Poster Communications: Physical activity confers neuroprotective benefits in young females; focus on improved cerebrovascular reactivity

The aged population are living longer and more sedentary lives, which in part contributes towards an increased prevalence of stroke and neurodegenerative disease. This is especially apparent in females (1, 2), however the fundamental mechanisms remain unclear. It has previously been demonstrated that lifelong physical activity in males can attenuate the inexorable age-related decline in cerebral perfusion and vasoreactivity (3), though to what extent comparable neuroprotection is conferred among females remains to be established. To force the “adaptive” signal out of the background “biological” noise, the current study examined the potential relationship between cardiorespiratory fitness and cerebral perfusion both at rest and in response to an acute vascular stressor (high-fat meal) known to incur cerebrovascular impairment subsequent to elevated oxidative-nitrosative stress (4). Eight active (21 ± 2 years of age; maximal oxygen consumption (VO2max) = 40 ± 3 ml/kg/min) and eight inactive (21 ± 2 years of age; VO2max = 31 ± 3 ml/kg/min) females participated in the study. On the first visit, VO2max was assessed via a standardised incremental exercise test. During the second visit, transcranial Doppler ultrasound and capnography were employed to establish middle cerebral artery blood flow velocity (MCAv) and cerebrovascular reactivity to hypercapnia (CVRCO2HYPER) and hypocapnia (CVRCO2HYPO) (4), which subsequently determined cerebrovasomotor range (CVRCO2RANGE). Measurements were obtained prior to and four hours following consumption of a standardised high-fat meal (1362 kcal; 130 g of fat) to induce post-prandial lipaemia (PPL) and elicit peak systemic oxidative-nitrosative stress. Comparative data were analysed via a two-way repeated measures analysis of variance and relationships via a Pearson product-moment correlation. The active group exhibited elevated CVRCO2HYPO and CVRCO2RANGE (P < 0.05 vs. inactive group). Furthermore, a positive relationship between VO2max and CVRCO2HYPER was observed (r = 0.6; P < 0.05). No between group differences were observed in resting cerebral perfusion and PPL-induced hypoperfusion was also comparable (P > 0.05 between groups). Collectively, our findings highlight a selective improvement in CVRCO2HYPO but not CVRCO2HYPER implying that the neuroprotection afforded by physical activity appears to be more related to changes in calcium sensitivity and not purely ascribed to vascular NO bioavailability. Given that the ageing female brain is more vulnerable to stroke and neurodegenerative disease in later life (1, 2), it would appear that they may likely suffer more pronounced cerebrovascular impairment during the critical phase of middle-age reinforcing the importance of lifelong physical activity.