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Biomedical subjects

D R Seals

Publications and source records attributed to D R Seals.

At least 37 records · Page 2Linked to original sources

Carotid artery wall hypertrophy with age is related to local systolic blood pressure in healthy men.

Carotid artery intima-media thickness (IMT) increases with advancing age in humans. The underlying mechanism of this increase is unknown, but data from animal studies suggest that a chronic increase in local distending pressure can act as a stimulus. To test this hypothesis, we studied a total of 129 healthy normotensive, nonobese, nonsmoking men aged 18 to 77 years. Brachial systolic blood pressure (SBP) was unchanged, but carotid SBP increased progressively with age (P<0.05). Carotid IMT and the ratio of carotid IMT to lumen (ultrasonography) increased progressively with age (P<0.05). Carotid IMT was approximately 50% greater in the older compared with the young men. Carotid SBP was positively related to carotid IMT (r=0.55, P<0.001). After carotid SBP was taken into account (ANCOVA), the age-related difference in carotid IMT was no longer statistically significant (P=0.22). We conclude that carotid IMT increases with age in healthy men in the absence of elevations in peripheral SBP. Carotid SBP increases progressively with advancing age in this population and is significantly related to the corresponding carotid wall hypertrophy. These results support the hypothesis that chronic increases in local distending pressure may be an important mechanism in the wall thickening that occurs with human aging in central elastic arteries.

Adolescent↗

Tonic sympathetic support of metabolic rate is attenuated with age, sedentary lifestyle, and female sex in healthy adults.

We recently demonstrated in young adult humans that the sympathetic nervous system contributes to the control of resting metabolic rate via tonic beta-adrenergic receptor stimulation. In the present follow-up study we determined the respective effects of age, habitual exercise status, and sex on this regulatory mechanism. Resting metabolic rate (ventilated hood, indirect calorimetry) was determined in 55 healthy sedentary or endurance exercise-trained adults, aged 18-35 or 60-75 yr (29 men and 26 women), before (baseline) and during the infusion of either a nonselective beta-adrenergic receptor antagonist (propranolol) or saline (control). Relative to baseline values, during beta-adrenergic receptor antagonism resting metabolic rate adjusted for fat-free mass was reduced to a lesser extent in older (mean +/- SE, -130 +/- 46 kJ/d) compared with young (-297 +/- 46) adults, sedentary (-151 +/- 50) compared with endurance exercise-trained (-268 +/- 46) adults, and women (-105 +/- 33) compared with men (-318 +/- 50; all P < 0.01). Reductions in resting metabolic rate during beta-adrenergic receptor antagonism were positively related to higher baseline resting metabolic rate and plasma catecholamine concentrations and negatively related to adiposity (all P < 0.05). Resting metabolic rate was unchanged in response to saline control in all groups. These results provide experimental support for the hypothesis that aging, sedentary living, and female sex are associated with attenuated sympathetic nervous system support of resting metabolic rate in healthy adult humans.

Adolescent↗

Regular aerobic exercise modulates age-associated declines in cardiovagal baroreflex sensitivity in healthy men.

1. Cardiovagal baroreflex sensitivity (BRS), the arterial baroreflex-mediated change in the R-R interval per unit change in systolic blood pressure, decreases with advancing age in sedentary adult humans. We determined the effects of regular aerobic exercise on the age-related decline in cardiovagal BRS. 2. In the cross-sectional study, 133 healthy men 18-79 years of age who were either sedentary, performing moderate aerobic exercise, or endurance exercise trained were studied. Among the sedentary men, cardiovagal BRS (phase IV of Valsalva's manoeuvre) was progressively lower (P < 0.05) in the middle-aged ( approximately 33 %) and older ( approximately 60 %) groups compared with the young group. In contrast, cardiovagal BRS was similar in the young and middle-aged men in the moderate exercise and endurance-trained groups. Cardiovagal BRS was lower (P < 0.05) in the older exercising men, but the magnitude of decline across age ( approximately 30 %) was only half as great as that in sedentary men. Cardiovagal BRS was 40-75 % greater (P < 0.05) in middle-aged and older men who exercised regularly compared with their sedentary peers. 3. In the intervention study, a 3 month aerobic exercise intervention (primarily walking) increased cardiovagal BRS by an average of 25 % (P < 0.05) in 13 previously sedentary middle-aged and older (56 +/- 1 years) healthy men. 4. Our results demonstrate for the first time that regular aerobic exercise: (1) attenuates the age-associated decline in cardiovagal BRS; and (2) partially restores the loss of cardiovagal BRS in previously sedentary middle-aged and older healthy men.

Aged↗

Human ageing and the sympathoadrenal system.

Over the past three decades the changes in sympathoadrenal function that occur with age in healthy adult humans have been systematically studied using a combination of neurochemical, neurophysiological and haemodynamic experimental approaches. The available experimental evidence indicates that tonic whole-body sympathetic nervous system (SNS) activity increases with age. The elevations in SNS activity appear to be region specific, targeting skeletal muscle and the gut, but not obviously the kidney. The SNS tone of the heart is increased, although this appears to be due in part to reduced neuronal reuptake of noradrenaline (norepinephrine). In contrast to SNS activity, tonic adrenaline (epinephrine) secretion from the adrenal medulla is markedly reduced with age. This is not reflected in plasma adrenaline concentrations because of reduced plasma clearance. Despite widely held beliefs to the contrary, sympathoadrenal responsiveness to acute stress is not exaggerated with age in healthy adults. Indeed, adrenaline release in response to acute stress is substantially attenuated in older men. The mechanisms underlying the age-associated increases in SNS activity have not been established, but our preliminary data are consistent with increased subcortical central nervous system (CNS) sympathetic drive. These changes in sympathoadrenal function with advancing age may have a number of important physiological and pathophysiological consequences for human health and disease.

Acute Disease↗

Regular aerobic exercise prevents and restores age-related declines in endothelium-dependent vasodilation in healthy men.

BACKGROUND: In sedentary humans endothelium-dependent vasodilation is impaired with advancing age contributing to their increased cardiovascular risk, whereas endurance-trained adults demonstrate lower age-related risk. We determined the influence of regular aerobic exercise on the age-related decline in endothelium-dependent vasodilation. METHODS AND RESULTS: In a cross-sectional study, 68 healthy men 22 to 35 or 50 to 76 years of age who were either sedentary or endurance exercise-trained were studied. Forearm blood flow (FBF) responses to intra-arterial infusions of acetylcholine and sodium nitroprusside were measured by strain-gauge plethysmography. Among the sedentary men, the maximum FBF response to acetylcholine was 25% lower in the middle aged and older compared with the young group (P:<0.01). In contrast, there was no age-related difference in the vasodilatory response to acetylcholine among the endurance-trained men. FBF at the highest acetylcholine dose was almost identical in the middle aged and older (17.3+/-1.3 mL/100 mL tissue per minute) and young (17.7+/-1.4 mL/100 mL tissue per minute) endurance-trained groups. There were no differences in the FBF responses to sodium nitroprusside among the sedentary and endurance- trained groups. In an exercise intervention study, 13 previously sedentary middle aged and older healthy men completed a 3-month, home-based aerobic exercise intervention (primarily walking). After the exercise intervention, acetylcholine-mediated vasodilation increased approximately 30% (P:<0.01) to levels similar to those in young adults and middle aged and older endurance-trained men. CONCLUSIONS: Our results indicate that regular aerobic exercise can prevent the age-associated loss in endothelium-dependent vasodilation and restore levels in previously sedentary middle aged and older healthy men. This may represent an important mechanism by which regular aerobic exercise lowers the risk of cardiovascular disease in this population.

Acetylcholine↗

Aging, habitual exercise, and dynamic arterial compliance.

BACKGROUND: A reduction in compliance of the large-sized cardiothoracic (central) arteries is an independent risk factor for the development of cardiovascular disease with advancing age. METHODS AND RESULTS: We determined the role of habitual exercise on the age-related decrease in central arterial compliance by using both cross-sectional and interventional approaches. First, we studied 151 healthy men aged 18 to 77 years: 54 were sedentary, 45 were recreationally active, and 53 were endurance exercise-trained. Central arterial compliance (simultaneous B-mode ultrasound and arterial applanation tonometry on the common carotid artery) was lower (P:<0.05) in middle-aged and older men than in young men in all 3 groups. There were no significant differences between sedentary and recreationally active men at any age. However, arterial compliance in the endurance-trained middle-aged and older men was 20% to 35% higher than in the 2 less active groups (P:<0.01). As such, age-related differences in central arterial compliance were smaller in the endurance-trained men than in the sedentary and recreationally active men. Second, we studied 20 middle-aged and older (53+/-2 years) sedentary healthy men before and after a 3-month aerobic exercise intervention (primarily walking). Regular exercise increased central arterial compliance (P:<0.01) to levels similar to those of the middle-aged and older endurance-trained men. These effects were independent of changes in body mass, adiposity, arterial blood pressure, or maximal oxygen consumption. CONCLUSIONS: Regular aerobic-endurance exercise attenuates age-related reductions in central arterial compliance and restores levels in previously sedentary healthy middle-aged and older men. This may be one mechanism by which habitual exercise lowers the risk of cardiovascular disease in this population.

Adolescent↗

Relation of leptin and insulin to adiposity-associated elevations in sympathetic activity with age in humans.

OBJECTIVE: To determine whether plasma leptin and insulin concentrations are related to adiposity-associated elevations in muscle sympathetic nerve activity (MSNA) with age in healthy adult humans. DESIGN: Cross-sectional investigation of young and older adult men. SUBJECTS: Thirty healthy adult men, 16 young (25+/-1 y, mean+/-s.e.) and 14 older (61+/-1 y). MEASUREMENTS/RESULTS: The older men had higher (P<0.05) levels of body mass, BMI, total fat mass and truncal fat mass (dual energy X-ray absorptiometry) than the young men. MSNA burst frequency (microneurography) was approximately 75% higher in the older men (P<0.001). Plasma leptin concentrations were approximately 150% higher (P<0.01), whereas plasma insulin concentrations were approximately 70% higher (P<0.05) in the older subjects. MSNA was related to both total (r=0.51, P<0.01) and truncal (r=0.56, P<0.01) fat mass. Plasma leptin concentrations were related to total and truncal fat mass (both r=0.83, P<0.001), and to MSNA (r=0.49, P<0.01). Plasma insulin concentrations were related to MSNA (r=0.38, P<0.05). We used partial correlation analyses to assess whether leptin and/or insulin are potential contributors to the relation between body fat and MSNA. Adjusting for the effects of plasma leptin, but not insulin, concentrations eliminated the significant relations between MSNA and total and truncal fat mass. CONCLUSION: Our results: (1) demonstrate a positive relation between MSNA and plasma leptin concentrations in young and older healthy men; and (2) support the concept that circulating leptin concentrations may act as a humoral signal contributing to adiposity-associated elevations in MSNA with age in adult humans.

Absorptiometry, Photon↗

Age-related declines in knee extensor strength and physical performance in healthy Hispanic and Caucasian women.

Hispanic women may undergo greater age-related reductions in physical functional capacity compared with Caucasian women. If so, a greater rate of decline in muscle strength with age could contribute. We tested this hypothesis in 82 healthy sedentary Caucasian (n = 37) and Hispanic (n = 45) adult women aged 21-78 years of similar socioeconomic status. Absolute one-repetition maximum (1-RM) strength of the knee extensors (KE) declined with advancing age in the Caucasian (r = -.55, p < .01) and Hispanic (r = -.45, p < .01) women; the rates of decline were similar in the two groups (-7% to 8% x decade(-1), p = .60). KE strength normalized for thigh fat-free mass (FFM) also declined with age in the Caucasian (r = .52, p < .01) and Hispanic (r = -.41, p < .01) women, the rates of decline being similar (-6% to 7% x decade(-1), p = .66). For all functional performance tasks (10-m walk, stair ascent, stair descent, and chair stand), performance time increased with advancing age (mean of four tasks vs age: Caucasian, r = .64, p < .01; Hispanic, r = .56, p < .01). Absolute and normalized KE 1-RM were inversely related to the mean time for the four performance tasks (r = -.34 to -.58, all p < .01). Normalized KE 1-RM was the best independent predictor of the age-related decline in task performance in both groups. These cross-sectional findings do not support the hypothesis that Hispanic ethnicity per se is associated with a greater decline in KE strength and performance tasks associated with KE strength in healthy women.

Adult↗

The 'adrenaline hypothesis' of hypertension revisited: evidence for adrenaline release from the heart of patients with essential hypertension.

OBJECTIVE: Whether adrenaline acts as a sympathetic nervous cotransmitter in humans and stimulates beta2-adrenoceptors to augment neuronal noradrenaline release remains a subject of considerable dispute. The aim of this study was to test if adrenaline is released from regional sympathetic nerves (in the heart) in patients with essential hypertension, and to investigate whether locally released adrenaline might enhance cardiac noradrenaline release. METHODS: Using dual isotope dilution methodology, adrenaline and noradrenaline plasma kinetics was measured for the whole body and in the heart in 13 untreated patients with essential hypertension and 27 healthy volunteers. All research participants underwent cardiac catheterization under resting conditions. RESULTS: At rest, there was negligible adrenaline release from the sympathetic nerves of the heart in healthy subjects, 0.27 +/- 1.62 ng/min. In contrast, in patients with essential hypertension, adrenaline was released from the heart at a rate of 1.46 +/- 1.73 ng/min, equivalent on a molar basis to approximately 5% of the associated cardiac noradrenaline spillover value. Cardiac noradrenaline spillover was higher in hypertensive patients, 24.9 +/- 17.0 ng/min compared to 15.4 +/- 11.7 ng/min in healthy volunteers (P< 0.05). Among patients, rates of cardiac adrenaline and noradrenaline spillover correlated directly (r= 0.59, P< 0.05). CONCLUSIONS: This study, in demonstrating release of adrenaline from the heart in patients with essential hypertension, and in disclosing a proportionality between rates of cardiac adrenaline and noradrenaline release, provides perhaps the most direct evidence to date in support of the 'adrenaline hypothesis' of essential hypertension.

Adult↗

Manuscript peer review: a helpful checklist for students and novice referees.

The ability to contribute consistent, fundamentally sound critiques is an essential element of the scientific peer review process and an important professional skill for investigators. Despite its importance, many students and junior scientists do not have an adequate working knowledge of how to effectively critique research manuscripts. Part of the problem, in our view, is that novice referees often lack a comprehensive understanding of the basic issues that should be considered in evaluating scientific articles. Specifically, they tend to overemphasize certain limitations (usually methodological), while missing other key points related to the scientific method that should be weighed much more heavily. In our journal club and graduate courses we have been using a "checklist" to help graduate students and postdoctoral fellows critically analyze original research papers. In this article we present these guidelines in the hope that they will serve as a helpful resource for students and other novice reviewers when critiquing scientific manuscripts.

Manuscripts as Topic↗

Age-associated arterial wall thickening is related to elevations in sympathetic activity in healthy humans.

Arterial wall hypertrophy occurs with age in humans and is a strong predictor of cardiovascular disease risk. The responsible mechanism is unknown, but data from studies in experimental animals suggest that elevated sympathetic-adrenergic tone may be involved. To test this hypothesis in humans we studied 11 young (29 +/- 1 yr; means +/- SE) and 13 older (63 +/- 1) healthy normotensive men under supine resting conditions. Muscle sympathetic nerve activity (MSNA) burst frequency (peroneal microneurography) was 70% higher in the older men (39 +/- 1 vs. 23 +/- 2 bursts/min; P < 0.001). Femoral artery intima media thickness (IMT; B-mode ultrasound) and the femoral IMT-to-lumen diameter ratio (IMT/lumen) were approximately 75% greater in the older men (both P < 0.001). Femoral IMT (r = 0. 82) and the femoral IMT/lumen (r = 0.85) were strongly and positively related to MSNA (both P < 0.001). The significant age group differences in femoral IMT and the IMT/lumen were abolished when the influence of MSNA was removed. In contrast, the relationship between MSNA and femoral wall thickness remained significant after removing the influence of age. We conclude that 1) primary aging is associated with femoral artery hypertrophy in humans and 2) this is strongly related to elevations in sympathetic nerve activity to the vasculature. These results support the hypothesis that tonic elevations in sympathetic nerve activity may be an important mechanism in the arterial remodeling that occurs with human aging.

Adult↗

Limb blood flow and vascular conductance are reduced with age in healthy humans: relation to elevations in sympathetic nerve activity and declines in oxygen demand.

BACKGROUND: We tested the hypothesis that basal (resting) limb blood flow and vascular conductance are reduced with age in adult humans and that these changes are related to elevations in sympathetic vasoconstrictor nerve activity and reductions in limb oxygen demand. METHODS AND RESULTS: Sixteen young (28+/-1 years; mean+/-SEM) and 15 older (63+/-1 years) healthy normotensive adult men were studied. Diastolic blood pressure and body fat were higher (P<0.005) in the older men, but there were no other age-related differences in subject characteristics. Femoral artery blood flow (Doppler ultrasound) was 26% lower in the older men (P<0.005), despite similar levels of cardiac output (systemic arterial blood flow) in the 2 groups. Femoral artery vascular conductance was 32% lower and femoral vascular resistance was 45% higher in the older men (P<0. 005). Muscle sympathetic nerve activity (peroneal microneurography) was 74% higher in the older men (P<0.001) and correlated with femoral artery blood flow (r=-0.55, P<0.005), vascular conductance (r=-0.65, P<0.001), and vascular resistance (r=0.61, P<0.001). The age-related differences in femoral hemodynamics were no longer significant after correction for the influence of muscle sympathetic nerve activity. There were no significant age-group differences in leg tissue mass (by dual-energy x-ray absorptiometry), but estimated leg oxygen consumption was 15% lower in the older men (P<0.001). Femoral artery blood flow was directly related to estimated leg oxygen consumption (r=0.78, P<0.001). The age-group differences in femoral artery blood flow were no longer significant after correction for estimated leg oxygen consumption by ANCOVA. CONCLUSIONS: (1) Basal whole-leg arterial blood flow and vascular conductance are reduced with age in healthy adult men; (2) these changes are associated with elevations in sympathetic vasoconstrictor nerve activity; and (3) the lower whole-limb blood flow is related to a lower oxygen demand that is independent of tissue mass.

Adult↗

Cardiopulmonary baroreflex inhibition of sympathetic nerve activity is preserved with age in healthy humans.

1. We tested the hypothesis that the ability of the cardiopulmonary baroreflex to produce sympathoinhibition is reduced with age in humans. Eleven young (23 +/- 1 years, mean +/- s.e.m.) and ten older (64 +/- 1) healthy adult males were studied under supine conditions (control) and in response to cardiopulmonary baroreflex stimulation evoked by acute central circulatory hypervolaemia (10 deg head-down tilt). The two groups were normotensive and free of overt cardiovascular disease. 2. Supine baseline (control) levels of efferent muscle sympathetic nerve activity (MSNA) burst frequency were twice as high in the older men (41 +/- 2 vs. 21 +/- 2 bursts min-1, P < 0.05). In both groups in response to head-down tilt arterial blood pressure and heart rate were unchanged, peripheral venous pressure (PVP) increased (P < 0.05), MSNA total activity decreased (P < 0.05), antecubital venous plasma noradrenaline concentrations did not change significantly, and forearm blood flow and vascular conductance increased (vascular resistance decreased) (all P < 0.05). The mean absolute DeltaMSNA/DeltaPVP was similar in the young and older men, although the higher control levels of MSNA in the older men resulted in a smaller percentage DeltaMSNA/DeltaPVP (P < 0.05). Per DeltaPVP, the reduction in forearm vascular resistance was smaller in the older men, but there were no age group differences when expressed as increases in forearm vascular conductance. 3. These results indicate that the ability of the cardiopulmonary baroreflex to inhibit MSNA is well preserved with age in healthy adult humans. As such, these findings are not consistent with the concept that this mechanism plays a role in the age-associated elevation in basal MSNA.

Adult↗

Influence of gender on the sympathetic neural adjustments to alterations in systemic oxygen levels in humans.

The purpose of this investigation was to determine whether gender influences the muscle sympathetic nerve activity (MSA) and systemic cardiovascular adjustments to alterations in systemic oxygen levels. To accomplish this, we performed direct (intraneural) measurements of muscle sympathetic nerve activity in 11 male and seven female young healthy adults during room air breathing, moderate isocapnic hypoxaemia and hyperoxaemia. During hypoxaemia, arterial oxygen saturation declined similarly in men and women. The magnitudes of the peak increases in MSA and stimulus-response 'gain' were not different between groups. However, the women had a shorter latency of response (P < 0.05). Women also demonstrated a greater increase in heart rate and a modest elevation in diastolic blood pressure, whereas the ventilatory responses were identical in the two groups. During normoxic recovery, MSA returned to baseline more quickly in women than in men (P < 0.05). During hyperoxaemia, muscle sympathetic nerve activity decreased only in the men (P < 0.05). Heart rate decreased slightly (P < 0.05) in both men and women, whereas blood pressure and minute ventilation were unchanged from normoxic control levels. Our findings fail to support an effect of gender on the peak muscle sympathetic nerve activity response to moderate isocapnic hypoxaemia in healthy young adult humans, although women demonstrate a shorter latency for sympathoexcitation and recovery under these conditions. In response to hyperoxaemia, women fail to demonstrate the sympathoinhibition consistently observed in men, possibly because of the low resting levels of MSA characteristic of young adult women. Thus, gender appears to contribute to the interindividual variability in sympathetic and cardiovascular responses to alterations in systemic oxygen levels.

Adult↗

Neural mechanisms in human obesity-related hypertension.

OBJECTIVE: Two hypotheses concerning mechanisms of weight gain and of blood pressure elevation in obesity were tested. The first hypothesis is that in human obesity sympathetic nervous system underactivity is present, as a metabolic basis for the obesity. The second hypothesis, attributable to Landsberg, is that sympathetic nervous activation occurs with chronic overeating, elevating blood pressure. These are not mutually exclusive hypotheses, since obesity is a heterogeneous disorder. DESIGN AND METHODS: Whole body and regional sympathetic nervous system activity, in the kidneys and heart, was measured at rest using noradrenaline isotope dilution methodology in a total of 86 research voluteers in four different subject groups, in lean and in obese people who either did, or did not, have high blood pressure. RESULTS: In the lean hypertensive patients, noradrenaline spillover for the whole body, and from the heart and kidneys was substantially higher than in the healthy lean volunteers. In normotensive obesity, the whole body noradrenaline spillover rate was normal, mean renal noradrenaline spillover was elevated (twice normal), and cardiac noradrenaline spillover reduced by approximately 50%. In obesity-related hypertension, there was elevation of renal noradrenaline spillover, comparable to that present in normotensive obese individuals but not accompanied by suppression of cardiac noradrenaline spillover, which was more than double that of normotensive obese individuals (P<0.05), and 25% higher than in healthy volunteers. There was a parallel elevation of heart rate in hypertensive obese individuals. CONCLUSIONS: The sympathetic underactivity hypothesis of obesity causation now looks untenable, as based on measures of noradrenaline spillover, sympathetic nervous system activity was normal for the whole body and increased for the kidneys; the low sympathetic activity in the heart would have only a trifling impact on total energy balance. The increase in renal sympathetic activity in obesity may possibly be a necessary cause for the development of hypertension in obese individuals, although clearly not a sufficient cause, being present in both normotensive and hypertensive obese individuals. The discriminating feature of obesity-related hypertension was an absence of the suppression of the cardiac sympathetic outflow seen in normotensive obese individuals. Sympathetic nervous changes in obesity-related hypertension conformed rather closely to those expected from the Landsberg hypothesis.

Adolescent↗

Lack of age-associated elevations in 24-h systolic and pulse pressures in women who exercise regularly.

We tested the hypothesis that the elevations in 24-h arterial systolic (SBP) and pulse (PP) pressures with age in sedentary adult females are absent or smaller in women who exercise regularly. Four groups of healthy normotensive women were studied: premenopausal (n = 12; 29 +/- 1 yr, mean +/- SE) and postmenopausal (n = 20; 62 +/- 1) sedentary, and premenopausal (n = 14; 30 +/- 1) and postmenopausal (n = 12; 58 +/- 1) endurance-exercise trained (distance runners). In the sedentary group, 24-h SBP and PP (Spacelabs ambulatory monitor 90207) were approximately 10 mmHg higher (P < 0.05) in the postmenopausal women than in the premenopausal controls; this was because of higher daytime and nighttime SBP and PP levels in the postmenopausal women. In contrast, 24-h, daytime and nighttime SBP and PP were not different with age in the endurance-trained women. SBP variability and SBP load (% of all recordings > 140 mmHg) generally were greater with age in the sedentary women (e.g., SBP load = 14 +/- 4 vs. 3 +/- 1%, P < 0.05) but not in the endurance-trained women. In the pooled population, 24-h SBP and PP were related to waist-to-hip ratio (measure of abdominal adiposity) (r = 0.48 and 0.49, respectively, P < 0.001) and carotid augmentation index (measure of arterial stiffness) (r = 0.43 and 0.53, P < 0.005). In the sedentary women, accounting for the influence of either of these factors eliminated the significant age-associated differences in 24-h SBP and PP (P > 0.3). Our results suggest that the elevations in 24-h SBP and PP with age in sedentary adult females may not occur in women who regularly perform endurance exercise. This appears to be related to the absence of age-associated increases in abdominal adiposity and arterial stiffness in the exercising women.

Adult↗

Hemodynamic sequelae of age-related increases in arterial stiffness in healthy women.

Stiffening of central arteries is believed to contribute to the increase in the incidence of cardiovascular disease with age, presumably through its adverse influence on arterial blood pressure. We found that (1) the physiologic link between age-related increases in arterial stiffness and blood pressure appears to be elevated systemic vascular resistance, and (2) increased arterial stiffness and systemic vascular resistance with age were inversely related to blood volume, stroke volume, and cardiac output.

Adult↗