We tested the hypothesis that hypotension occurred in older adults at the onset of orthostatic challenge as a result of vagal dysfunction. Responses of heart rate (HR) and mean arterial pressure (MAP) were compared between 10 healthy older and younger adults during onset and sustained lower body negative pressure (LBNP). A younger group was also assessed after blockade of the parasympathetic nervous system with the use of atropine or glycopyrrolate and after blockade of the beta(1)-adrenoceptor by use of metoprolol. Baseline HR (older vs. younger: 59 +/- 4 vs. 54 +/- 1 beats/min) and MAP (83 +/- 2 vs. 89 +/- 3 mmHg) were not significantly different between the groups. During -40 Torr, significant tachycardia occurred at the first HR response in the younger subjects without hypotension, whereas significant hypotension [change in MAP (DeltaMAP) -7 +/- 2 mmHg] was observed in the elderly without tachycardia. After the parasympathetic blockade, tachycardiac responses of younger subjects were diminished and associated with a significant hypotension at the onset of LBNP. However, MAP was not affected after the cardiac sympathetic blockade. We concluded that the elderly experienced orthostatic hypotension at the onset of orthostatic challenge because of a diminished HR response. However, an augmented vasoconstriction helped with the maintenance of their blood pressure during sustained LBNP.

This study was designed to investigate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability before and after glycopyrrolate or atropine treatment. Changes in R-R interval (RRI) and ABP were assessed in 10 healthy young (age, 22 +/- 1.8 yr) volunteers during graded lower body negative pressure (LBNP) before and after muscarinic cholinergic (MC) blockade. Transient hypertension was induced by phenylephrine (1 microg/kg body wt), whereas systemic hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. Power spectral densities of systolic [systolic blood pressure (SBP)] and diastolic ABP variability were examined. Both antimuscarinic agents elicited tachycardia similarly without significantly affecting baseline ABP. The increase in SBP after phenylephrine injection (+14 +/- 2 mmHg) was significantly augmented with atropine (+26 +/- 2 mmHg) or glycopyrrolate (+27 +/- 3 mmHg) and associated with a diminished reflex bradycardia. The decrease in SBP after cuff deflation (-9.2 +/- 1.2 mmHg) was significantly greater after atropine (-15 +/- 1 mmHg) or glycopyrrolate (-14 +/- 1 mmHg), with abolished reflex tachycardia. LBNP significantly decreased both SBP and RRI. However, after antimuscarinic agents, the reduction in SBP was greater (P < 0.05) and was associated with less tachycardia. Antimuscarinic agents reduced (P < 0.05) the low-frequency (LF; 0.04-0.12 Hz) power of ABP variability at rest. The LF SBP oscillation was significantly augmented during LBNP, which was accentuated (P < 0.05) after antimuscarinic agents and was correlated (r = -0.79) with the decrease in SBP. We conclude that antimuscarinic agents compromised ABP stability by diminishing baroreflex sensitivity, reflecting the importance of vagal cardiac function in hemodynamic homeostasis. The difference between atropine and glycopyrrolate was not significant.

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.

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.

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