrations of these mediators, including in individuals post stroke, and change functional outcomes. It can modulate neuroplasticity mechanisms during the rehabilitation process. However, most of these studies used a single bout of exercise, have small sample sizes and show inconsistent results. OBJECTIVE: The aim of this study was compare the effectiveness of a high-intensity aerobic training (AT) program (walking on the treadmill between 60-80% of heart rate reserve, HRR) versus a low-intensity AT program (walking on the ground, below 40% of HRR), for 12 weeks, on interleukin 6 (IL- 6), soluble tumor necrosis factor receptors (sTNFR1 and sTNFR2), IL-10 and BDNF concentrations in peripheral blood, in individuals with chronic post-stroke (after 6 months) and functional outcomes (gait speed, mobility, and exercise capacity). METHODS: This is a controlled, double-blinded, randomized clinical trial. Thirty-eight post-stroke individuals, recruited from the community, received group interventions three times a week for 12 weeks. Primary outcomes were IL-6, IL-10, sTNFR1, sTNFR2 and BDNF peripheral concentrations. Secondary outcomes were comfortable and fast gait speed (10-meter walk test, 10MWT), functional mobility (Timed Up and Go, TUG), and exercise capacity (6-minute walk test, 6MWT). All the outcomes were measured at baseline, postintervention (at 12 weeks), and at the 4-week follow-up (at 16 weeks). RESULTS: There is no statistically significant change over time in BDNF serum concentrations, regardless of the group. There was a decrease in sTNFR1 (Wald=18,344; p < 0,001) from baseline to reassesment, and sTNFR2 from baseline to reassesment, and from baseline to follow-up (Wald=15,142; p = 0,001), regardless of training intensity. There were no time, group, and group-by-time interaction effect for IL-10. It was not possible to measure IL-6 concentrations. There is statistically significant change over time with increase in comfortable gait speed of 0,10 m/s (F = 16,942, p =0,001) and fast gait speed of 0.08 m/s (F = 9,518, p = 0,006), decrease in TUG of 1,16 s (F = 9,513, p = 0,006) and a median increase of 56 meters in 6MWT (F = 36,491, p < 0,001). DISCUSSION: A high-intensity AT was not superior to a low-intensity AT to promote changes in inflammatory and neurotrophic variables, as well as in gait speed, functional mobility and exercise capacity in individuals with chronic post-stroke. The functional changes in both groups were clinically significant. CONCLUSION: AT in both intensities promoted changes in biological (TNF-α soluble receptors) and functional (10MWT, TUG and 6MWT) measures in individuals with chronic post-stroke in both groups.