Feter_2019_Physiol.Behav_201_42

The present study investigated the chronic effects of different physical exercise and physical activity models on cognitive function, cholinergic activity, and oxidative stress markers in the cerebral cortex and hippocampus. Eighty 60-day old C57BL/6 mice were divided into the following five groups: Sedentary (SED), moderate-intensity continuous training (MICT), high-intensity interval training (HIIT), resistance training (RT), and physical activity (RW, for "running wheel"). Cognitive function (recognition and spatial memory), oxidative stress parameters, and acetylcholinesterase (AChE) activity in the cerebral cortex and hippocampus were evaluated. MICT mice exhibited enhanced recognition memory compared to SED mice (p=.046) and other exercised groups (HIIT: p<.001; RW: p=.003; RT: p<.001). The RT group showed better spatial memory compared to the SED (p=.004), MICT (p=.019), and RW (p=.003) groups. RW, MICT, HIIT, and RT training models reduced nitrites in the hippocampus compared to the SED group. RT led to a significant increase in both lipid peroxidation (p=.01) and reactive oxygen species (ROS) (p<.001) levels compared to the SED group in the hippocampus. MICT promoted an increase in catalase (CAT) activity (p=.002), while superoxide dismutase (SOD) activity was diminished by RT compared to MICT and HIIT (p=.008). In the cerebral cortex, RT increased ROS levels, but exhibited the lowest lipid peroxidation level among the groups (p<.001). The RW group showed an activity-induced increase in lipid peroxidation level compared to the SED group, and the highest level of CAT activity among all groups (p<.001). AChE activity was higher in the RT group compared to the SED, MICT, and RW groups (p=.039) in the cerebral cortex. In summary, nitrite levels in the hippocampus were decreased in all intervention groups regardless of activity or exercise model. Likewise, MICT improved recognition memory besides increasing CAT activity. We conclude that the MICT and RT protocols seem to act as oxidative stress regulators and non-pharmacological strategies to improve cognitive function.