Effects of exercise timing and intensity on neuroplasticity in a rat model of cerebral infarction

Exercise therapy plays key roles in functional improvements during neurorehabilitation. However, it may be difficult for some people to properly perform exercise because mobility and endurance might be restricted by neurological deficits due to stroke. Additionally, there is little evidence detailing the biological mechanisms underlying the most effective swimming exercise protocols for neuroplasticity after stroke. Thus, the present study investigated the effects of swimming exercise on neuroplasticity in a cerebral infarction rat model according to the timing and intensity of exercise. A total of 45 male Sprague-Dawley rats (300 ± 50 g, 10 weeks old) were subjected to photothrombotic cerebral infarction and randomly divided into five groups: non-exercise (group A, n = 9); early submaximal (group B, n = 9); early maximal (group C, n = 9); late submaximal (group D, n = 9); and late maximal (group E, n = 9). Swimming exercise was performed five times a week for 4 weeks, and cognition was evaluated with the Morris water maze (MWM) test. Assessments of superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels and immunohistochemical analyses of brain-derived neurotrophic factor (BDNF) were conducted in the ipsilesional hippocampus region. After 4 weeks of exercise, the escape latency was shorter and velocity was greater in group B than in groups A, C, D, and E (p = 0.046, p <  0.001, respectively). Furthermore, SOD activity was higher and MDA levels were lower in group B than in groups A, C, D, and E (p = 0.004, p = 0.019). The immunohistochemistry results revealed that the greatest BDNF immunoreactivity was in group B. Taken together, these results indicate that early submaximal swimming exercise may be the most effective protocol for the recovery of neurological deficits in a rat model of cerebral infarction.