Disentangling the genetic effects of refugial isolation and range expansion in a trans-continentally distributed species.

In wide-ranging taxa with historically dynamic ranges, past allopatric isolation and range expansion can both influence the current structure of genetic diversity. Considering alternate historical scenarios involving expansion from either a single refugium or from multiple refugia can be useful in differentiating the effects of isolation and expansion. Here, we examined patterns of genetic variability in the trans-continentally distributed painted turtle (Chrysemys picta). We utilized an existing phylogeographic dataset for the mitochondrial control region and generated additional data from nine populations for the mitochondrial control region (n = 302) and for eleven nuclear microsatellite loci (n = 247). We created a present-day ecological niche model (ENM) for C. picta and hindcast this model to three reconstructions of historical climate to define three potential scenarios with one, two, or three refugia. Finally, we employed spatially-explicit coalescent simulations and an approximate Bayesian computation (ABC) framework to test which scenario best fit the observed genetic data. Simulations indicated that phylogeographic and multilocus population-level sampling both could differentiate among refugial scenarios, although inferences made using mitochondrial data were less accurate when a longer coalescence time was assumed. Furthermore, all empirical genetic datasets were most consistent with expansion from a single refugium based on ABC. Our results indicate a stronger role for post-glacial range expansion, rather than isolation in allopatric refugia followed by range expansion, in structuring diversity in this species. To distinguish among complex historical scenarios, we recommend explicitly modeling the effects of range expansion and evaluating alternate refugial scenarios for wide-ranging taxa.

A coupled SAFE-2.5D BEM approach for the dispersion analysis of damped leaky guided waves in embedded waveguides of arbitrary cross-section.

The paper presents a Semi-Analytical Finite Element (SAFE) formulation coupled with a 2.5D Boundary Element Method (BEM) for the computation of the dispersion properties of viscoelastic waveguides with arbitrary cross-section and embedded in unbounded isotropic viscoelastic media. Attenuation of guided modes is described through the imaginary component of the axial wavenumber, which accounts for material damping, introduced via linear viscoelastic constitutive relations, as well as energy loss due to radiation of bulk waves in the surrounding media. Energy radiation is accounted in the SAFE model by introducing an equivalent dynamic stiffness matrix for the surrounding medium, which is derived from a regularized 2.5D boundary element formulation. The resulting dispersive wave equation is configured as a nonlinear eigenvalue problem in the complex axial wavenumber. The eigenvalue problem is reduced to a linear one inside a chosen contour in the complex plane of the axial wavenumber by using a contour integral method. Poles of leaky and evanescent modes are obtained by choosing appropriately the phase of the wavenumbers normal to the interface in compliance with the nature of the waves in the surrounding medium. Finally, the obtained eigensolutions are post-processed to compute the energy velocity and the radiated wavefield in the surrounding domain. The reliability of the method is first validated on existing results for waveguides of circular cross sections embedded in elastic and viscoelastic media. Next, the potential of the proposed numerical framework is shown by computing the dispersion properties for a square steel bar embedded in grout and for an H-shaped steel pile embedded in soil.

Processing cereal straws by steam explosion in a pilot plant to enhance digestibility in ruminants.

Wheat, barley and oat straws were treated by steam explosion (SE) and then washed with 50g/l NaOH solution. The SE treatment was optimized at batch scale on the basis of carbohydrate recovery. Stocks of fodder (300kg) were produced at 198 degrees C for 2.5min by a continuous reactor and used for in vivo digestibility tests carried out on sheep. The flow-sheet and the mass balances were obtained for the entire process. For the three straws, the water consumption has been 7.3kg/kg of straw. To delignify and improve the digestibility of the straws, 20g of NaOH/kg straw was used. The yield of fodder, lignin and hemicellulose is dependant on the nature of the starting straw. Delignified fodder (insoluble fraction) can be produced with a yield of 0.64, 0.59, 0.55, respectively, from wheat, barley and oat straw. SE improved the digestibility of the straw by 25%; alkaline washing further increased it by 9%. Balanced rations containing, on a DM basis, 1/4 of treated straw, had digestibility coefficients similar to those of commercial rations based on alfalfa.

[Milwaukee shoulder syndrome (apatite associated destructive arthritis): therapeutic aspects]. / Milwaukee shoulder syndrome (artropatia destruente apatite-associata): aspetti terapeutici.

Milwaukee shoulder is a well defined clinical entity that can be observed in particular in older women. It is a destructive arthropathy associated with the deposition of calcium pyrophosphate dihydrate crystals, characterized by the presence of large amount of synovial fluid and a complete tear of the rotator cuff. Clinical features include pain, swelling and progressive functional impairment. The first-line treatment include the use of analgesic drugs and repeated arthrocentesis followed by intra-articular steroid administration; closed-needle tidal irrigation has been reported to be useful. In late phase we can observe narrowing of the acromion-humeral and of the gleno-humeral joint and progressive degenerative changes at the humeral head, leading to almost complete functional impairment. In these cases a surgical approach with total shoulder arthroplasty may be considered.

Influence of aging on cardiac baroreflex sensitivity determined non-invasively by power spectral analysis.

Aging reduces cardiac baroreflex sensitivity. Our primary aim in the present study was to assess the effects of aging on cardiac baroreflex sensitivity, as determined by power spectral analysis (alpha index), in a large population of healthy subjects. We also compared the alpha indexes determined by power spectral analysis with cardiac baroreflex sensitivity measured by the phenylephrine method (BS(phen)). We studied 142 subjects (79 males/63 females; age range 9-94 years), who were subdivided into five groups according to percentiles of age (25, 50, 75 and 95). Power spectral analysis yields three alpha indexes: an alpha low-frequency (LF) index of cardiac baroreflex sensitivity that ranges around 0.1 Hz; an alpha high-frequency (HF) index reflecting cardiac baroreflex sensitivity corresponding to the respiratory rate; and alpha total frequency (alpha TF), a new index whose spectral window includes all power in the range 0.03-0.42 Hz. Spectra were recorded during controlled and uncontrolled respiration. Under both conditions, all three alpha indexes were higher in the youngest age group (< or =34 years old) than in the three oldest groups. Notably, alpha TF was significantly higher in younger subjects than in the three oldest groups [14+/-1 ms/mmHg compared with 9+/-1 (P<0.05), 8.1+/-1 (P<0.001) and 8.1+/-1 (P<0.05) ms/mmHg respectively]. BS(phen) showed a similar pattern [12+/-1 ms/mmHg compared with 8+/-0.5 (P<0.001), 6+/-0.5 (P<0.05) and 6+/-1 (P<0.05) ms/mmHg respectively]. No significant differences were found for cardiac baroreflex sensitivity among the three oldest groups. All alpha indexes were correlated inversely with age. The index yielding the closest correlation with BS(phen) was alpha TF (r=0.81, P<0.001). Cardiac baroreflex sensitivity in normotensive individuals declines with age. It falls predominantly in middle age (from approx. 48 years onwards) and remains substantially unchanged thereafter. The elderly subjects we selected for this study probably had greater resistance to cardiovascular disease that is manifested clinically, with preserved cardiac baroreceptor sensitivity.

Autonomic modulation of heart rate and blood pressure in normotensive offspring of hypertensive subjects.

Predominant sympathetic cardiovascular modulation in the hyperkinetic phase of arterial hypertension has been well described. Less information is available on autonomic control in persons with a family history of arterial hypertension. To investigate this question, we selected 61 normotensive subjects (mean age 30.9 +/- 1.8 years) whose mother or father or both had arterial hypertension and 30 normotensive patients (mean age 30.1 +/- 1.4 years) whose parents had not had arterial hypertension (neither mother nor father) to undergo short-term power spectral analysis of RR interval and arterial pressure variabilities. The same recordings were used to determine baroreflex sensitivity or the alpha index by means of the transfer function. Normotensive offspring of hypertensive subjects had higher diastolic blood pressures (P < .05) and left ventricular mass index (P < .05) than did normotensive offspring of non-hypertensive subjects. They also had higher spectral densities of low frequency expressed in normalized units, both for R-R intervals (P < .05) and systolic pressure variabilities (P < .05); they also had a greater ratio of low-frequency to high-frequency powers of R-R interval variability (P < .05). No difference was observed between the two normotensive groups for baroreflex sensitivity. Our spectral data indicate that normotensive persons with a positive family history of arterial hypertension have lower parasympathetic modulation than those with a negative history. In normotensive persons with a family history of arterial hypertension, normal baroreflex sensitivity could be the mechanism that buffers the tendency for pressures to increase. The gradual loss of this regulatory mechanism may favor rising arterial pressures.

Autonomic modulation and QT interval dispersion in hypertensive subjects with anxiety.

Anxiety is associated with an increased risk of sudden death. QT dispersion is a marker of cardiac repolarization instability and is seen in conditions of high risk of sudden death. The purpose of this study was to evaluate autonomic nervous system control and QT dispersion in hypertensive subjects with anxiety symptoms. In a recent preliminary study, we observed that hypertensive individuals reporting high scores on a self-assessment anxiety scale had more marked left ventricular hypertrophy. In 105 hypertensive subjects divided into 3 groups according to severity of anxiety, we evaluated autonomic control by short-term power spectral analysis of RR and arterial pressure variability at rest (baseline) and during sympathetic stress (tilt test), left ventricular mass index, and heart rate-corrected QT (QTc) dispersion. At baseline, hypertensive subjects with higher anxiety symptom scores had significantly lower high-frequency RR values expressed in absolute terms (P<0.05) and in normalized units (P<0.05) than their counterparts without anxiety symptoms. Hypertensive subjects with anxiety also had a higher mean left ventricular mass index (P<0.001) and greater QTc dispersion (P<0.001). Both indexes and high frequency (P<0.05) correlated with severity of anxiety. These findings suggest that anxiety is associated with autonomic imbalance. This condition could favor an increase in left ventricular mass. Myocardial hypertrophy alone or combined with neuroautonomic imbalance may lead to QT dispersion.

QT interval dispersion and autonomic modulation in subjects with anxiety.

This study was designed to assess Q-T interval dispersion as a marker of electrical instability in subjects with anxiety. Recent observations have shown that the presence of anxiety symptoms increases the risk of sudden death. The Kawachi anxiety questionnaire identified 29 subjects (male/female ratio 13:16) who scored 0, 22 subjects (male/female ratio 14:8) who scored 1, and 37 subjects (male/female ratio 13:24) who scored 2 or more. In all subjects we measured electrocardiographic interlead QT dispersion and autonomic function through spectral analysis of R-R interval and blood pressure variabilities and left ventricular mass. Compared with subjects who scored 0, those reporting 2 or more symptoms showed increased heart rate-corrected QT dispersion (54.9+/-1.7 ms vs. 34.9+/-3.2 ms, P<.001), sympathetic modulation (normal logarithm low-frequency power/high-frequency power 0.59+/-0.1 vs. 0.12+/-0.04, P<.05), and left ventricular mass (120.7+/-3.5 g/m2 vs. 97.9+/-2.8 g/m2, P<.001). Probably because it augments sympathetic activity, anxiety causes left ventricular mass to increase and, like hypertension, increases heart rate-corrected Q-T interval dispersion. The consequent electrical instability could be the substrate responsible for inducing fatal ventricular arrhythmias.

Neer capsular shift surgery in the treatment of recurrent antero-inferior shoulder dislocations.

A total of 47 patients affected with recurrent multidirectional shoulder dislocation with a prevalent anteroinferior component were submitted to Neer inferior capsular shift surgery. Bankart lesion, present in 24 patients, was repaired prior to performing capsuloligamentous surgery. The patients included in the study presented with generalized ligamentous hyperlaxity in 20 cases, while hyperlaxity was localized in the pathological shoulder in the remaining cases, presumably related to the high number of dislocations. The choice of performing Neer inferior capsular shift surgery was initially based on the data and the modern conceptions that emerged in the literature. Successively, the good results obtained encouraged us to follow the path taken, and we are currently encouraged to advise this surgical procedure for the category of patients mentioned above.

Left ventricular mass and heart rate variability in middle-aged and elderly salt-sensitive hypertensive subjects.

Previous reports have shown that in salt-sensitive hypertension a high dietary salt intake can increase sympathetic activity. We evaluated the influence of the autonomic nervous system on myocardial hypertrophy by power spectral analysis of heart rate variability in middle-aged and elderly salt-sensitive hypertensive subjects. We compared autonomic nervous system activity in 32 salt-sensitive hypertensive patients (15 subjects with mean age, 42.4+/-2.4 years and 17 subjects with mean age, 74.6+/-1.6 years) and 20 age-matched normotensive controls. Power spectral analysis detects four spectral components: total power (TP), high-frequency (HF), low-frequency (LF) and very-low-frequency (VLF) power. In the elderly subjects we found an association between the left ventricular mass index (LVMI) and the following variables: very-low frequency (P<0.0001), 24-h urinary sodium excretion (P<0.0001) and diastolic blood pressure (DBP) (P<0.0001). In contrast, in middle-aged subjects we found a significant association between the LVMI and LF (P<0.001). In middle-aged, but not in elderly salt-sensitive hypertensive subjects, increased sympathetic activity correlated with the LVMI (P<0.0001). Our findings suggest an association between sympathetic hyperactivity and the LVMI in middle-aged subjects with salt-sensitive hypertension.

Heart rate and blood pressure variability in obese normotensive subjects.

OBJECTIVE: To assess autonomic modulation of cardiovascular activity in massively obese subjects. DESIGN: Cross-sectional clinical study. SUBJECTS: 43 age-matched normotensive subjects: 15 moderately obese (body mass index (BMI) < 40); 14 massively obese (BMI > 40) and 14 nonobese controls (BMI < 26). MEASUREMENTS: Using power spectral analysis, heart rate and arterial pressure variability were determined at rest and after sympathetic stress (tilt). Two spectral components were analysed: a low-frequency (LF) component at around 0.1 Hz, predominantly reflecting sympathetic modulation and a high-frequency (HF) component at around 0.26 Hz, reflecting parasympathetic modulation. RESULTS: Spectral data for heart rate showed that the massively obese subjects had lower LF [mean +/- s.e.m.] normalized units (NUs) at rest (35.1 +/- 0.9) and after tilt (56.1 +/- 2.1), than the moderately obese subjects (LF NUs at rest 53.9 +/- 4.2, P < 0.001; LF NUs tilt: 66.8 +/- 5.6, P < 0.001) and nonobese control subjects (LF NUs at rest, 56.6 +/- 3.0, P < 0.001); (LF NUs tilt: 81.7 +/- 1.7, P < 0.001). Data for systolic arterial pressure variability measured at rest exhibited the inverse pattern, the massively obese group having higher mean LF values (LF mm Hg2 rest: 15.0 +/- 1.4; LF mm Hg2 tilt: 15.7 +/- 1.5) than the moderately obese group (LF mm Hg2 rest 3.2 +/- 0.7, P < 0.001; LF mm Hg2 tilt: 7.2 +/- 2.0, P < 0.001) and than the nonobese control subjects (LF mm Hg2 rest 3.5 +/- 0.5, LF mm Hg2 tilt 8.5 +/- 0.8, P < 0.001). Regression detected a significant association between BMI and LF of systolic pressure (beta = 0.364; P = 0.0007), In LF of heart rate (beta = -5.555; P = 0.00001) and very low frequency (VLF) of diastolic pressure (beta = -3.305; P = 0.0020). CONCLUSION: Obesity seems to increase sympathetic modulation of arterial pressure, but diminishes modulation of heart rate. Because our obese subjects had high plasma noradrenaline levels, their low LF power of heart rate could reflect diminished adrenoceptor responsiveness.

Autonomic modulation of heart rate and blood pressure in hypertensive subjects with symptoms of anxiety.

1. The influence of anxiety symptoms on autonomic nervous system cardiovascular control has never been studied in hypertensive subjects. This study was designed to verify the presence of sympathetic hyperactivity in hypertension associated with anxiety symptoms. 2. Neuroautonomic cardiovascular control was evaluated using short-time power spectral analysis of RR and arterial pressure variability at baseline and after the head-up tilt test. The two spectral components principally influenced by the autonomic nervous system are the low-frequency (LF) component, mainly though not exclusively due to sympathetic modulation, and the high-frequency (HF) component, due to parasympathetic activity. The ratio of LF to HF powers (LF:HF) provides an index of the sympathovagal sinus balance. 3. We studied 33 hypertensive subjects (mean age 47+/-1 years; M:F=19:14) and 37 normotensive control subjects (mean age: 47+/-2 years; M:F=20:17) divided into four subgroups: hypertensive subjects who scored 2 or more on a 5-item anxiety symptom scale, hypertensive subjects who scored 0, normotensive controls who scored 2 or more and normotensive controls who scored 0. LF:HF and LF during rest were significantly higher (P<0.05) in hypertensive and normotensive groups with an anxiety score of 2 or more compared with the two groups who scored 0. HF of systolic blood pressure was significantly lower in the hypertensive group who scored 2 or more than in the hypertensive group who scored 0 (P<0.05). Tilt in both hypertensive groups reporting anxiety symptoms left the indexes of sympathetic modulation unchanged. Tilt in hypertensive subjects reporting anxiety symptoms also induced a significant fall in arterial pressure (P<0.05). The mean left ventricular mass index was significantly higher in the hypertensive subjects who had anxiety scores of 2 or more than in those scoring 0 (144.7+/-3.0 versus 133. 4+/-2.31, P<0.05). 4. In conclusion, normotensive and hypertensive subjects reporting anxiety symptoms showed increased sympathetic modulation of heart rate at rest. Higher anxiety scores seem to be associated with the development of left ventricular hypertrophy.

Baroreflex sensitivity in the elderly with silent myocardial ischemia.

In order to assess high-pressure baroceptor sensitivity and parasympathetic function in elderly patients with silent myocardial ischemia, we selected 45 inpatients in our geriatric unit for a prospective cohort study of patients with coronary heart disease. All patients were over 65 years of age (37 men and 8 women) and had coronary heart disease, documented by an angiographic study and electrocardiographic evidence of myocardial ischemia during exercise stress testing, performed according to the Bruce protocol. The subjects were divided in three subgroups: group 1 (22 patients) with electrocardiographic and echocardiographic history of myocardial infarction but no angina chest pain during exercise testing; group 2 (13 patients) with no exercise induced chest pain; and group 3 (10 patients) with exercise-induced chest pain. Baroceptor sensitivity was assessed in all subjects, by evaluating heart rate changes expressed in RR interval on the basis of changes in the mean arterial pressure during intravenous infusion of stepwise doses (50-100 and 150 microg) of phenylephrine hydrochloride. Heart rate changes were also evaluated during overshoot of the Valsalva maneuver (Valsalva max.), providing an index of parasympathetic activity. Our results showed that group two patients (only silent ischemia) had significantly (P>0.001) greater baroceptor sensitivity than the other two groups (group 2; 15.2+/-1.9 ms/mmHg; group 1: 10.0+/-1.7 ms/mmHg; and group 3: 9.8+/-1.7 ms/mmHg). Group two also showed a significant positive correlation (r=0.58; P<0.05) between baroceptor sensitivity and end-diastolic pressure and a significant inverse correlation (r=-0.672; P<0.05) between baroceptor sensitivity and the ejection fraction. Group 2 patients had a significantly longer RR interval than group 1 (P<0.05) and group 3 (P<0.05); a significant positive correlation (r=0.620; P<0.05) between Valsalva max. and end-diastolic pressure; and a significant inverse correlation (r=0.694; P<0.05) between Valsalva max. and the ejection fraction. Valsalva max. and baroceptor sensitivity correlated significantly in all three groups (group 1, r=0.707; P<0.001; group 2, r=0.94; P<0.001; and group 3; r=0.833; P<0.05). In conclusion our data suggest that elderly patients with silent ischemia appear to have an increased capacity for evoking parasympathetic reflexes that could inhibit pain perception.

Abnormal passive head-up tilt test in subjects with symptoms of anxiety power spectral analysis study of heart rate and blood pressure.

Previous reports that subjects with anxiety symptoms are at higher risk of sudden death may imply that anxiety induces stable sympathetic hyperactivity. To address this subject, in persons with and without anxiety symptoms, we evaluated autonomic nervous system activity by power spectral analysis of heart-rate and arterial-pressure variability at baseline (rest) and after sympathetic stress (tilt). The 117 subjects selected (56 men and 61 women, age range 23-87 years) were subdivided by questionnaire into three groups: 49 subjects (mean age 55.8+/-2.8 years) had no anxiety symptoms; 36 (mean age 56.8+/-3.6 years) had one anxiety symptom; and 32 (mean age 55.0+/-2.9 years) had two or more anxiety symptoms. Power spectral analysis recognizes three main components: high frequency (HF), chiefly reflecting vagal efferent activity; low frequency (LF), reflecting sympathetic activity; and very-low-frequency (VLF). The ratio of low- to high-frequency powers (LF:HF) of heart rate variability provides a measure of sympathovagal balance. Power spectral analysis showed that subjects with two or more anxiety symptoms had significantly lower resting values for all power spectral components of heart rate variability: total power (TP), VLF, LF, and HF than did symptomless controls (P<0.05). The highest anxiety-score groups also had a higher baseline LF:HF than the other two groups (P<0.05). Their resting LF:HF ratio correlated positively with anxiety symptom scores (r=0.72, P<0.0001). Tilt induced opposite results: the highest anxiety-score groups had a significantly lower LF:HF ratio; the ratio correlated inversely with their anxiety scores (r=-0.69; P<0.0001). Recordings of resting systolic arterial pressure variability showed that the group with two or more anxiety symptoms had significantly higher LF power (P<0.05) than symptomless controls. Our findings suggest that persons with high anxiety scores have baseline cardiac sympathetic hyperactivity. They also have low heart-rate variability, possibly explaining their susceptibility to sudden cardiac death.

Ni++ as a competitive inhibitor of calcium transport in mitochondria.

The kinetics of Ca++ uptake in rat liver mitochondria have been studied using the potassium diffusion potential. The advantage of this approach is that in this condition, the mitochondrial respiratory rate is not the limiting step, and therefore the effects of Ni++ on the Ca++ carrier can be studied. Our results suggest that Ni++ is a competitive inhibitor of the Ca++ carrier, but it is not transported into the mitochondria.

Power spectral analysis of heart rate in elderly hypertensive subjects with or without silent coronary disease.

Much evidence indicates an involvement of the sympathetic nervous system in the genesis of silent myocardial ischemia. The authors assessed autonomic system activity by power spectrum analysis of heart rate variability in 21 elderly hypertensive men with and without angiographically confirmed coronary artery disease and compared the results with those from an age-matched control group. In the analysis an autoregressive algorithm was used to determine the power spectrum from an electrocardiographic recording of 512 consecutive RR intervals. The autonomic nervous system induces two distinct sinusoids: a low-frequency signal attributable to sympathetic activity and a high-frequency vagal response. In the hypertensive patients with coronary disease the authors also evaluated sympathetic activation after double-blind, placebo-controlled administration of metoprolol (100 mg/day), followed by amlodipine (10 mg/day), quinapril (20 mg/day), and amlodipine (5 mg/day) plus quinapril (10 mg/day).

The effects of antihypertensive drugs on the autonomic nervous system in elderly hypertensive patients with silent myocardial ischemia.

To seek further evidence for the participation of sympathetic nervous system in the onset of transient episodes of painless ischemia, we compared the behavior of the autonomic nervous system by means of power spectrum analysis of heart rate variability in 15 elderly hypertensive men with angiographically confirmed painless coronary artery disease, and in 10 similar patients without coronary artery disease. An autoregressive algorithm was used to calculate the power spectrum density from an electrocardiographic (ECG) recording of 512 consecutive RR intervals. The power spectrum comprised two main bandwidths: a high-frequency band reflecting parasympathetic and a low-frequency band reflecting sympathetic activity. In the hypertensives with painless coronary disease sympathetic tone was also assessed after double-blind placebo-controlled administration of metoprolol (100 mg/day), amlodipine (10 mg/day), quinapril (20 mg/day), and amlodipine (5 mg/day) plus quinapril (10 mg/day). The hypertensives with painless coronary disease had significantly higher sympathetic activity than those without (low frequency: 58.0 +/- 2.0 vs 25.0 +/- 1.0, p < 0.001) but significantly lower parasympathetic activity (high frequency: 39.0 +/- 2.0 vs 60.0 +/- 2.0, p < 0.001). Treatment with metoprolol, quinapril and amlodipine plus quinapril significantly depressed sympathetic activity (p < 0.05).

Age-adjusted normal confidence intervals for heart rate variability in healthy subjects during head-up tilt.

PURPOSE: Aging leads to a decline in autonomic nervous system function. In this study, designed to assess the influence of age on neuroautonomic regulation of cardiac activity, heart rate variability was measured by power spectral analysis and normal ranges were determined in a population of healthy subjects. PATIENTS AND METHODS: In 83 healthy volunteers (42 men and 41 women; age range 25-85 years) autonomic nervous system function was assessed by autoregressive spectral analysis of heart rate variability in clinostatism and after passive orthostatic load (head-up tilt). The analysis considered two spectral components relevant to the study of the autonomic nervous system--high-frequency power (approximately 0.05 Hz) and low-frequency power (approximately 0.10 Hz)--and the ratio between them. Low-frequency spectral components, in particular the ratio between low- and high-frequency spectra, reflect sympathetic activity; high-frequency components reflect parasympathetic activity. RESULTS: For data comparison, the study group was subdivided into three age groups: 25 subjects (12 men and 13 women) under 44 years of age; 28 (15 men and 13 women) aged 44-64 years; and 30 (15 men and 15 women) over 64 years of age. The natural logarithms and normalized units of low- and high-frequency power, and the low-to-high power ratio were used to calculate 95% confidence intervals. Power spectral analysis at baseline and after postural tilt showed significantly higher low-frequency power of heart rate variability (P < 0.05), natural logarithm of power (P < 0.001) and normalized units (P < 0.001) in the two younger groups than in the oldest group. The two younger age-groups also had significantly increased high-frequency power (P < 0.05) and natural logarithm of power (P < 0.05). The oldest age group had significantly increased high-frequency power analyzed in normalized units (P < 0.001). CONCLUSION: The age-related lowering observed in nearly all the spectral frequency components of heart rate variability confirms in healthy subjects that autonomic nervous system function declines with age.