
Clinical and neuroimaging correlates in a pilot randomized trial of aerobic exercise for major depression
2023; Elsevier BV; Volume: 347; Linguagem: Inglês
10.1016/j.jad.2023.12.025
ISSN1573-2517
AutoresAcácio Moreira‐Neto, Lucas Melo Neves, Angelo Corrêa de Lima Miliatto, Valéria Juday, Raquel Marquesini, Beny Lafer, Ellison Fernando Cardoso, Carlos Ugrinowitsch, Mariana Penteado Nucci, Carla Silva‐Batista,
Tópico(s)Heart Rate Variability and Autonomic Control
ResumoAerobic exercise (AE) combined with pharmacotherapy is known to reduce depressive symptoms; however, studies have not focused on long-term AE for volumetric changes of brain regions (amygdala, thalamus, and nucleus accumbens [NAcc]) linked to the control of affective responses and hopelessness in individuals with major depression (MD). In addition, AE with motor complexity (AEMC) would be more effective than AE in causing brain plasticity. We compared the effects of 24 weeks of AE and AEMC combined with pharmacotherapy on clinical and volumetric outcomes in individuals with MD. Forty medicated individuals with MD were randomly assigned to nonexercising control (C), AE, and AEMC groups. The training groups exercised for 60 min, twice a week for 24 weeks. Clinical and volumetric outcomes were assessed before and after the 24 weeks. Effect size (ES) and confidence interval (CI) were calculated for within-group and between-groups changes. AE and AEMC reduced hopelessness (ES = −0.73 and ES = −0.62, respectively) and increased affective responses (ES = 1.24 and ES = 1.56, respectively). Only AE increased amygdala (ES = 0.27 left and ES = 0.34 right), thalamus (ES = 0.33 left and ES = 0.26 right) and left NAcc (ES = 0.54) volumes. AE was more effective than the C group in reducing hopelessness and causing brain plasticity. The changes in the right amygdala volume showed a strong trend in explaining 72 % of the changes in affective responses following AE (p = 0.06). Lack of posttraining follow-up and small sample size. These preliminary data indicate that AE combined with pharmacotherapy can cause clinical improvement and brain plasticity in individuals with MD.
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