![]() For example, the aforementioned studies reported a variety of exercise participation from sedentary to recreationally active. These discrepancies in the literature may be due to methodological differences as well as participants’ underlying comorbidities, biological sex, medication use, or habitual exercise status. There are conflicting reports regarding the changes in cerebrovascular reactivity to hypercapnia related to primary aging with some studies demonstrating age-associated declines ( Rogers et al., 1985 Reich and Rusinek, 1989 Tsuda and Hartmann, 1989 Matteis et al., 1998 Barnes et al., 2012), some demonstrating age-associated increases ( Zhu et al., 2013) while others show no age-associated declines ( Schieve and Wilson, 1953 Schwertfeger et al., 2006 Galvin et al., 2010 Oudegeest-Sander et al., 2014 Coverdale et al., 2017). Importantly, cerebrovascular reactivity is lower in individuals with a history of stroke, patients with dementia or Alzheimer’s disease, and may be a biomarker of risk of cognitive decline ( Iadecola, 2004 Silvestrini et al., 2006 Glodzik et al., 2013).Īs advancing age increases the risk for development of cerebrovascular disease and cognitive decline ( Choi et al., 1998), it is important to distinguish physiological or primary aging from pathology. Measuring the CBF response to hypercapnia is often used to test cerebrovascular function and is termed cerebrovascular reactivity ( Iliff et al., 1974). This suggests an age-associated difference in the reliance on MAP to increase cerebral blood flow during hypercapnia.Ī healthy brain is highly sensitive to changes in arterial carbon dioxide (CO 2) such that elevations in the arterial partial pressure of carbon dioxide (P aCO 2) can cause profound vasodilation of cerebral vasculature and hypercapnia is associated with augmentation of global cerebral blood flow (CBF) ( Kety and Schmidt, 1948). Our results demonstrate that cerebrovascular reactivity was not different between young and older adults who habitually exercise however, MAP reactivity was augmented in older adults. ![]() There were no associations between PWV and cerebrovascular reactivity (range: r = 0.00–0.39 p = 0.07–0.99). MCAv and CVCi reactivity to hypercapnia were not different between young and older adults (MCAv reactivity, YA: 2.0 ± 0.2 cm/s/mmHg OA: 2.0 ± 0.2 cm/s/mmHg p = 0.77, CVCi reactivity, YA: 0.018 ± 0.002 cm/s/mmHg 2 OA: 0.015 ± 0.001 cm/s/mmHg 2 p = 0.27) however, older adults demonstrated higher MAP reactivity to hypercapnia (YA: 0.4 ± 0.1 mmHg/mmHg OA: 0.7 ± 0.1 mmHg/mmHg p < 0.05). Older adults had higher PWV (YA: 6.2 ± 1.2 m/s OA: 7.5 ± 1.3 m/s p < 0.05) compared with young adults. Central arterial stiffness was assessed using carotid–femoral pulse wave velocity (PWV). Cerebrovascular conductance index (CVCi) was calculated as MCAv/MAP. In order to assess cerebrovascular reactivity, MCAv, end-tidal carbon dioxide (ETCO 2), and mean arterial pressure (MAP) were continuously recorded at rest and during stepwise elevations of 2, 4, and 6% inhaled CO 2. Middle cerebral artery velocity (MCAv) was recorded using transcranial Doppler ultrasound. We recruited 22 young (YA: age = 27 ± 5 years, range 18–35 years) and 21 older (OA: age = 60 ± 4 years, range 56–68 years) habitual exercisers who partake in at least 150 min of structured aerobic exercise each week. In addition, we sought to determine the association between central arterial stiffness and cerebrovascular reactivity. In this context, we evaluated the age-related differences in cerebrovascular reactivity in healthy adults who habitually exercise. Habitual exercise is protective against cognitive decline and is associated with reduced stiffness of the large central arteries that perfuse the brain. Reduced cerebrovascular reactivity to a vasoactive stimulus is associated with age-related diseases such as stroke and cognitive decline.
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