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Although physical exercise has emerged as a potential therapeutic modality for functional deficits following ischemic stroke, the extent of this effect appears to be contingent upon the time of exercise initiation. In the present study, we assessed how exercise timing affected brain damage through hyperglycolysis-associated NADPH oxidase (NOX) activation.

Using an intraluminal filament, adult male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h and assigned to one non-exercise and three exercise groups. Exercise on Rota-rod was initiated for 30 min at 6 h (considered very early), at 24 h (early), and at day 3 (relatively late) after reperfusion. Lactate production was measured 30 min after exercise completion, and NOX activity and protein expression of NOX subunits (p47^phox, gp91^phox, p22^phox and p67^phox) and glucose transporter 1 and 3 (Glut-1 and …