Chronic physical activity mitigates cerebral hypoperfusion during central hypovolemia in elderly humans.

This study sought to test the hypothesis that orthostasis-induced cerebral hypoperfusion would be less severe in physically active elderly humans (ACT group) than in sedentary elderly humans (SED group). The peak O(2) uptake of 10 SED (67.1 +/- 1.4 yr) and 9 ACT (68.0 +/- 1.1 yr) volunteers was determined by a graded cycling exercise test (22.1 +/- 1.2 vs 35.8 +/- 1.3 ml.min(-1).kg(-1), P < 0.01). Baseline mean arterial pressure (MAP; tonometry) and middle cerebral arterial blood flow velocity (V(MCA); transcranial Doppler) were similar between the groups (SED vs. ACT group: 91 +/- 3 vs. 87 +/- 3 mmHg and 54.9 +/- 2.3 vs. 57.8 +/- 3.2 cm/s, respectively), whereas heart rate was higher and stroke volume (bioimpedance) was smaller in the SED group than in the ACT group. Central hypovolemia during graded lower body negative pressure (LBNP) was larger (P < 0.01) in the ACT group than in the SED group. However, the slope of V(MCA)/LBNP was smaller (P < 0.05) in the ACT group (0.159 +/- 0.016 cm/s/Torr) than in the SED group (0.211 +/- 0.008 cm/s/Torr). During LBNP, the SED group had a greater augmentation of cerebral vasomotor tone (P < 0.05) and hypocapnia (P < 0.001) compared with the ACT group. Baseline MAP variability and V(MCA) variability were significantly smaller in the SED group than in the ACT group, i.e., 0.49 +/- 0.07 vs. 1.04 +/- 0.16 (mmHg)(2) and 1.06 +/- 0.19 vs. 4.24 +/- 1.59 (cm/s)(2), respectively. However, transfer function gain, coherence, and phase between MAP and V(MCA) signals (Welch spectral estimator) from 0.08-0.18 Hz were not different between SED (1.41 +/- 0.18 cm.s(-1).mmHg(-1), 0.63 +/- 0.06 units, and 38.03 +/- 6.57 degrees ) and ACT (1.65 +/- 0.44 cm.s(-1).mmHg(-1), 0.56 +/- 0.05 units, and 48.55 +/- 11.84 degrees ) groups. We conclude that a physically active lifestyle improves the intrinsic mechanism of cerebral autoregulation and helps mitigate cerebral hypoperfusion during central hypovolemia in healthy elderly adults.

Sympathetic cardiac influence and arterial blood pressure instability.

Previous studies have suggested that sympathetic cardiac blockade enhances baroreflex function, whereas parasympathetic blockade diminishes baroreflex sensitivity and elicits arterial blood pressure (ABP) instability. The aim of this project was to test the hypothesis that sympathetic cardiac blockade was beneficial in maintaining ABP stability during orthostatic challenge. In 8 young healthy subjects, measurements were taken before and after sympathetic cardiac blockade (beta1-adrenoceptor blockade via metoprolol) in combination with or without parasympathetic blockade (atropine) at rest and during lower body negative pressure (LBNP). Arterial blood samples were obtained to evaluate plasma renin activity (PRA) and norepinephrine (NE). Power spectral analyses were performed on heart rate (HR) and ABP variability. LBNP -50 Torr significantly decreased systolic blood pressure (SBP, -6+/-3 mm Hg) and increased PRA (from 0.72+/-0.23 to 1.75+/-0.24 ng ml(-1) h(-1)) and NE (from 1.02+/-0.11 to 2.13+/-0.32 pg ml(-1)). Low frequency (LF, 0.04-0.12 Hz) SBP and diastolic blood pressure (DBP) variability were significantly augmented by LBNP (4.1+/-1.6 vs. 10.8+/-3.0 mm Hg2, and 3.1+/-1.0 vs. 7.9+/-1.9 mm Hg2, respectively). Following metoprolol, arterial baroreflex sensitivity (assessed by the slope of HR interval to SBP during injection with 1 mug kg(-1) phenylephrine) increased significantly (9.9+/-2.2 to 19.6+/-4.1 ms mm Hg(-1)). With beta1-adrenoceptor blockade, LBNP still decreased SBP (-10+/-2 mm Hg) and increased NE, but did not significantly augment PRA (0.59+/-0.22 vs. 1.03+/-0.18 ng ml(-1) h(-1)), or LF SBP and DBP variability (3.3+/-0.6 vs. 5.7+/-1.3 mm Hg2, and 3.1+/-0.7 vs. 5.4+/-1.1 mm Hg2, respectively). The increased PRA during LBNP remained non-significant following metoprolol combined with atropine, whereas the augmented LF SBP (2.6+/-0.7 vs. 9.9+/-2.8 mm Hg2) and DBP (2.5+/-0.7 vs. 11.1+/-3.0 mm Hg2) variability were significantly accentuated compared to both metoprolol alone and control conditions, accompanied by a greater delta SBP (-17+/-7 mm Hg) and significantly diminished baroreflex gain (0.91+/-0.05 ms/mm Hg). These data suggested that removal of sympathetic cardiac influence improved cardiovascular stability as indicated by a diminished LF ABP variability, which was related to an enhanced cardiac responsiveness.

Aging and arterial blood pressure variability during orthostatic challenge.

BACKGROUND: It has been demonstrated that a decrease in vagal cardiac function compromises arterial blood pressure (ABP) stability during orthostatic challenge. Augmentations in low-frequency (LF) ABP oscillations are indicative of this change in autonomic hemodynamic control. Aging is associated with diminished arterial baroreflex sensitivity and vagal cardiac dysfunction. However, the effect of aging on the stability of ABP during an orthostatic challenge remains to be elucidated. OBJECTIVE: The purpose of this study was to investigate ABP stability with aging during central hypovolemia induced by lower-body negative pressure (LBNP). METHODS: Graded LBNP up to -40 mm Hg was applied in 16 older (65 +/- 3 years of age) and 16 younger (25 +/- 3 years of age) healthy adults. ABP variability was analyzed by fast Fourier transform. LF spectral density (0.04-0.15 Hz) was extracted to provide an index of vasomotor responsiveness. RESULTS: Both LF systolic blood pressure (SBP) variability and diastolic blood pressure variability were augmented with LBNP. The rate of increase in LF SBP variability was augmented significantly greater in older as compared with younger subjects (p = 0.049). In addition, LF SBP variability was inversely correlated with decreases in pulse pressure in both age groups (r = -0.84, p = 0.01). The magnitude of the decreases in SBP and pulse pressure during LBNP was significantly affected by age, with the largest changes occurring in older subjects. The altered ABP response that manifested in older individuals was associated with a significant diminution in the reflex tachycardiac response elicited by LBNP. CONCLUSIONS: Induction of central hypovolemia via graded LBNP augments LF ABP variability. This increased ABP variability is significantly greater in older individuals. Our data suggest that aging is associated with ABP instability during orthostatic challenge.