White matter hyperintensities in the brain are small areas of damage most likely produced by the rupture or other loss of integrity of tiny blood vessels. In effect they are miniscule strokes, individually unnoticed, but collectively a form of damage to the brain that adds up over time. Since white matter hyperintensities are connected to vascular health, it isn’t too surprising to see that old people possessed of better vascular function, as a consequence of maintaining physical fitness into later life, exhibit a lower burden of this form of damage in the brain. It should be expected that this lesser degree of structural damage contributes to the slower cognitive decline that accompanies higher levels of fitness in later life.
White matter (WM) hyperintensities (WMHs) are one of the most ubiquitous age-related structural changes observed via MRI, yet they are of unknown etiology. WMHs are presumed to be a consequence of age-related vascular changes. Arterial stiffness is associated with WMHs and is the most influential hemodynamic factor in individuals over the age of 60. Age-related arterial dysfunction is the result of a variety of deleterious changes that include intimal remodeling, increased arterial stiffness, and endothelial dysfunction. Age-related changes in the physical properties of, and the interaction between, macrovasculature and microvasculature contribute to the development of WMHs. For example, large artery stiffening transmits increases in pulsatility, the variation of blood pressure throughout the cardiac cycle, to small cerebral vessels. Excessive pulsatility to small cerebral vessels is associated with WMHs.
While cerebrovascular changes are endemic to aging, older adults show considerable variability in vascular brain health. One variable known to positively impact the brain’s vascular health is cardiorespiratory fitness (CRF), a product of regular exercise. However, little is known about the effects of CRF on WMH volume per se. In contrast, higher CRF has been linked to higher WM microstructure in older adults. Since low WM microstructure in normal appearing WM precedes conversion to WMHs, WMHs may also be positively influenced by high CRF. If so, CRF may attenuate the development of WMHs in older adults.
This study explored the effects of CRF on WMH volume in community-dwelling older adults. We further tested the possibility of an interaction between CRF and age on WMH volume. Participants were 76 adults between the ages of 59 and 77 who underwent a maximal graded exercise test and structural brain imaging. Results indicated that age was a predictor of WMH volume. However, an age-by-CRF interaction was observed such that higher CRF was associated with lower WMH volume in older participants. Our findings suggest that higher levels of aerobic fitness may protect cerebrovascular health in older adults.