Efeito do destreinamento na aptidão cardiorrespiratória de indivíduos pós-acidente vascular encefálico

Abstract

Stroke is a highly prevalent cerebrovascular disease that affected around 795000 people worldwide each year, and 610000 of these were characterized as the first episode. These data show that the recurrence of the disease is more common and this increases its severity. High physical activity levels are associated with reduced incidence of stroke and the risk of cardiovascular disease. Cardiorespiratory fitness, expressed by VO2peak, is reduced in individuals after stroke, and may indicate a limitation in performing activities of daily living. One of the trainings often performed by individuals after stroke that can improve cardiorespiratory fitness is aerobic exercise. However, interruption may lead to detraining, defined as partial or complete loss of training-induced anatomical, physiological, and performance adaptations. Nevertheless, no studies were found on the effect of short-term detraining (one month) in individuals after stroke. In addition, the results of the long-term (more than one month) effects when studied in these individuals are conflicting. Therefore, the aim of this study was to determine the short-term (one month) and long-term (six month) effect of detraining on cardiorespiratory fitness (VO2peak) of individuals after stroke who participated in aerobic training. Participants of the present study were divided into gain group, those who presented a minimum increase of 1.3 ml.kg-1.min-1 in the absolute VO2peak value between the initial evaluation and immediately after the intervention and no-gain group those with a change inferior to that value. The outcome of this study was cardiorespiratory fitness, characterized by VO2peak obtained by the cardiopulmonary exercise test (CPET) performed one and six months after the end of the aerobic training. Statistical analyzes were performed by an independent researcher. Two-way analysis of variance (ANOVA) with two factors (time x group) with repeated measures in the time factor and previously planned contrasts was used to compare the VO2peak between the two groups at the four assessment moments: pre-intervention, post-intervention, short-term detraining (one month post-intervention) and long-term detraining (six months post-intervention). Twenty individuals participated in the study, 12 in the gain group and 8 in the no-gain group, with a mean age of 57 ± 11 years and an average time since the onset of stroke of 56 ± 52 months. According to ANOVA, there was a significant interaction between group and time factors (F = 6.11; p = 0.001). Previously planned contrasts showed that the gain group showed significantly higher VO2peak than the no-gain group immediately after the intervention (F = 25.86; p <0.001). With short-term detraining, there was a significant reduction in the VO2peak in the gain group, reaching values similar to the no-gain group and to the baseline (F = 14.81; p = 0.001). Both groups had similar VO2peak values with long-term detraining (F = 2.70; p = 0.12), with no significant differences from the values observed at baseline and the short-term detraining (0.11≤ p≤1.00). The results of this study demonstrated that the gain in cardiorespiratory fitness, expressed through increased VO2peak, was completely lost after one month of detraining. These findings reinforce that the detraining of this population resembles that of the healthy population, as well as the importance of maintaining and not interrupting physical training to retain the gains obtained in the cardiorespiratory fitness of subjects in the chronic phase of stroke.