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Pain is a complex phenomenon, the experience of which varies widely across individuals. At worst, chronic pain can lead to anxiety and depression. Cost-effective strategies are urgently needed to improve the treatment of pain, and thus we propose a novel home-based pain measurement system for the longitudinal monitoring of pain experience and variation in different patients with chronic low back pain. The autonomous nervous system and audio-visual features are analyzed from heart rate signals, voice characteristics and facial expressions using a unique measurement protocol. Self-reporting is utilized for the follow-up of changes in pain intensity, induced by well-designed physical maneuvers, and for studying the consecutive trends in pain. We describe the study protocol, including hospital measurements and questionnaires and the implementation of the home measurement devices. We also present different methods for analyzing the multimodal data: electroencephalography, audio, video and heart rate. Our intention is to provide new insights using technical methodologies that will be beneficial in the future not only for patients with low back pain but also patients suffering from any chronic pain. [ABSTRACT FROM AUTHOR]

This study was designed to assess the effect of aerobic training on the dynamics between the R-R interval length and the high-frequency (HF) oscillation of the R-R interval. Seventeen healthy males (26+/-2 years) participated in an 8-week aerobic training intervention. The mean HF spectral power (0.15-0.4 Hz) of the R-R interval and the mean R-R interval length were analyzed from 24-h recordings. HF power was also analyzed in 5-min sequences and plotted as a function of the corresponding mean R-R interval length. The relationship between the R-R interval length and the HF power was analyzed by a quadratic regression model. The relationship was defined as saturated if the distinct deflection point of the model occurred before the maximum R-R interval. Otherwise, the relationship was defined as linear. Additionally, the mean HF power was calculated from the linear portion of the R-R interval versus the HF power regression curve (HF index). Before the training intervention, seven subjects had a saturated HF power. After the intervention, five new cases of saturated HF power were observed. The mean HF power of the 24-h recording did not change in the group with a saturated HF power before training (7.4+/-0.8 vs. 7.6+/-0.8 ms(2)), but the HF index increased (6.7+/-0.7 vs. 7.1+/-0.7 ms(2), P<0.05). We conclude that enhanced vagal activity due to aerobic training increases the prevalence of the saturation of the HF oscillation of the R-R interval variability in healthy subjects. HF power calculated from unsaturated area detects more accurately subtle changes in the vagally mediated beat-to-beat variability of the R-R interval after aerobic training than the mean 24-h HF power. [ABSTRACT FROM AUTHOR]

Allergic rhinitis is a major chronic respiratory disease and an immunoneuronal disorder. We aimed at providing further knowledge on the function of the neural system in nasal allergic reaction. Here, a method to assess simultaneously the nasal airflow resistance and the underlying function of autonomic nervous system (ANS) is presented and used during the nasal provocation of allergic and nonallergic subjects. Continuous nasal airflow resistance and spectral heart rate variability parameters show in detail the timing and intensity differences in subjects’ reactions. After the provocation, the nasal airflow resistance of allergic subjects showed a positive trend, whereas LF/HF (Low Frequency/High Frequency) ratio and LF power showed a negative trend. This could imply a gradual sympathetic withdrawal in allergic subjects after the allergen provocation. The groups differed significantly by these physiological descriptors. The proposed method opens entirely new opportunities to research accurately concomitant changes in nasal breathing function and ANS. [ABSTRACT FROM AUTHOR]

Reciprocal autonomic regulation occurs during incremental exercise. We hypothesized that sympatho-vagal interplay may become altered after exercise because of the differences in recovery patterns of autonomic arms. The cardiac vagal activity was assessed by measurement of beat-to-beat R-R interval oscillations using a Poincaré plot method (SD1), and muscle sympathetic nervous activity (MSNA) was measured from peroneus nerve by a microneurography technique during and after exercise in 16 healthy subjects. Autonomic regulation was compared between the rest and after exercise (3·5 ± 1·0 min after exercise) at equal heart rates (HR). SD1 was at the equal level at the recovery phase (40 ± 21 ms) compared to the resting condition (38 ± 16 ms, P = ns) at comparable HR (57 ± 10 for both). MSNA was higher at the recovery phase (40 ± 19 burst per 100 heartbeats) than at rest (25 ± 13 burst per 100 heartbeats, P<0·0001). The difference of MSNA activity between rest and late recovery phase had a strong positive correlation with the difference in SD1 ( r = 0·78, P<0·001) at equal HRs. Subjects who have a higher sympathetic activity in the recovery phase of exercise have a more augmented cardiac vagal activity resulting in an accentuated sympatho-vagal outflow. The altered autonomic interaction observed here may partly explain the clustering of various cardiovascular events to the recovery phase of exercise. [ABSTRACT FROM AUTHOR]

Cardiovascular autonomic function is associated with physical performance and exercise training adaptation. The association between physical performance and sympathetic regulation is not well known. We hypothesized that sympathetic nervous system activity is associated with physical performance among male runners. The study population included 26 healthy male club runners [age 33 +/- 5 years, body mass index (BMI) 24 +/- 1 kg/m(2), VO(2max) 58 +/- 5 ml kg(-1) min(-1); mean +/- SD]. Muscle sympathetic nerve activity (MSNA) was assessed from the peroneal nerve by the microneurography technique during 5 min of supine rest. Physical performance was assessed by time to exhaustion during treadmill running. The mean resting MSNA was 20 +/- 6 bursts min(-1) (range 6-34). The mean time to exhaustion was 1,005 +/- 136 s (range 720-1260). When the study group was divided into tertiles according to their running performance (866 +/- 69, 994 +/- 30 and 1154 +/- 71 s in time to exhaustion, P < 0.0001 between the groups), MSNA was lower (P = 0.032) in the group with the best running performance (16 +/- 5 bursts min(-1)) compared to those with the worst running performance (23 +/- 7 bursts min(-1)). In conclusion, baseline sympathetic activity, measured by a microneurography at rest, may be associated with the maximal running performance of healthy subjects. [ABSTRACT FROM AUTHOR]

Cardiac baroreflex is described by baroreflex sensitivity (BRS) from blood pressure and heart rate interval (RRi) fluctuations. However, respiration affects both blood pressure and RRi via mechanisms that are not necessarily of baroreflex origin. To separate the effects of baroreflex and respiration, metronome-guided breathing in a high frequency band (HF, 0.25-0.4 Hz) and a low frequency spectral band (LF, 0.04-0.15 Hz) have therefore been commonly used for BRS estimation. The controlled breathing may, however, change the natural functioning of the autonomic system and interfere BRS estimates. To enable usage of spontaneous breathing, we propose an adaptive LMS-based filter for removing the respiration effect from the BRS estimates. ECG, continuous blood pressure and respiration were measured during 5 min spontaneous and 5 min controlled breathing at 0.25 Hz in healthy males ( N = 24, 33±7 years). BRS was calculated with spectral methods from the LF band with and without filtering. In those subjects whose spontaneous breathing rate was <0.15 Hz, the BRS(LF) values were overestimated, whereas the adaptive filtering reduced the bias significantly. As a conclusion, the adaptive filter reduces the distorting effect of respiration on BRS values, which enables more accurate estimation of BRS and the usage of spontaneous breathing as a measurement protocol. [ABSTRACT FROM AUTHOR]

This study was designed to assess the relationship between R-R interval length and heart rate (HR) variability in healthy subjects and patients after an acute myocardial infarction (AMI). Twenty-four-hour ambulatory ECG recordings were obtained for 76 healthy subjects and 82 post-AMI patients. The high-frequency (HF, 0.15–0.4 Hz) spectral power of R-R intervals was analyzed in 5-min sequences over 24 h and plotted as a function of the corresponding mean R-R interval length. Quadratic regression model was used to study the relationship between R-R interval length and HF power. If a distinct deflection point (R-R0) occurred in the quadratic regression (r > 0.50) model before maximum R-R interval, indicating the plateau of HF power, the relationship between R-R interval and HF power was defined as saturated. Otherwise, the relationship was defined as linear (r > 0.50) or low correlated (r > 0.50). The relationship was saturated in 35, linear in 38, and low correlated in 3 healthy subjects. In post-AMI patients, the relationship was saturated in 9 subjects, linear in 44 subjects, and low correlated in 29 patients. The HF power analyzed from the 24-h period did not differ between the saturated and linear groups, but when analyzed from the linear portion only, HF spectral power was smaller in the linear than the saturated group both among healthy subjects (P < 0.05) and post-AMI patients (P < 0.05). Saturation of the HF oscillations of R-R intervals is a common phenomenon in healthy subjects and also present in post-AMI patients during ambulatory conditions. This saturation effect may bias the quantification of cardiac vagal function when HR variability is analyzed from Holter recordings. [ABSTRACT FROM AUTHOR]

Background: Premature beats (PBs) have been considered as artifacts producing a bias in the traditional analysis of heart rate (HR) variability. We assessed the effects and significance of PBs on fractal scaling exponents in healthy subjects and patients with a recent myocardial infarction (AMI).Methods: Artificial PBs were first generated into a time series of pure sinus beats in 20 healthy subjects and 20 post-AMI patients. Thereafter, a case-control approach was used to compare the prognostic significance of edited and nonedited fractal scaling exponents in a random elderly population and in a post-AMI population. Detrended fluctuation analysis (DFA) was used to measure the short-term (α1) and long-term (α2) fractal scaling exponents.Results: Artificial PBs caused a more pronounced reduction ofα1 value among the post-AMI patients than the healthy subjects, for example, if>0.25% of the beats were premature a>25% decrease in theα1 was observed in post-AMI patients, but 4% of the premature beats were needed to cause a 25% reduction inα1 in healthy subjects. Both edited (1.01± 0.31 vs 1.19± 0.27, P<0.01) and uneditedα1 (0.71± 0.33 vs 0.89± 0.36, P<0.05) differed between the patients who died (n= 42) and those who survived (n= 42) after an AMI. In the general population, only uneditedα1 differed significantly between survivors and those who died (0.96± 0.19 vs 0.83± 0.27, P<0.05).Conclusions: Unedited premature beats result in an increase in the randomness of short-term R-R interval dynamics, particularly in post-AMI patients. Premature beats must not necessarily be edited when fractal analysis is used for risk stratification. [ABSTRACT FROM AUTHOR]

Summary Methods based on non-linear heart rate (HR) dynamics have been suggested to probe features in HR behaviour that are not easily detected by the traditional HR variability indices. This study tested the hypothesis that analysis of correlation properties of R–R intervals provides useful information on HR fluctuation during exercise. High- (HF) and low-frequency (LF) spectral components and a short-term scaling exponent (α 1 ) of HR variability, were analysed for nine healthy subjects at rest, during incremental and steady-state exercise, during atropine infusion and during incremental exercise after atropine administration. During the incremental exercise test α 1 increased from rest to an intensity level of ∼40% of &formmu0; (from 1·07 ± 0·24 to 1·50 ± 0·25, P <0·001) and thereafter decreased linearly until the end of exercise (from 1·50 ± 0·25 to 0·38 ± 0·10, P <0·001). Atropine infusion increased the scaling exponent α 1 value from 0·91 ± 0·23 to 1·37 ± 0·31 (P <0·001). During exercise after atropine infusion, a linear reduction was observed in the scaling exponent α 1 from 1·37 ± 0·23 to 0·25 ± 0·08 (P <0·001). Analogous changes in α 1 were seen during long-term steady-state exercise compared to incremental exercise. Conventional HR variability indices did not show any significant changes during exercise at high exercise intensity levels. α 1 correlated with the LF/HF ratio at rest (r = 0·90, P <0·001), but the correlation was weaker after atropine (r = 0·71, P <0·05) and during exercise (e.g. r = 0·33, P = NS at the level of 40% of &formmu1;). In conclusion, incremental exercise test until exhaustion results in bidirectional changes in correlation properties of R–R interval... [ABSTRACT FROM AUTHOR]

R-R Interval Dynamics After Premature Beats. Introduction: Studies assessing heart rate (HR) behavior after premature beats have focused on HR responses to ventricular premature beats (VBPs), but there is less information of HR behavior after atrial premature beats (APBs). Methods and Results: HR turbulence after VPBs and APBs was first measured in response to ambient APBs and VPBs occurring during 24-hour ambulatory ECG recordings in 29 subjects without structural heart disease, and in response to programmed atrial (AE) and ventricular extrastimuli (VE) in 6 subjects undergoing electrophysiologic (EP) examination. Turbulence onset (TO) was more negative (-2.3 ± 3.2% vs -0.9 ± 2.8%, P < 0.01) and turbulence slope (TS) was steeper (11 ± 11 vs 5.1 ± 4.1 msec/R-R interval, P < 0.05) after VPBs than APBs. Compared to VPBs, the acceleration of HR after APBs was delayed by one beat, and APBs were associated with a short R-R interval preceding the APB, resulting in a blunted TO. Studies of patients undergoing an EP test confirmed the one-beat delay of HR acceleration and the blunted TO after programmed AE compared to VE (P < 0.05) . TO and TS after VPBs were related to baroreflex sensitivity. TO also was related to 24-hour standard deviation of N-N intervals (SDNN). However, the TO or TS following APBs was not related to either SDNN or baroreflex sensitivity. Conclusion: HR behavior is different in response to APBs and VBPs among subjects without structural heart disease. Different definitions and calculation formulas should be used in the analysis of HR turbulence after APBs and VPBs.(J Cardiovasc Electrophysiol, Vol. 14, pp. 447-452, May 2003). [ABSTRACT FROM AUTHOR]

Breakdown of short-term fractal-like behaviour of HR indicates an increased risk for adverse cardiovascular events and mortality, but the pathophysiological background for altered fractal HR dynamics is not known. Our aim was to study the effects of pharmacological modulation of autonomic function on fractal correlation properties of heart rate (HR) variability in healthy subjects. Short-term fractal scaling exponent (α1) along with spectral components of HR variability were analysed during the following pharmacological interventions in healthy subjects: (i) noradrenaline (NE) infusion (n=22), (ii) NE infusion after phentolamine (PHE) (n=8), (iii) combined NE + adrenaline (EPI) infusion (n=12), (iv) vagal blockade with high dose of atropine (n=10), (v) and vagal activation by low dose of atropine (n=10). Then α1 decreased progressively during the incremental doses of NE (from 0·85 ± 0·250 to 0.55 ± 0·23, P<0·0001). NE also decreased the average HR (P<0·001) and increased the high frequency spectral power (P<0·001). Vagal blockade with atropine increased the α1 value (from 0·82 ± 0·22 to 1·24 ± 0·41, P<0·05). Combined NE + EPI infusion and vagal activation with a low dose atropine did not result in any changes in α1, and α-adrenergic blockade by PHE did not completely reverse the effects of NE on α1. Increased levels of circulating NE result in reduction of short-term correlation properties of HR dynamics. The results suggest that coactivation of cardiac vagal outflow at the time of high levels of a circulating sympathetic transmitter explains the breakdown of fractal-like behaviour of human HR dynamics. [ABSTRACT FROM AUTHOR]

Studies the heart rate (HR) behaviors during accentuated sympathovagal interaction by generating power spectra and Poincare plots of successive R-R intervals at the baseline and during infusion of incremental doses of noepinephrine in young healthy males. Unstableness of HR behavior during accentuated sympathovagal interaction; Changes in HR dynamics during norepinephrine infusion.

Discusses the effects of age and physical fitness on the vagal modulation of heart rate during exercise. Characteristics of subjects at different age-matched fitness tertiles; Measurement of peak oxygen consumption; Analysis of heart rate variability.

Background: We study the estimation of breathing frequency (BF) derived from wearable single-channel ECG signal in the context of mobile daily life activities. Although respiration effects on heart rate variability and ECG morphology have been well established, studies on ECG-derived respiration in daily living settings are scarce; possibly due to considerable amount of disturbances in such data. Yet, unobtrusive BF estimation during everyday activities can provide vital information for both disease management and athletic performance optimization.Method and Data: For robust ECG-derived BF estimation, we combine the respiratory information derived from R-R interval (RRI) variability and morphological scale variation of QRS complexes (MSV), acquired from ECG signals. Two different fusion techniques are applied on MSV and RRI signals: cross-power spectral density (CPSD) estimation and power spectrum multiplication (PSM). The algorithms were tested on large sets of data collected from 67 participants during office, household and sport activities, simulating daily living activities. We use spirometer reference BF to evaluate and compare our estimations made by different models.Results and Conclusion: PSM acquires the least average error of BF estimation, [Formula: see text] and [Formula: see text], compared to the reference spirometer values. PSM offers approximately 25 and 75% less error in comparison with the CPSD fusion estimation and the estimation by those two exclusive sources, respectively. Our results demonstrate the superiority of both of the fusion approaches, compared to the estimation derived from either of RRI or MSV signals exclusively. [ABSTRACT FROM AUTHOR]

Previous studies have shown that indexes describing heart rate (HR) dynamics may predict subsequent deaths of patients after an acute myocardial infarction (AMI). Because β-blocking (BB) drugs affect both mortality and HR dynamics, the prognostic power of measurements of HR dynamics may have changed in the current era of BB therapy. This study assessed the temporal changes and prognostic significance of time-domain, spectral, and fractal indexes of HR variability along with HR turbulence after an AMI among patients with optimized BB medication. SD of NN intervals, spectral indexes, the short-term fractal scaling exponent (α1), power-law slope (β), and turbulence onset and slope were measured in 600 patients at 5 to 7 days after AMI and in 416 patients at 12 months after AMI. In the multivariate analysis, after adjusting for clinical variables, only reduced fractal HR indexes, α1 and β (p <0.01 for both), turbulence onset, and slope (p <0.05 for both), measured at the convalescent phase after AMI, predicted subsequent cardiac death. All time-domain and spectral HR variability indexes and turbulence onset increased significantly during the 12-month period after AMI (p <0.001 for all), whereas the fractal indexes and turbulence slope remained unchanged. Late after AMI, reduced β (p <0.05) and turbulence slope (p <0.01) were the only independent predictors of cardiac mortality. Traditional time-domain and spectral measurements of HR variability and turbulence onset improved significantly after AMI, whereas the fractal HR dynamics and turbulence slope remained stable. Fractal HR variability and HR turbulence retain their prognostic power in the BB era, when measured either at the convalescent or late phase after AMI. [Copyright &y& Elsevier]

• The purpose of the study was to examine effects of verbalization of affective experience on heart-rate variability (HRV). • We examined HRV of 35 subjects while they were viewing and reporting on 48 affective pictures (IAPS). The subjects produced oral reports through instant recall and imagery of the stimuli. • Our results showed that sympathetic activity was lower and parasympathetic activity higher when subjects were reporting on unpleasant pictures than it was when they were reporting on pleasant pictures. To the best of our knowledge similar findings have not been earlier reported in oral reporting studies. • Our results suggest that: 1. the effect of verbalization on heart-rate variability is determined by the valence of the stimuli and 2. oral reporting may have regulatory influences on autonomic activity during recall of unpleasant experiences. • Overall, our findings show:. ○ that there are functional differences between reporting and viewing of unpleasant stimuli and between reporting and viewing of pleasant stimuli. Our findings indicate that reporting of unpleasant stimuli is functionally different when compared to reporting to pleasant, less reactive stimuli. ○ Our findings indicate that there are functional differences between the conditions that are connected to the task and emotion at hand. ■ First, verbalization has built-in strong intentionality that prevents avoidant behaviour during reporting of unpleasant stimuli. ■ Second, the function of the reporting changes depending on the valence of the stimuli. Subjects show higher sympathetic reactivity to unpleasant stimuli and emotional confrontation is emphasized in the reporting task. During reporting of pleasant stimuli, subjects show lower sympathetic reactivity and focus on the task or the performance is emphasized. This is observed as higher sympathetic activity while reporting on pleasant stimuli. ○ The effect of verbalization on subjects' emotions can perhaps be best explained with unified exposure and regulatory effects that are facilitated by the reporting task of unpleasant stimuli. Active and intentional focus on unpleasant stimuli prevents avoidant behaviour and the use of language dampens subjects' autonomic activity via amygdaloid-hypothalamic connections to autonomic nervous system. The purpose of the study was to examine effects of verbalization of affective experience on heart-rate variability and emotions (HRV). We measured HRV of 35 subjects while they were viewing and verbalizing 48 affective pictures (IAPS). Our results showed that sympathetic activity was lower and parasympathetic activity higher when subjects were verbalizing unpleasant pictures than it was when they were verbalizing pleasant pictures. To the best of our knowledge similar findings have not been earlier reported. Our results suggest that: 1. the effect of verbalization on heart-rate variability is determined by the valence of the stimuli and 2. verbalization has regulatory influences on autonomic activity during recall of unpleasant experiences. The effect of verbalization on subjects' HRV and emotions can perhaps be best explained with unified exposure and regulatory effects that are facilitated by the reporting task of unpleasant stimuli. Active and intentional focus on unpleasant stimuli prevents avoidant behaviour by exposing subjects to unpleasant contents and language processing dampens subjects' autonomic activity via amygdaloid-hypothalamic connections. [ABSTRACT FROM AUTHOR]

Abstract: The purpose of this study was to assess the differences in cardiac autonomic modulation during maximal static (SA) and dynamic (DA) underwater apneas. Arterial oxygen saturation (SpO2), heart rate (HR) and HR variability (SD1 from Poincaré plot and short-term fractal-like scaling exponent, α1) were analyzed at the immersed baseline (3min) and initial, mid- and end-phases (each 30s) of SA and DA in nine elite breath-hold divers. DA and SA lasted 78±8 and 225±20s (mean±SEM), respectively, and resulted in similar decrements in end-stage SpO2 (78±3 and 75±3%, p=0.352). During DA, initial increase in HR (from 80±5 to 122±5bpm, p<0.001) was followed by gradual decrease towards the baseline at mid-apnea and end-apnea phase (101±6 and 80±8bpm, respectively). During SA, HR decreased at mid-apnea (from 78±4 to 66±3bpm, p=0.004) but did not decrease further at end-apnea phase (66±4bpm). Decreased SD1 was observed at the initial phase of DA (from 28±5 to 10±4ms, p=0.005) being lower compared with SA (24±4ms, p=0.005). At the end of DA and SA, SD1 tended to increase above the baseline (62±16 and 66±10ms, p=0.128 and p=0.093, respectively, p=0.602 DA vs. SA). α1 tended to be higher at the end of DA compared with SA (1.17±0.10 vs. 0.79±0.10, p=0.059). We concluded that apnea blunts the effects of exercise on cardiac vagal activity at the end of DA. However, higher HR during DA compared with SA indicates larger cardiac sympathetic activity during DA, as suggested also by slightly higher α1. [Copyright &y& Elsevier]

Abstract: The purpose of this study was to assess the power and the frequency of low-frequency (LF; 0.04–<0.15Hz) oscillations in systolic blood pressure (SBP) and R–R interval (RRi) across the continuum of risk of cardiovascular disease, including age. A potential confound in such determinations is low spontaneous breathing frequency in some individuals. We measured beat-to-beat SBP, RRi and respiration in healthy YOUNG (33±3years) and OLDER subjects (62±5years) and older patients with hypertension (HT, 61±5years), coronary artery disease without (CAD, 62±5years) and with type 2 diabetes (CAD+DM, 62±4years, n =28 for all groups) during spontaneous breathing at supine rest. Power (PowerLF) and median frequency (MedLF) of LF oscillations were calculated by power spectral analysis after removing respiratory effects by least-mean-square adaptive filtering. OLDER had higher PowerLF-SBP (5.5±3.0 vs. 3.4±2.5mmHg2, p =0.002) and lower PowerLF-RRi than YOUNG (339±460 vs. 575±422ms2, p =0.001) whereas neither variable differed between OLDER and patient groups. MedLF-SBP (0.072±0.009 vs. 0.080±0.011Hz, p =0.005) and MedLF-RRi (0.072±0.010 vs. 0.079±0.013Hz, p =0.027) were lower in OLDER compared with YOUNG. Compared with OLDER, MedLF-RRi was lower in CAD (0.065±0.006Hz, p =0.015) and CAD +DM (0.066±0.008Hz, p =0.012); whereas CAD+DM had also lower MedLF-SBP (0.065±0.006Hz, p =0.012). No differences were observed between OLDER and HT and between CAD and CAD+DM in these variables. We concluded that age is major determinant of the power of LF oscillations in SBP and RRi at rest, whereas the median frequency of these oscillations is altered also by coronary artery disease. [Copyright &y& Elsevier]

Abstract: Altered frequency of slow (0.04–0.15Hz) arterial pressure and R–R interval oscillations has been observed in various diseases but the mechanisms for this frequency shift are unclear. The median (Med) frequencies of slow R–R interval and blood pressure (BP) oscillations were recorded in 11 healthy subjects with paced breathing (0.25Hz) during muscle metaboreflex and baroreflex mediated sympathetic stimuli: 1) handgrip exercise (HG) followed by post-exercise circulatory occlusion (PECO), 2) handgrip exercise during ischemia by circulatory occlusion (IHG) and 3) passive head-up tilt (TILT). MedBP shifted to the higher frequency during HG, PECO and IHG (from 0.070±0.009Hz to 0.088±0.013, 0.085±0.015 and 0.099±0.013Hz, respectively, p <0.01 for all) but not during TILT (0.078±0.012Hz). Similarly, MedR–R shifted to the higher frequency during HG, PECO and IHG (from 0.072±0.009Hz to 0.085±0.014, 0.085±0.016 and 0.095±0.015Hz, respectively, p <0.01 for all) but not during TILT (0.075±0.012Hz). MedBP and MedR–R were higher during IHG compared to HG and lower during TILT compared to both HG and IHG (p <0.01 for all). We conclude that the sympathetic stimulus induced by muscle metaboreflex is an important mechanism increasing the frequency of slow oscillations in arterial pressure and R–R intervals. The present results give new insight to understand the physiology underlying the frequency of slow arterial pressure and R–R interval oscillations. [Copyright &y& Elsevier]