Swim training attenuates oxidative damage and promotes neuroprotection in cerebral cortical slices submitted to oxygen glucose deprivation

Abstract

Although it is well known that regular exercise may promote neuroprotection, the mechanisms underlying this effect are still not fully understood. We investigated if swim training promotes neuroprotection by potentiating antioxidant pathways, thereby decreasing the effects of oxidative stress on glutamate and nitric oxide release. Male Wistar rats (n=36) were evenly randomized into a trained group (TRA) (5 days/week, 8 weeks, 30 min) and a sedentary group (SED). Forty-eight hours after the last session of exercise, animals were killed and brain was collected for in vitro ischemia. Cortical slices were divided into two groups: a group in which oxidative stress was induced by oxygen and glucose deprivation (OGD), and a group of nondeprived controls (nOGD). Interestingly, exercise by itself increased superoxide dismutase activity (nOGD, SED vs. TRA animals) with no effect on pro-oxidative markers. In fact, TRA-OGD slices showed lowered levels of lactate dehydrogenase when compared with SED-OGD controls, reinforcing the idea that exercise affords a neuroprotective effect. We also demonstrated that exercise decreased glutamate and nitrite release as well as lipid membrane damage in the OGD cortical slices. Our data suggest that under conditions of metabolic stress, swim training prevents oxidative damage caused by glutamate and nitric oxide release.

Neuroprotective effect of exercise in rat hippocampal slices submitted to in vitro ischemia is promoted by decrease of glutamate release and pro‐apoptotic markers

“…; Leite et al . ). The exercise would have to be much more intense (close to maximum workload capacity) to induce significant changes in physiological variables associated with stress (Scopel et al .…”

“…In fact, our group has already shown that regular physical exercise sessions are able to decrease glutamate and nitrite release as well as membrane damage in the OGD cortical slices (Leite et al . ). Therefore, physical exercise may result in an improvement of neuronal ability to endure energetic depletion, as well as the changes of apoptosis regulation.…”

“…; Leite et al . ), oxygen consumption and mitochondrial biogenesis (Boveris and Navarro ; Packer et al . ).…”

“…At this point, animals were randomized into two groups: (i) The exercise group ( n = 25), which underwent a swim training for 30 min/day, 5 days/week, over 8 weeks in individual water tanks, 50 cm in depth, and (ii) the sedentary group ( n = 25), which was placed on an acrylic platform in individual tanks with shallow water (5 cm) (Leite et al . ). Two other maximal workload capacity tests were conducted in the fourth and eighth week of physical training (Gobatto et al .…”

Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain

“…Physical training impacts several body systems including cardiovascular, musculoskeletal and nervous system ( 1 ). Studies have showed that regular exercise improves brain health and prevents or improves recovery from brain injuries ( 1 ) by enhancing neurotrophic factor levels ( 2 ) and modulating oxidative status ( 1 ).…”