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Objective: The current study aimed to assess the effects of five cycles of automated mechanical somatosensory stimulation (AMSS) of the fore-feet on blood pressure (BP) and cardiovascular autonomic control in Parkinson's Disease patients., Methods: Out of 23 patients, 16 underwent an AMSS session every 72 h, for a total of five sessions per patient. Electrocardiogram, noninvasive beat-to-beat blood pressure and respiratory activity were recorded for 20 min in supine position at baseline and after the AMSS sessions. Main outcomes were the changes in SBP and DBP, in the spectral indices of cardiac sympathetic (LFRRn.u.) and vagal (HFRR) modulatory activities, cardiac sympathovagal relationship (LF/HF), vascular sympathetic modulation (LFSAP) and arterial baroreflex sensitivity (sequence technique). Symbolic analysis of heart rate variability provided additional indices of cardiac sympathetic (0V%) and vagal (2UV%) modulation to the sinoatrial node., Results: After five AMSS trials a reduction in SBP (baseline: 131.2 ± 15.5 mmHg; post-AMSS: 122.4 ± 16.2 mmHg; P = 0.0004) and DBP (baseline: 73.2 ± 6.1 mmHg; post-AMSS: 68.9 ± 6.2 mmHg; P = 0.008) was observed. Post-AMSS, spectral and symbolic indices of cardiovascular sympathetic control decreased and arterial baroreflex sensitivity increased (baseline: 5.7 ± 1.3 ms/mmHg; post-AMSS: 11.27 ± 2.7 ms/mmHg)., Conclusion: AMSS sessions were effective in reducing BP, increasing baroreflex sensitivity and decreasing cardiovascular sympathetic modulation in Parkinson's disease patients. AMSS might be useful to control supine hypertension in Parkinson's disease.

We studied the autonomic response to an orthostatic challenge (i.e. head-up tilt) in 52 amyotrophic lateral sclerosis (ALS) patients and 16 healthy subjects by means of power spectral analysis of heart period (HP) and systolic arterial pressure (SAP) variability. In addition, we verified the correlation of spectral indexes with clinical features of the ALS patients. Results showed that cardiovascular control of the ALS patients was impaired and this impairment was more evident from SAP series. While the revised Functional Rating Scale score, its bulbar subscore, and disease duration were uncorrelated with spectral indexes, the rate of the disease progression was positively correlated with the absolute low frequency power of SAP variability at rest and negatively correlated with the normalized high frequency power of HP variability during head-up tilt. We conclude that: i) spectral analysis of HP and SAP variability provides indexes helpful to quantify the impairment of the cardiovascular neural control in ALS patients; ii) patients with a faster disease progression are characterized by a higher vascular sympathetic drive and/or a depressed vagal cardiac regulation.

The study investigates the two different aspects of the baroreflex control resulting in two baroreflex sensitivity (BRS) indexes: i) sympathetic BRS (sBRS); ii) cardiac BRS (cBRS). sBRS was assessed as the slope of the regression line of the conditional probability of detecting a burst on the integrated muscle nerve sympathetic activity (MSNA) given an assigned diastolic arterial pressure (DAP) on DAP. cBRS was estimated from spontaneous heart period (HP) and systolic arterial pressure (SAP) via a spectral approach in the low (0.04-0-15 Hz) and high (0.15-0.5 Hz) frequency bands respectively. Both sBRS and cBRS were assessed in eight healthy subjects undergoing three experimental sessions: supine resting position (REST), 80 degrees head-up tilt test (TILT) and before the occurrence of pre-syncope symptoms (TILT_PRE). Results showed a decrease of both sBRS and cBRS during TILT and a baroreflex impairment during TILT_PRE. sBRS and cBRS were linearly correlated during TILT but became uncorrelated during TILT_PRE. Findings suggest a failure of both "baroreflexes" and their disassociation during TILT_PRE.

Leptin exists in a free form and a receptor-bound form. Protein-bound rather than free leptin levels may be associated with regulation of muscle sympathetic nerve activity (MSNA). We determined MSNA and bound leptin concentrations in 25 men [age, 29 +/- 6 yr, body mass index (BMI), 24 +/- 3 kg/m(2)]. Baroreflex sensitivity was measured using phenylephrine and nitroprusside infusions. We measured bound leptin in patients with central (multiple system atrophy, n = 8; age, 59 +/- 8 yr; BMI, 23 +/- 2 kg/m(2)) and peripheral autonomic failure (pure autonomic failure, n = 4; age, 71 +/- 10 yr; BMI, 25 +/- 3 kg/m(2)). MSNA was correlated with protein-bound leptin concentrations (r(2) = 0.35; P < 0.01) but not with free leptin levels (r(2) = 0.09). MSNA at baseline was 15 +/- 2 bursts x minutes(-1) in subjects with lower and 24 +/- 3 bursts x minutes(-1) in subjects with higher bound leptin concentrations (P < 0.05). Blood pressure as well as baroreflex regulation of heart rate and MSNA was similar in both groups. Phenylephrine and nitroprusside responses were similar. Patients with multiple system atrophy and autonomic failure featured similar bound leptin levels. We conclude that protein-bound rather than free leptin levels are correlated with basal sympathetic outflow in normotensive, nonobese men. This relationship cannot be explained by a direct central nervous effect of protein-bound leptin. Instead, protein-bound leptin may increase sympathetic vasomotor tone indirectly via a baroreflex mechanism.

Stage 2 sleep is characterized by the EEG appearance of "K-complexes" and blood pressure oscillations. K-complexes may be directly related to blood pressure changes or they may reflect central sympathetic activation. We analyzed the temporal relationship among K-complexes, heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) during sleep in eight healthy volunteers (3 men and 5 women, age 22-41 yr). Most K-complexes presented as single large complexes (56 +/- 20%), followed by single small complexes (15 +/- 14%) and as couplets or triplets (13 +/- 6%). Single large K-complexes were preceded by a baroreflex-mediated increase of MSNA in approximately one-half (55%) of the cases. Detailed analysis of HR, BP, and MSNA was possible in 63 (45%) large single K-complexes not disturbed by preceding baroreflex-related changes. Systolic and diastolic BP and MSNA increased significantly after single events (22.5 +/- 13, 5.2 +/- 2.1, and 6.5 +/- 3.0%). Mean sympathetic baroreflex latency was similar after the single large K-complexes compared with the mean value during stage 2 sleep (1,290 +/- 126 vs. 1,279 +/- 61 ms). The area under the burst was significantly increased after single large K-complexes (median 3.9 vs. 9.0 arbitrary units, P < 0.03). The results support the hypothesis that K-complexes express cortical activation leading to temporary facilitation of sympathetic outflow in a graded fashion. Their functional effects appear to be independent of baroreflex modulation of MSNA in approximately 50% of the cases.

This document is an editorial published in the journal Clinical Autonomic Research. It pays tribute to the late David H. Robertson, a physician, scientist, mentor, and founder of the Autonomic Dysfunction Center at Vanderbilt University Medical Center. The authors highlight Robertson's significant contributions to the autonomic field, including his discoveries related to postprandial hypotension, the water pressor effect, congenital autonomic diseases, baroreflex failure, and Postural Tachycardia Syndrome (POTS). They also mention his role in the creation of the American Autonomic Society. The authors express their gratitude for Robertson's mentorship and describe him as a caring and approachable individual. Robertson is survived by his family and the many trainees and collaborators he influenced throughout his career. [Extracted from the article]

Pure autonomic failure (PAF) is a rare disorder belonging to the group of synucleinopathies, characterized by autonomic nervous system degeneration. Severe orthostatic intolerance with recurrent syncope while standing are the two most disabling manifestations. Symptoms may start at middle age, thus affecting people at their working age. The aims of this study were to evaluate the autonomic and work ability impairment of a group of PAF patients and assess the relationships between cardiovascular autonomic control and work ability in these patients. Eleven PAF patients (age 57.3 ± 6.7 years), engaged in work activity, participated in the study. They completed the Composite Autonomic Symptom Score (COMPASS-31, range 0 no symptom-100 maximum symptom intensity) and Work Ability questionnaires (Work Ability Index, WAI, range 7–49; higher values indicate better work ability and lower values indicating unsatisfactory or jeopardized work ability). Electrocardiogram, blood pressure and respiratory activity were continuously recorded for 10 min while supine and during 75° head-up tilt (HUT). Autoregressive spectral analysis of cardiac cycle length approximated as the time distance between two consecutive R-wave peaks (RR) and systolic arterial pressure (SAP) variabilities provided the power in the high frequency (HF, 0.15–0.40 Hz) and low frequency (LF, 0.04–0.15 Hz) bands of RR and SAP variabilities. Cardiac sympatho-vagal interaction was assessed by LF to HF ratio (LF/HF), while the LF power of SAP (LFSAP) quantified the vascular sympathetic modulation. Changes in cardiovascular autonomic indexes induced by HUT were calculated as the delta (Δ) between HUT and supine resting positions. Spearman correlation analysis was applied. PAF patients were characterized by a moderate autonomic dysfunction (COMPASS-31 total score 47.08 ± 20.2) and by a reduction of work ability (WAI 26.88 ± 10.72). Direct significant correlations were found between WAI and ΔLFRR (r = 0.66, p = 0.03) and ΔLF/HFRR (r = 0.70, p = 0.02). Results indicate that patients who were better able to modulate heart rate, as revealed by a greater cardiac sympathetic increase and/or vagal withdrawal during the orthostatic stimulus, were those who reported higher values of WAI. This finding could be relevant to propose new strategies in the occupational environment to prevent early retirement or to extend the working life of these patients. [ABSTRACT FROM AUTHOR]

Primary Sjögren's syndrome (pSS) is an autoimmune disease affecting exocrine glands and extra-glandular organs. There are conflicting reports on the presence of autonomic dysfunction in pSS and no data are available on the functional status of sympathetic outflow to the vessels and baroreceptor [baroreflex sensitivity (BRS)] control mechanisms. We investigated the cardiac (cBRS) and sympathetic (sBRS) baroreceptor modulation in both time and frequency domains and the cardiovascular autonomic profile in pSS patients compared to healthy controls. Autonomic symptoms were quantified by the Composite Autonomic Symptom Scale (COMPASS31) three-item questionnaire. The EULAR Sjogren's syndrome patient reported index (ESSPRI) questionnaire evaluated the magnitude of pSS clinical symptoms, i.e., fatigue, pain, and sicca symptoms. Electrocardiogram, beat-by-beat arterial pressure (AP) and respiratory activity were continuously recorded in 17 pSS patients and 16 healthy controls, while supine and during 75° head-up tilt. In seven patients and seven controls, muscle sympathetic nerve activity (MSNA) was measured. Spectrum analysis of RR variability provided markers of cardiac vagal modulation (HFRR nu) and sympatho-vagal balance [low frequency (LF)/high frequency (HF)]. The power of LF (0.1 Hz) oscillations of systolic arterial pressure (SAP) variability (LFSAP) evaluated the vasomotor response to sympathetic stimulation. Compared to controls, pSS patients scored higher in total COMPASS31 (p < 0.0001) and all ESSPRI subdomains (fatigue, p = 0.005; pain, p = 0.0057; dryness, p < 0.0001). Abnormal scialometry (<1.5 ml/15 min) and Schirmer tests (<5 mm/5 min) were found in pSS patients and salivary flow rate was negatively associated with ESSPRI dryness (p = 0.0014). While supine, pSS patients had lower SEQcBRS index of cardiac baroreceptor sensitivity, higher HFRRnu (p = 0.021), lower LF/HF (p = 0.007), and greater MSNA (p = 0.038) than controls. No differences were observed in LFSAP between groups. During orthostatic challenge, although LFSAP increased similarly in both groups, MSNA was greater in pSS patients (p = 0.003). At rest pSS patients showed lower cBR control and greater parasympathetic modulation. Furthermore, greater sympathetic nerve activity was observed in pSS patients while supine and in response to gravitational challenge. We hypothesized that such enhanced sympathetic vasoconstrictor activity might reflect an attempt to maintain blood pressure in a setting of likely reduced vascular responsiveness. [ABSTRACT FROM AUTHOR]

Orthostatic intolerance commonly occurs after prolonged bed rest, thus increasing the risk of syncope and falls. Baroreflex-mediated adjustments of heart rate and sympathetic vasomotor activity (muscle sympathetic nerve activity – MSNA) are crucial for orthostatic tolerance. We hypothesized that prolonged bed rest deconditioning alters overall baroreceptor functioning, thereby reducing orthostatic tolerance in healthy volunteers. As part of the European Space Agency Medium-term Bed Rest protocol, 10 volunteers were studied before and after 21 days of −6° head down bed rest (HDBR). In both conditions, subjects underwent ECG, beat-by-beat blood pressure, respiratory activity, and MSNA recordings while supine (REST) and during a 15-min 80° head-up tilt (TILT) followed by a 3-min −10 mmHg stepwise increase of lower body negative pressure to pre-syncope. Cardiac baroreflex sensitivity (cBRS) was obtained in the time (sequence method) and frequency domain (spectrum and cross-spectrum analyses of RR interval and systolic arterial pressure – SAP, variability). Baroreceptor modulation of sympathetic discharge activity to the vessels (sBRS) was estimated by the slope of the regression line between the percentage of MSNA burst occurrence and diastolic arterial pressure. Orthostatic tolerance significantly decreased after HDBR (12 ± 0.6 min) compared to before (21 ± 0.6 min). While supine, heart rate, SAP, and cBRS were unchanged before and after HDBR, sBRS gain was slightly depressed after than before HDBR (sBRS: −6.0 ± 1.1 versus −2.9 ± 1.5 burst% × mmHg−1, respectively). During TILT, HR was higher after than before HDBR (116 ± 4 b/min versus 100 ± 4 b/min, respectively), SAP was unmodified in both conditions, and cBRS indexes were lower after HDBR (α index: 3.4 ± 0.7 ms/mmHg; BRSSEQ 4.0 ± 1.0) than before (α index: 6.4 ± 1.0 ms/mmHg; BRSSEQ 6.8 ± 1.2). sBRS gain was significantly more depressed after HDBR than before (sBRS: −2.3 ± 0.7 versus −4.4 ± 0.4 burst% × mmHg−1, respectively). Our findings suggest that baroreflex-mediated adjustments in heart rate and MSNA are impaired after prolonged bed rest. The mechanism likely contributes to the decrease in orthostatic tolerance. [ABSTRACT FROM AUTHOR]

Regular exercise is recommended to improve the cardiovascular risk profile. However, there is growing evidence that extreme volumes and intensity of long-term exertion may increase the risk of acute cardiac events. The aim of this study is to investigate the after-effects of regular, strenuous physical training on the cardiovascular neural regulation in a group of amateur triathletes compared to age-matched sedentary controls. We enrolled 11 non-elite triathletes (4 women, age 24±4 years), who had refrained from exercise for 72 hours, and 11 age-matched healthy non-athletes (3 women, age 25±2 years). Comprehensive echocardiographic and cardiopulmonary exercise tests were performed at baseline. Electrocardiogram, non-invasive blood pressure, respiratory activity, and muscle sympathetic nerve activity (MSNA) were continuously recorded in a supine position (REST) and during an incremental 15° step-wise head-up tilt test up to 75° (TILT). Blood samples were collected for determination of stress mediators. Autoregressive spectral analysis provided the indices of the cardiac sympathetic (LFRR) and vagal (HFRR) activity, the vascular sympathetic control (LFSAP), and the cardiac sympatho-vagal modulation (LF/HF). Compared to controls, triathletes were characterized by greater LFRR, LF/HF ratio, LFSAP, MSNA, and lower HFRR at REST and during TILT, i.e. greater overall cardiovascular sympathetic modulation together with lower cardiac vagal activity. Cortisol and adrenocorticotropic hormone concentrations were also higher in triathletes. In conclusion, triathletes were characterized by signs of sustained cardiovascular sympathetic overactivity. This might represent a risk factor for future cardiovascular events, given the known association between chronic excessive sympathetic activity and increased cardiovascular risk. [ABSTRACT FROM AUTHOR]

Fibromyalgia syndrome (FMS) is a rheumatologic disorder characterized by chronic widespread pain, fatigue and other symptoms. Baroreflex dysfunction has been observed in women with FMS. However, it is unknown whether the limited involvement of the baroreflex control during an orthostatic stimulus has some impact on the quality of life of the FMS patient. Therefore, the aim of the study is evaluate the relationship between the quality of life of the FMS patient and indexes of the cardiovascular autonomic control as estimated from spontaneous fluctuations of heart period (HP) and systolic arterial pressure (SAP). We enrolled 35 women with FMS (age: 48.8±8.9 years; body mass index: 29.3±4.3 Kg/m2). The electrocardiogram, non-invasive finger blood pressure and respiratory activity were continuously recorded during 15 minutes at rest in supine position (REST) and in orthostatic position during active standing (STAND). Traditional cardiovascular autonomic control markers were assessed along with a Granger causality index assessing the strength of the causal relation from SAP to HP (CRSAP→HP) and measuring the degree of involvement of the cardiac baroreflex. The impact of FMS on quality of life was quantified by the fibromyalgia impact questionnaire (FIQ) and visual analog score for pain (VAS pain). No significant linear association was found between FIQ scores and the traditional cardiovascular indexes both at REST and during STAND (p>0.05). However, a negative relationship between CRSAP→HP during STAND and FIQ score was found (r = -0.56, p<0.01). Similar results were found with VAS pain. In conclusion, the lower the degree of cardiac baroreflex involvement during STAND in women with FMS, the higher the impact of FMS on the quality of life, thus suggesting that Granger causality analysis might be clinically helpful in assessing the state of the FMS patient. [ABSTRACT FROM AUTHOR]