Endogenous neuroprotective potential due to preconditioning exercise in stroke

Abstract

Stroke is a leading cause of serious long-term physical disability due to insufficient neurorepair mechanisms. In general, physical activity is an important modifiable risk factor, particularly for stroke and cardiovascular diseases. Physical exercise has shown to be neuroprotective in both animal experiments and clinical settings. Exercise can be considered a mild stressor and follows the prototypical preconditioning stimulus. It has beneficial effects on brain health and cognitive function. Preconditioning exercise, which is prophylactic exercise prior to ischemia, can protect the brain from subsequent serious injury through promotion of angiogenesis, mediation of inflammatory responses, inhibition of glutamate over-activation, protection of the blood-brain barrier, and inhibition of apoptosis. Preconditioning exercise appears to induce brain ischemic tolerance and it has been shown to exert beneficial effects. It is clinically safe and feasible and represents an exciting new paradigm in endogenous neuroprotection for patients with acute stroke. In this review, we describe the neuroprotective potential of preconditioning exercise and clinical applications in patients with acute ischemic stroke.

Role of Regular Physical Activity in Neuroprotection against Acute Ischemia

“…Finally, exercise's anti-ischemic effect may be also linked to the mechanism of preconditioning [134]. Preconditioning is defined as the exposure of a system or an organ to a conditioning stimulus to induce tolerance or resistance to a subsequent injury [135] by triggering cells and organisms to express intrinsic protective factors, thus helping them acquire tolerance and self-defense against later possible damage [136].…”

“…Preconditioning is defined as the exposure of a system or an organ to a conditioning stimulus to induce tolerance or resistance to a subsequent injury [135] by triggering cells and organisms to express intrinsic protective factors, thus helping them acquire tolerance and self-defense against later possible damage [136]. Several studies have demonstrated that preconditioning exercise (i.e., prophylactic exercise prior to stroke) provides significant neuroprotection against acute stroke through the promotion of angiogenesis, mediation of inflammatory responses, and inhibition of neuronal apoptosis [134]. In the 2,3,5-triphenyltetrazorlium chloride (TTC) study, the tissue infarction in rats with preconditioning exercise was decreased compared with the brain of rats without preconditioning [134].…”

“…Several studies have demonstrated that preconditioning exercise (i.e., prophylactic exercise prior to stroke) provides significant neuroprotection against acute stroke through the promotion of angiogenesis, mediation of inflammatory responses, and inhibition of neuronal apoptosis [134]. In the 2,3,5-triphenyltetrazorlium chloride (TTC) study, the tissue infarction in rats with preconditioning exercise was decreased compared with the brain of rats without preconditioning [134]. Preconditioning with different exercise protocols such as moderate continuous training (MCT) and high-intensity interval training (HIIT) confers similar protection against neurological deficits and tissue injury following an acute stroke [137] although the benefit seems to be directly proportional to the intensity of training [138] and to a longer period of exercising before the ischemic injury [139,140].…”

“…infarction in rats with preconditioning exercise was decreased compared with the brain of rats without preconditioning [134]. Preconditioning with different exercise protocols such as moderate continuous training (MCT) and high-intensity interval training (HIIT) confers similar protection against neurological deficits and tissue injury following an acute stroke [137] although the benefit seems to be directly proportional to the intensity of training [138] and to a longer period of exercising before the ischemic injury [139,140].…”

“…Moreover, preconditioning exercise improves different structural and functional components of the blood-brain barrier (BBB) [134] whose dysfunction is one of the key pathobiological mechanisms leading to local and systemic immuno-inflammatory activation and to increase local injury via cerebral edema.…”