Pre-stroke exercise does not reduce atrophy in healthy young adult mice

Abstract

Stroke is the main cause of acquired disability in adults. Exercise reduces the risk for stroke and protects against functional loss after stroke. An exercise-induced reduction in key risk factors probably contributes to the protective effect, but direct effects on the brain may also contribute to stroke protection. We previously reported that exercise increases angiogenesis and neurogenesis through activation of the lactate receptor HCA₁. Here we exposed young adult wild-type mice and HCA₁ knockout mice to interval exercise at high or medium intensity, or to intraperitoneal injections of L-lactate or saline for seven weeks before we induced experimental stroke by permanent occlusion of the distal medial cerebral artery (dMCA). The resulting cortical atrophy measured three weeks after stroke was unaffected by exercise or L-lactate pre-treatments, and independent of HCA₁ activation. Our results suggest that the beneficial effect of exercise prior to stroke where no reperfusion occurs is limited in individuals who do not carry risk factors.

Keywords: Exercise; HCA(1); HCAR1; Lactate; Stroke.