It is known that cerebral blood flow declines with age in sedentary adults, although previous studies have involved small sample sizes, making the exact estimate of decline imprecise and the effects of possible moderator variables unknown. Animal studies indicate that aerobic exercise can elevate cerebral blood flow; however, this possibility has not been examined in humans. We examined how regular aerobic exercise affects the age-related decline in blood flow velocity in the middle cerebral artery (MCAv) in healthy humans. Maximal oxygen consumption, body mass index (BMI), blood pressure and MCAv were measured in healthy sedentary (n = 153) and endurance-trained (n = 154) men aged between 18 and 79 years. The relationships between age, training status, BMI and MCAv were examined using analysis of covariance methods. Mean ± s.e.m. estimates of regression coefficients and 95% confidence intervals (95% CI) were calculated. The age-related decline in MCAv was −0.76 ± 0.04 cm s −1 year −1 (95% CI = −0.69 to −0.83, r 2 = 0.66, P < 0.0005) and was independent of training status (P = 0.65). Nevertheless, MCAv was consistently elevated by 9.1 ± 3.3 cm s −1 (CI = 2.7-15.6, P = 0.006) in endurance-trained men throughout the age range. This ∼17% difference between trained and sedentary men amounted to an approximate 10 year reduction in MCAv 'age' and was robust to between-group differences in BMI and blood pressure. Regular aerobic-endurance exercise is associated with higher MCAv in men aged 18-79 years. The persistence of this finding in older endurance-trained men may therefore help explain why there is a lower risk of cerebrovascular disease in this population.
Highlights d NR supplementation in aged subjects augments the skeletal muscle NAD + metabolome d NR supplementation does not affect skeletal muscle mitochondrial bioenergetics d NR supplementation reduces levels of circulating inflammatory cytokines
Abstract-Cerebral autoregulation (CA) is a critical process for the maintenance of cerebral blood flow and oxygenation.Assessment of CA is frequently used for experimental research and in the diagnosis, monitoring, or prognosis of cerebrovascular disease; however, despite the extensive use and reference to static CA, a valid quantification of "normal" CA has not been clearly identified. While controlling for the influence of arterial PCO 2 , we provide the first clear examination of static CA in healthy humans over a wide range of blood pressure. In 11 healthy humans, beat-to-beat blood pressure (radial arterial), middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound), end-tidal PCO 2 , and cerebral oxygenation (near infrared spectroscopy) were recorded continuously during pharmacological-induced changes in mean blood pressure. In a randomized order, steady-state decreases and increases in mean blood pressure (8 to 14 levels; range: Ϸ40 to Ϸ125 mm Hg) were achieved using intravenous infusions of sodium nitroprusside or phenylephrine, respectively. MCAv mean was altered by 0.82Ϯ0.35% per millimeter of mercury change in mean blood pressure (R 2 ϭ0.82). Changes in cortical oxygenation index were inversely related to changes in mean blood pressure (slopeϭϪ0.18%/mm Hg; R 2 ϭ0.60) and MCAv mean (slopeϭϪ0.26%/cm ⅐ s
Ϫ1; R 2 ϭ0.54). There was a progressive increase in MCAv pulsatility with hypotension. These findings indicate that cerebral blood flow closely follows pharmacological-induced changes in blood pressure in otherwise healthy humans. Thus, a finite slope of the plateau region does not necessarily imply a defective CA. Moreover, with progressive hypotension and hypertension there are differential changes in cerebral oxygenation and MCAv mean . (Hypertension. 2010;55:698-705.)
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