Age, aerobic fitness, and cerebral perfusion during exercise: role of carbon dioxide

Abstract

Middle cerebral artery mean velocity (MCAvmean) is attenuated with increasing age both at rest and during exercise. The aim of this study was to determine the influence of the age-dependent reduction in arterial PCO2 (PaCO2) and physical fitness herein. We administered supplemental CO2 (CO2 trial) or no additional gas (control trial) to the inspired air in a blinded and randomized manner, and assessed middle cerebral artery mean flow velocity during graded exercise in 1) 21 young [Y; age 24 Ϯ 3 yr (ϮSD)] volunteers of whom 11 were trained (YT) and 10 considered untrained (YUT), and 2) 17 old (O; 66 Ϯ 4 yr) volunteers of whom 8 and 9 were considered trained (OT) and untrained (OUT), respectively. A resting hypercapnic reactivity test was also performed. MCAvmean and PaCO2 were lower in O [44.9 Ϯ 3.1 cm/s and 30 Ϯ 1 mmHg (ϮSE)] compared with Y (59.3 Ϯ 2.3 cm/s and 34 Ϯ 1 mmHg, P Ͻ 0.01) at rest, independent of aerobic fitness level. The age-related decreases in MCAvmean and PaCO2 persisted during exercise. Supplemental CO2 reduced the age-associated decline in MCAv mean by 50%, suggesting that PaCO2 is a major component in the decline. On the other hand, relative hypercapnic reactivity was neither influenced by age (P ϭ 0.46) nor aerobic fitness (P ϭ 0.36). Although supplemental CO2 attenuated exercise-induced reduction in cerebral oxygenation (near-infrared spectroscopy), this did not influence exercise performance. In conclusion, PaCO2 contributes to the age-associated decline in MCAvmean at rest and during exercise; however exercise capacity did not diminish this age effect. brain blood flow; middle cerebral artery; old; transcranial Doppler CEREBRAL BLOOD FLOW (CBF) is meticulously regulated to ensure an adequate perfusion of the brain. With exercise middle cerebral artery mean velocity (MCAv mean ; a surrogate measure of CBF) is increased until ϳ60% of maximal oxygen uptake (V O 2max ) but thereafter declines toward resting levels (10,20,28). In young healthy individuals this drop in cerebral perfusion is likely the consequence of a hyperventilation facilitated reduction in PaCO 2 and hence augmented cerebral vasoconstriction (39). Accordingly, administration of CO 2 to the inspired air during exercise abolishes the decrease in MCAv mean (44,45), and during vigorous exercise MCAv mean is regulated by PaCO 2 and only to a lesser extent influenced by cerebral metabolism, mean arterial pressure (MAP), cardiac output, or sympathetic nerve activity (35).Compared with young healthy individuals a reduced CBF (24) and MCAv mean has consistently been reported in the aged population both at rest (2,7,9,15,25,27,49) and during exercise (9,10,28,32). Although a reduced MCAv mean response in aged humans is observed with exercise, its pattern follows that of young individuals, i.e., an initial increase which is then followed by a decline as the exercise intensity becomes intense (9,10,28,32). The regulating mechanisms for the reduction in CBF with age remain uncertain and global brain atrophy (11), decreased neuronal activ...

Restoring heat stress‐associated reduction in middle cerebral artery velocity does not reduce fatigue in the heat

“…Flück et al. () recently demonstrated that the age‐induced decrease in cerebral perfusion is related to concomitant reductions in PaCO 2 , but that normalization of MCAv mean to that of healthy young volunteers did not affect exercise performance, which is also in agreement with the current study. Thus, the present study is the first to mechanistically address the importance of a heat‐induced reduction of MCAv mean on incremental exercise performance in the heat, and as previously reported in other settings, the diminished MCAv mean when exercising in a warm environment seems of only very limited importance for exercise performance.…”

“…(b) Centrally mediated fatigue may be promoted by an insufficient O 2 delivery to the brain (Amann & Kayser, ; Rasmussen et al., ), which could become the consequence when cerebral perfusion is reduced. However, recent studies augmenting MCAv mean in hypoxic (Subudhi et al., ; Fan et al., ; Siebenmann et al., ) and normoxic (Subudhi et al., ; Flück et al., ) conditions have demonstrated that exercise capacity is not affected by changes in cerebral oxygenation, suggesting that this might also not be the case in heat‐stressed humans. Nonetheless, this remains unknown.…”

The impact of age on cerebral perfusion, oxygenation and metabolism during exercise in humans

“…; Flück et al . ). Interestingly, no significant interaction between age and exercise intensity was observed for MCA V mean by Fisher et al .…”

“…) or absolute exercise intensities (Flück et al . ) examined. These conflicting findings may relate to the smaller age difference between the groups in Fisher et al .…”

“…() (44 years) and Flück et al . () (42 years). Indeed, the normal age‐related reduction in resting MCA V mean was not observed in Fisher et al .…”