Cerebral vasomotor reactivity during hypo- and hypercapnia in sedentary elderly and Masters athletes

Abstract

Physical activity may influence cerebrovascular function. The objective of this study was to determine the impact of life-long aerobic exercise training on cerebral vasomotor reactivity (CVMR) to changes in end-tidal CO2 (EtCO2) in older adults. Eleven sedentary young (SY, 27±5 years), 10 sedentary elderly (SE, 72±4 years), and 11 Masters athletes (MA, 72±6 years) underwent the measurements of cerebral blood flow velocity (CBFV), arterial blood pressure, and EtCO2 during hypocapnic hyperventilation and hypercapnic rebreathing. Baseline CBFV was lower in SE and MA than in SY while no difference was observed between SE and MA. During hypocapnia, CVMR was lower in SE and MA compared with SY (1.87±0.42 and 1.47±0.21 vs. 2.18±0.28 CBFV%/mm Hg, P<0.05) while being lowest in MA among all groups (P<0.05). In response to hypercapnia, SE and MA exhibited greater CVMR than SY (6.00±0.94 and 6.67±1.09 vs. 3.70±1.08 CBFV1%/mm Hg, P<0.05) while no difference was observed between SE and MA. A negative linear correlation between hypo- and hypercapnic CVMR (R(2)=0.37, P<0.001) was observed across all groups. Advanced age was associated with lower resting CBFV and lower hypocapnic but greater hypercapnic CVMR. However, life-long aerobic exercise training appears to have minimal effects on these age-related differences in cerebral hemodynamics.

Figure 1

Linear regression analysis of group-averaged data showing the associations among the changes in cerebral blood flow velocity (CBFV%), cerebrovascular conductance index (CVCi%), and end-tidal CO₂ (EtCO2) during hypercapnic rebreathing in the sedentary young (SY), the sedentary elderly (SE), and Masters athletes (MA). The error bars represent standard deviations. SY: CBFV%=105.44+2.82*ΔEtCO₂, R²=0.94, P<0.001; CVCi%=109.54+1.46*ΔEtCO₂, R²=0.83; P<0.001. SE: CBFV%=88.94+5.44*ΔEtCO₂, R²=0.99, P<0.001; CVCi%=92.32+3.65*ΔEtCO₂, R²=0.99; P<0.001. MA: CBFV%=82.39+6.01*ΔEtCO₂, R²=0.99, P<0.001; CVCi%=92.79+3.67*ΔEtCO₂, R²=0.99; P<0.001.

Figure 2

Multivariate linear regression analysis of group-averaged and individual data exhibiting the contributions of hypercapnic changes in end-tidal CO₂ and arterial blood pressure to cerebral blood flow velocity in the sedentary young, sedentary elderly, and Masters athletes. The error bars represent standard deviations.

Figure 3

Linear correlation between hypo- and hypercapnic cerebral CO2 reactivity from each subject. Both reactivity measurements were calculated as the ratio of maximal changes in cerebral blood flow velocity (%) in response to the corresponding changes in end-tidal CO2 (mm Hg).

Figure 4

A hypothetical drawing to illustrate an age-related down-and-rightward shift of cerebral blood flow velocity (CBFV) and end-tidal CO2 (EtCO2) curve. During hypocapnic hyperventilation, cerebral vasomotor reactivity (slope of the curve) would be reduced in old when compared with young because reduction in basal CBFV would lead the operating point (*) being closer to the level of maximal vasoconstriction. Conversely, during hypercapnic rebreathing, the slope of the curve in the young would be attenuated when EtCO2 reached approximately 50 mm Hg while CBFV may continue to increase in old leading to higher cerebral vasomotor reactivity.