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Hypertension is recognised as a leading attributable risk factor for cardiovascular disease and premature mortality. Global initiatives towards the prevention and treatment of arterial hypertension are centred around non-pharmacological lifestyle modification. Exercise recommendations differ between professional and scientific organisations, but are generally unanimous on the primary role of traditional aerobic and dynamic resistance exercise. In recent years, isometric exercise training (IET) has emerged as an effective novel exercise intervention with consistent evidence of reductions in blood pressure (BP) superior to that reported from traditional guideline-recommended exercise modes. Despite a wealth of emerging new data and endorsement by select governing bodies, IET remains underutilised and is not widely prescribed in clinical practice. This expert-informed review critically examines the role of IET as a potential adjuvant tool in the future clinical management of BP. We explore the efficacy, prescription protocols, evidence quality and certainty, acute cardiovascular stimulus, and physiological mechanisms underpinning its anti-hypertensive effects. We end the review with take-home suggestions regarding the direction of future IET research. [ABSTRACT FROM AUTHOR]

Background: Autonomic nervous system (ANS) testing has aided in our ability to evaluate autonomic dysfunction in migraine patients. We reviewed the literature in multiple databases which investigate ANS function in migraine patients and healthy subjects. Methods: This systematic review and meta-analysis examined the respective deep breathing, Valsalva manoeuvre, orthostatic and isometric challenge results, using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and Meta-analyses of Observational Studies in Epidemiology (MOOSE) statements. Results: Seven articles met all inclusion criteria. Fixed-effects meta-analysis showed migraine patients (n = 424), collectively, had lower interictal autonomic test results compared with healthy controls (n = 268). In detail, this was true for the standardized mean difference (g) of deep breathing (g= -0.32; 95% confidence interval (CI) -0.48, -0.16), orthostatic challenge (g= -0.28; 95% CI -0.44, -0.13) and isometric challenge (g= -0.55; 95% CI -0.71, -0.39) and for the difference of means (MD) of the Valsalva ratio (MD = -0.17; 95% CI -0.23, -0.10). Conclusions: Interictal ANS dysfunction can be identified in migraine patients when compared to healthy controls. These findings indicate the importance to evaluate ANS function in migraine patients - especially, as migraine-specific prophylactic therapies (such as anti-calcitonin gene-related peptide (CGRP) antibodies) may affect the function of the ANS. [ABSTRACT FROM AUTHOR]

Both anxiety and autism spectrum disorder (ASD) are associated with atypical physiological activity. Few studies have systematically assessed the resting physiological activity in ASD with co-occurring anxiety disorders. We tested 75 participants divided in four groups: youth with ASD, with (ASD + Anxiety = 22, 6F, 12.29 ± 2.83 years old) and without co-occurring anxiety (ASD Alone = 15, 6F, 11.59 ± 2.85 years old) and compared their physiological profile with that of matched typically developing controls (TDC) with (Anxiety Alone = 16, 6F, 11.24 ± 3.36 years old) and without co-occurring anxiety disorders (TDC = 22, 8F, 11.88 ± 2.88 years old). Results indicated reduced sympathetic and parasympathetic activity at rest in ASD as compared to TDC youth. ASD + Anxiety and Anxiety Alone groups showed different sympathetic, but similar parasympathetic activity. These findings suggest that autonomic profile-based approaches may advance research, diagnosis, and treatment of ASD and anxiety. [ABSTRACT FROM AUTHOR]

Purpose: We evaluated the impact of menopause-associated vasomotor symptoms (VMS) on sleep. We also sought to establish the content validity of Patient-Reported Outcomes Measurement Information System (PROMIS) short form Sleep-Related Impairment and Sleep Disturbance measures in postmenopausal women with moderate to severe VMS. Methods: Cross-sectional, in-person, qualitative interviews were conducted in the United States (Texas, Illinois) and European Union (UK, France) with women aged 40–64 years experiencing moderate to severe VMS (≥35/wk). Main outcomes were impact of VMS on sleep based on concept elicitation and content validity of PROMIS Sleep-Related Impairment and Sleep Disturbance short forms via cognitive debriefing. Results: Thirty-two women (US: n = 16; EU: n = 16) participated. A majority (US: 93.8%; EU: 93.8%) said VMS affected sleep; specifically, they had sleep interrupted by sweating or overheating and had difficulty returning to sleep. Sleep disturbance was the most bothersome aspect of VMS (US: 75%; EU: 50%). VMS-associated sleep disturbance affected next-day work productivity, mood, relationships, daily activities, concentration, social activities, and physical health. Participants found both PROMIS sleep measures relevant and easy to answer; the Sleep Disturbance measure was considered the most relevant. Participants had no difficulty remembering their experiences over the 7-day recall period and found the response options to be distinct. Conclusion: VMS associated with menopause significantly interferes with sleep and next-day functioning (e.g., work productivity), supporting assessment of sleep outcomes in studies evaluating treatment of VMS. Women with moderate to severe VMS found that the PROMIS Sleep-Related Impairment and Sleep Disturbance short forms assessed constructs important to understanding sleep in the context of menopause-associated VMS. [ABSTRACT FROM AUTHOR]

The 123I-labeled meta-iodobenzylguanidine (MIBG) is an analogue of noradrenaline that can evaluate cardiac sympathetic activity in scintigraphy. Quantitative analysis of 123I-MIBG images has been verified in patients with heart failure and neurodegenerative diseases. However, quantitative results differ due to variations in scintigraphic imaging procedures. Here, we created and assessed the clinical feasibility of a calibration method for 123I-MIBG imaging. The characteristics of scintigraphic imaging systems were determined using an acrylic calibration phantom to generate a multicenter phantom imaging database. Calibration factors corresponding to the scintigraphic imaging procedures were calculated from the database and applied to a clinical study. The results of this study showed that the calibrated analysis eliminated inter-institutional differences among normal individuals. In summary, our standardization methodology for 123I-MIBG scintigraphy could provide the basis for improved diagnostic precision and better outcomes for patients. [ABSTRACT FROM AUTHOR]

Purpose: Early weaning (EW) is a risk factor for obesity development. Brown adipose tissue (BAT) hypofunction is related to obesity onset. Here, we evaluated whether sympathetic nervous system (SNS) activity in BAT and the thermogenic function of BAT are decreased in adulthood in obese rats from two EW models. Methods: At the time of birth, lactating Wistar rats and their pups (three males and three females) were separated into three groups: the control group, in which pups consumed milk throughout lactation; the non-pharmacological EW (NPEW) group, in which suckling was interrupted with a bandage during the last 3 days of lactation; and the pharmacological EW (PEW) group, in which dams were treated with bromocriptine (0.5 mg/twice a day) 3 days before weaning. The offspring were sacrificed on PN180. Results: Adult male rats from both EW models exhibited lower BAT SNS activity. Female rats from the PEW group showed a decrease in BAT SNS activity. The protein levels of UCP1 were lower in the NPEW males, while PGC1α levels were lower in both PEW and NPEW males. Both groups of EW females showed reductions in the levels of β3-AR, TRβ1, and PGC1α. The UCP1 protein level was reduced only in the NPEW females. The EW groups of both sexes had lower AMPK protein levels in BAT. In the hypothalamus, only the PEW females showed an increase in AMPK protein levels. In both groups of EW males, adrenal catecholamine was increased and tyrosine hydroxylase was decreased, while in EW females, adrenal catecholamine was decreased. Conclusions: Early weaning alters the thermogenic capacity of BAT, which partially contributes to obesity in adulthood, and there are sex-related differences in these alterations. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to test our hypothesis that acute hypotension attenuates brachial flow-mediated dilation (FMD) as an index of endothelial function in healthy humans.Methods: Twelve healthy men (21.8 ± 1.6 years, body mass index; 22.2 ± 1.6 kg/m2) participated in this study. Brachial FMD was measured in three trials: standardized FMD protocol (control trial), abrupt decrease in blood pressure (BP) via thigh cuff inflation-deflation (hypotension trial) and decrease in shear rate (SR) via a shortened forearm occlusion time (SR reduction trial). Brachial diameter and blood velocity were measured using Duplex ultrasound.Results: Mean arterial pressure during reactive hyperaemia showed a marked decrease in the hypotension trial (- 23.7 ± 6.0 mmHg), but not in the control and SR reduction trials. SR area under the curve was attenuated in the SR reduction trial (P < 0.001), but not in the control and hypotension trials (P = 0.316). Consequently, FMD was attenuated in the hypotension and SR reduction trials compared with that in the control trial (P = 0.003 and P = 0.043, respectively), and was attenuated to a greater extent in the hypotension trial compared with the SR reduction trial (P = 0.006; control, 6.9 ± 3.5%; hypotension, 3.5 ± 1.7%; SR reduction, 5.0 ± 2.2%). After adjusting FMD using SR, FMD remained attenuated in the hypotension trial (P = 0.014), but not in the SR reduction trial.Conclusion: Our findings indicate that arterial pressure as well as sympathetic nervous system activation could be an important determinant of FMD. Blunted FMD of peripheral arteries may be a rational response to restore BP and/or prevent further reduction of BP following acute hypotension in healthy humans. [ABSTRACT FROM AUTHOR]

Social anxiety is characterized by maladaptive anticipation, avoidance, and post-avoidance processes in response to perceived threats. Exaggerated sympathetic activation to threats is proposed to play a key role in social anxiety, but has received inconsistent empirical support. To clarify this issue, we characterized social anxiety-related differences in the time course of sympathetic activation as a function of threat certainty and threat avoidance. While skin conductance was measured, adults (18–30 years old) reporting clinically elevated (n = 34) or low (n = 33) social anxiety symptoms completed a behavioral paradigm involving threat anticipation and the opportunity to avoid conditioned threat and non-threats. During threat anticipation, both groups exhibited increasing conditioned sympathetic activation when threat was certain; however, the high social anxiety group exhibited less conditioned sympathetic activation to threats vs. non-threats compared to the low social anxiety group, irrespective of threat certainty. Following threat anticipation, the high social anxiety group exhibited greater avoidance of both threats and non-threats. Following threat avoidance, the high social anxiety group exhibited comparatively smaller and slower sympathetic recovery. Taken together, our results suggest that social anxiety is characterized by indiscriminate sympathetic activation to both threat and safety cues, which facilitates maladaptive avoidance behaviors and impairs sympathetic recovery. [ABSTRACT FROM AUTHOR]

The fraction of repolarization variability independent of RR interval variability is of clinical interest. It has been linked to direct autonomic nervous system (ANS) regulation of the ventricles in healthy subjects and seems to reflect the instability of the ventricular repolarization process in heart disease. In this study, we sought to identify repolarization measures that best reflect the sympathetic influences on the ventricles independent of the RR interval. ECG was recorded in 46 young subjects during supine and then following 45 degrees head-up tilt. RR intervals and five repolarization features (QTend, QTpeak, RTend, RTpeak, and TpTe) were extracted from the ECG recordings. Repolarization variability was separated into RR-dependent and RR-independent variability using parametric spectral analysis. Results show that LF power of TpTe is independent of RR in both supine and tilt, while the LF power of QTend and RTend independent of RR and respiration increases following tilt. We conclude that TpTe is independent of RR and is highly affected by respiration. QTend and RTend LF power might reflect the sympathetic influences on the ventricles elicited by tilt. Graphical abstract. [ABSTRACT FROM AUTHOR]

Phenomenological studies suggest the existence of enhanced cognitive states, termed flow or peak experiences, in which specific cognitive processes (e.g., attention, perception) can be dramatically increased for limited durations. Here we review new scientific evidence that shows that specific types of meditation that developed out of certain religious traditions such as Vajrayana (Tantric Buddhism) and Hindu Tantra lead to the enhanced cognitive states, characterized by heightened sympathetic activation and phasic alertness (a significant temporary boost in focused attention). This is in contrast to the meditation practices (Shamatha, Vipassana) from other traditions such as Theravada and Mahayana that elicit heightened parasympathetic activity and tonic alertness. Such findings validate Buddhist scriptural descriptions of heightened arousal during Vajrayana practices and a calm and alert state of mind during Theravada and Mahayana types of meditation. The finding demonstrates the existence of enhanced cognitive states—the unique and energized states of consciousness characterized by a dramatic boost in focused attention. [ABSTRACT FROM AUTHOR]

Background: No study has evaluated the cardiovascular effects of diazepam in elderly subjects that assume diazepam to induce sleep. Purpose: The present study was carried out in order to evaluate the effects of chronic administration of diazepam as hypnotic drug on blood pressure (BP) and heart rate (HR) in healthy elderly subjects. Patients and methods: Healthy, elderly subjects, aged 65–74 years, were treated with diazepam 5 mg or placebo—both administered once a day in the evening—for 4 weeks in two cross-over periods, each separated by a 2-week placebo period, according to a randomized, double-blind, cross-over design. At the end of each study period, clinical as well as 24-h ambulatory BP and HR were evaluated. Results: A total of 25 subjects were included in the analysis. At the end of a 4-week diazepam treatment, clinical as well 24-h BP and HR mean values were not significantly affected. Analysis of sub-periods showed that during night-time, systolic BP (SBP) values under diazepam were 7.6% higher than under placebo, with a mean difference of 7.9 mmHg (p < 0.01), diastolic BP (DBP) values were 5.8% higher, with a mean difference of 3.7 mmHg (p < 0.05 vs placebo) and HR values were 6.6% higher with a mean difference of 4.2 b/min (p < 0.05). The HR increase observed with diazepam persisted during the morning hours, whereas during the afternoon and evening hours SBP, DBP and HR values were similar in the two treatment groups. Conclusions: In elderly subjects chronic assumption of diazepam as hypnotic agent produced an increase in BP, in particular SBP, during night-time and of HR during night-time and morning hours. These effects, which probably depend on a diazepam-mediated increase in sympathetic drive and decrease in vagal tone, might be of clinical relevance due to the role of increased BP and HR as independent predictors of cardiovascular morbidity and mortality. [ABSTRACT FROM AUTHOR]

Purpose: This preliminary study tested the hypothesis that the carotid baroreflex (CBR) mediated sympathoexcitation regulates cerebral blood flow (CBF) at rest and during dynamic exercise.Methods: In seven healthy subjects (26 ± 1 years), oscillatory neck pressure (NP) stimuli of + 40 mmHg were applied to the carotid baroreceptors at a pre-determined frequency of 0.1 Hz at rest, low (10 ± 1W), and heavy (30 ± 3W) exercise workloads (WLs) without (control) and with α - 1 adrenoreceptor blockade (prazosin). Spectral power analysis of the mean arterial blood pressure (MAP), mean middle cerebral artery blood velocity (MCAV), and cerebral tissue oxygenation index (ScO2) in the low-frequency range (0.07-0.20 Hz) was estimated to examine NP stimuli responses.Results: From rest to heavy exercise, WLs resulted in a greater than three-fold increase in MCAV power (42 ± 23.8-145.2 ± 78, p < 0.01) and an almost three-fold increase in ScO2 power (0.51 ± 0.3-1.53 ± 0.8, p = 0.01), even though there were no changes in MAP power (from 24.5 ± 21 to 22.9 ± 11.9) with NP stimuli. With prazosin, the overall MAP (p = 0.0017), MCAV (p = 0.019), and ScO2 (p = 0.049) power was blunted regardless of the exercise conditions. Prazosin blockade resulted in increases in the Tf gain index between MAP and MCAV compared to the control (p = 0.03).Conclusion: CBR-mediated changes in sympathetic activity contribute to dynamic regulation of the cerebral vasculature and CBF at rest and during dynamic exercise in humans. [ABSTRACT FROM AUTHOR]

Purpose: The primary purpose of this study was to determine the accuracy of the standard deviation of normal-to-normal intervals (SDNN) to root mean square of successive normal-to-normal interval differences (RMSSD) ratio from 1-min recordings (SDNN:RMSSD1-min) compared to criterion recordings, as well as its relationship to low-frequency-to-high-frequency ratio (LF:HF) at rest and following maximal exercise in a group of collegiate athletes.Method: Twenty athletes participated in the study. Heart rate variability (HRV) data were measured for 5 min before and at 5-10 and 25-30 min following a maximal exercise test. From each 5-min segment, the frequency-domain measures of HF, LF, and LF:HF ratio were analyzed. Time-domain measures of SDNN, RMSSD, and SDNN:RMSSD ratio were also analyzed from each 5-min segment, as well as from randomly selected 1-min recordings.Result: The 1-min values of SDNN, RMSSD, and SDNN:RMSSD provided no significant differences and nearly perfect intra-class correlations (ICCs ranged from 0.97 to 1.00, p < 0.001 for all) to the criterion measures from 5-min recordings. In addition, SDNN, RMSSD, and SDNN:RMSSD from the 1-min segments provided very large to nearly perfect correlations (r values ranged from 0.71 to 0.97, p < 0.001 for all) to LF, HF, and LF:HF, respectively, at each time point.Conclusion: The findings of the study suggest that ultra-shortened time-domain markers may be useful surrogates of the frequency-domain parameters for tracking changes in sympathovagal activity in athletes. [ABSTRACT FROM AUTHOR]

Background: Increased sympathetic nervous system activity has been proposed as a potential mechanism for the blood pressure (BP) elevation seen in individuals born small for gestational age (SGA). This study was carried out to detect the changes in BP and heart rate (HR) in children born SGA during exposure to stress and to assess for changes in urinary catecholamine excretion. Methods: Nineteen children aged 6-14 years born SGA and 17 age- and gender-matched healthy controls were included in the study. The stress test included a mathematical test and venipuncture. BP and HR were monitored during the test. Spot urine samples were collected at baseline and after the stress test to determine dopamine, epinephrine and norepinephrine levels. Results: At baseline, there was no difference in BP and HR between the SGA and control groups, but mean urinary norepinephrine levels were slightly higher in the SGA group (55.7 ± 16.1 vs. 43.4 ± 3.8 mcg/gCr; P = 0.10). Compared to the control group, mean maximal HR increase was higher in the SGA group (31.3 ± 3.1 vs. 19.2 ± 3.8%; P = 0.008), and mean duration of maximal HR to baseline HR was longer (186 ± 23 vs. 97 ± 13 s, respectively; P = 0.003). There was a significant negative correlation between birth weight and maximal HR increase ( r = −0.497, P = 0.003). Conclusion: Children born SGA showed significantly greater increases in HR and significantly longer periods of tachycardia during exposure to stress than did healthy controls. The rise in HR was inversely correlated with birth weight. These findings suggest that children born SGA have a greater increase in sympathetic response when exposed to stress than do healthy individuals. [ABSTRACT FROM AUTHOR]

Background: Salivary alpha amylase (sAA) and chromogranin A (sCgA) have both been suggested as non-invasive markers for sympathetic nervous system (SNS) activity. A complete cervical spinal cord injury leading to tetraplegia is accompanied with sympathetic dysfunction; the aim of this study was to establish the exercise response of these markers in this in vivo model. Methods: Twenty-six elite male wheelchair athletes (C6-C7 tetraplegia: N = 8, T6-L1 paraplegia: N = 10 and non-spinal cord injured controls: N = 8) performed treadmill exercise to exhaustion. Saliva and blood samples were taken pre, post and 30 min post exercise and analysed for sAA, sCgA and plasma adrenaline concentration, respectively. Results: In all three subgroups, sAA and sCgA were elevated post exercise ( P < 0.05). Whilst sCgA was not different between subgroups, a group × time interaction for sAA explained the reduced post-exercise sAA activity in tetraplegia (162 ± 127 vs 313 ± 99 (paraplegia) and 328 ± 131 U mL (controls), P = 0.005). The post-exercise increase in adrenaline was not apparent in tetraplegia ( P = 0.74). A significant correlation was found between adrenaline and sAA ( r = 0.60, P = 0.01), but not between adrenaline and sCgA ( r = 0.06, P = 0.79). Conclusions: The blunted post-exercise rise in sAA and adrenaline in tetraplegia implies that both reflect SNS activity to some degree. It is questionable whether sCgA should be used as a marker for SNS activity, both due to the exercise response which is not different between the subgroups and its non-significant relationship with adrenaline. [ABSTRACT FROM AUTHOR]

Despite increased application of the deceleration capacity (DC) and acceleration capacity (AC) of heart rate indices as indicators of autonomic nervous system (ANS) function, it remains controversial as to whether they reflect cardiac sympathetic or vagal activity. We addressed this problem using a cardiovascular system model that allows analysis of DC and AC under controllable levels of sympathetic and vagal activities. Multi-scale DCs and ACs with various timescales T and wavelet scales s were computed from the simulated RR interval series under randomly fluctuating levels of ANS activity, and the correlations of the indices to ANS functions were assessed. Results showed that under the conventional scales (T = 1, s = 2), both DC and AC were solely dependent on vagal activity. With higher scales (T = 3, s = 5), both DC and AC were positively correlated to sympathetic activity and negatively correlated to vagal activity. These data suggest that DC and AC provide information on the same aspects of ANS activity and that their physiological significance is highly influenced by the timescales and wavelet scales used in the computation. [ABSTRACT FROM AUTHOR]

It is generally acknowledged that for an orally administered ergogenic aid to enhance exercise performance it must first be absorbed by the gastrointestinal tract before exerting its effects. Recently, however, it has been reported that some ergogenic aids can affect exercise performance without prior absorption by the gastrointestinal tract. This is best illustrated by studies that have shown that rinsing the mouth with a carbohydrate (CHO) solution, without swallowing it, significantly improves exercise performance. The ergogenic effects of CHO mouth rinsing in these studies have been attributed to the activation of the brain by afferent taste signals, but the specific mechanisms by which this brain activation translates to enhanced exercise performance have not yet been elucidated. Given the benefits of CHO mouth rinsing for exercise performance, this raises the issue of whether other types of tastants, such as bitter-tasting solutions, may also improve exercise performance. Recently, we performed a series of studies investigating whether the bitter tastant quinine can improve maximal sprint performance in competitive male cyclists, and, if so, to examine some of the possible mechanisms whereby this effect may occur. These studies have shown that mouth rinsing and ingesting a bitter-tasting quinine solution can significantly improve the performance of a maximal cycling sprint. There is also evidence that the ergogenic effect of quinine is mediated, at least in part, by an increase in autonomic nervous system activation and/or corticomotor excitability. The purpose of this article is to discuss the results and implications of these recent studies and to suggest avenues for further research, which may add to the understanding of the way the brain integrates signals from the oral cavity with motor behaviour, as well as uncover novel strategies to improve exercise performance. [ABSTRACT FROM AUTHOR]

Experimental and clinical studies have clearly shown the role of the sympathetic nervous system in the pathophysiology of several cardiovascular and non-cardiovascular diseases. This short review will be aimed at focusing and discussing the new information collected on two specific clinical conditions such as obesity and metabolic syndrome. The paper will briefly describe the four main mechanisms that represent the common link between these two pathophysiological conditions and that through the sympathetic nervous system contribute to increase the cardiovascular risk. [ABSTRACT FROM AUTHOR]

Objective. Using data on the evolution of electrical brain stimulation and considering the pathophysiological aspect of neurostimulation correction of the sympathetic nervous system, the aim of the present work was to identify grounds for the potential of the use of this method in Korsakoff's psychosis. Materials and methods. Sixteen patients with Korsakoff's (amnestic) psychosis were treated using this method. Results and discussion. All patients showed improvements, which are illustrated by detailed description of a typical case. It is concluded that sympathetic correction has high therapeutic potential. [ABSTRACT FROM AUTHOR]

When studying factors that may heighten risk for relational aggression in youth, it is important to consider characteristics of both the individual and their environment. This research examined the associations between parental psychological control and reactive and proactive relational aggression in emerging adults in college. Given that sympathetic nervous system (SNS) activation may underlie differences between reactive and proactive aggression and has been shown to moderate the effects of parenting on youth development, the moderating role of SNS reactivity [indexed by skin conductance level reactivity (SCLR)] was also examined. Emerging adults (N = 180; 77.2 % female) self-reported on perceptions of parental psychological control and reactive and proactive relational aggression. SCLR was assessed in response to an interpersonal laboratory challenge task. Parental psychological control was positively associated with reactive relational aggression only for emerging adults who exhibited high SCLR. Parental psychological control was positively associated with proactive relational aggression only among emerging adults who showed low SCLR. This study extends previous research on parenting and aggression and suggests that parental psychological control is differentially associated with reactive versus proactive relational aggression, depending on emerging adults' SCLR to interpersonal stress. [ABSTRACT FROM AUTHOR]

Purpose: While non-noxious local cooling is widely used in physical medicine, its effect on muscle sympathetic nerve activity (MSNA) and cardiovascular regulation are not clear. The purpose of the present study was to assess the responses of MSNA, blood pressure (BP), heart rate (HR) and local blood flow during non-noxious local cooling.Methods: The study included two protocols. Both protocols consisted of 10-min rest in supine position, followed by 15-min local cooling (15 °C) of the shin and anterior foot, and 20-min recovery. MSNA of the right common peroneal nerve, BP, HR, and shin skin temperature (TSK) were recorded in eight men in the first protocol, while leg blood flow (LBF) was measured in the same subjects by strain-gauge plethysmography in the second protocol.Results: TSK gradually decreased from 31.5 ± 0.02 to 16.0 ± 1.01 °C (mean ± SEM) during local cooling, and gradually increased after the end of local cooling. No subject complained of pain, and BP and HR remained constant. The MSNA burst rate increased significantly (p < 0.05) to 141.1 ± 12.5 % during local cooling, but decreased significantly (p < 0.05) to 73.6 ± 5.9 % during the recovery period. Total MSNA also increased to 148.0 ± 14.2 % (p < 0.05) during local cooling, and decreased to 74.0 ± 13.9 % (p < 0.05) at recovery. LBF remained constant through the experiment.Conclusions: The results suggest that MSNA is activated by non-noxious local cooling, and attenuated after the end of local cooling without any changes in HR and BP. [ABSTRACT FROM AUTHOR]

Purpose: To determine whether frontotemporal lobar degeneration (FTLD) is associated with similar cardiovascular autonomic dysfunction to that seen in amyotrophic lateral sclerosis (ALS), we compared cardiovascular parameters between ALS patients and patients with FTLD. Methods: In ten patients with FTLD (mean age ± SD: 71.6 ± 4.6 years) and 12 patients with ALS (mean age ± SD: 71.4 ± 4.6 years), MSNA (using microneurography), heart rate (HR), and blood pressure (BP) were recorded simultaneously. Results: MSNA was significantly higher in both groups of patients compared with the controls ( p < 0.01), while there were no significant differences in MSNA between the patients with FTLD and those with ALS. During head-up tilt, changes in HR, BP, and the frequency of MSNA bursts were smaller in the patients than in controls ( p < 0.05 or p < 0.01). Conclusions: Patients with FTLD and ALS showed similar dysfunction of HR, BP, and sympathetic outflow to muscles. [ABSTRACT FROM AUTHOR]

Purpose: Increased arterial stiffness is associated with an impairment of ventricular-vascular coupling efficiency and increased risk of cardiovascular mortality. Recently, it has been suggested that an increase in arterial stiffness is associated with resistance exercise training. Therefore, the aims of this study were to compare augmentation index (AIx) and left ventricular wasted pressure energy (LVEW) as markers of arterial stiffness and ventricular-vascular coupling efficiency in young aerobic-trained (AT) and resistance (RT)-trained subjects. We also investigated the relationship of muscle sympathetic nerve activity (MSNA) and flow-mediated dilation (FMD) to AIx in both sets of subjects to determine if endothelial function or sympathetic outflow could explain any differences in arterial stiffness.Method: To achieve our aims, we measured MSNA in 15 male subjects (8 RT, 7 AT) using microneurography. We also used applanation tonometry of the radial pressure waveform to noninvasively synthesize aortic pressure waveforms. FMD was calculated as percent dilation of the radial artery from baseline following a 5 min occlusion.Result: RT subjects had an increased AIx (12 ± 3 vs. -7 ± 2; P < 0.01), LVEW (429 ± 111 vs. -360 ± 77; P < 0.01) and MSNA burst incidence (34 ± 4 vs. 26 ± 4; P < 0.01) when compared with AT subjects. There was no difference in FMD between groups. MSNA burst incidence was also significantly related to AIx in subjects (R (2) = 0.61; P < 0.01) with a distinct demarcation between RT and AT subjects.Conclusion: These results confirm previous reports of a positive association between MSNA and AIx in young male resistance-trained subjects. Furthermore, RT is associated with increased arterial stiffness and elevated sympathetic outflow. [ABSTRACT FROM AUTHOR]

This study aimed to clarify whether there is an association between ventricular sympathetic nervous activity (SNA) and clinically relevant ventricular arrhythmia (a run of ≥3 consecutive ventricular beats, RVA) in postoperative patients with tetralogy of Fallot (TOF). We performed a retrospective study in a national referral center of pediatric cardiology in Japan. Twenty-four postoperative TOF patients (13 males, median age 17 years) undergoing myocardial I metaiodobenzylguanidine (MIBG) scintigraphy were included. We measured the heart-to-mediastinum ratio (HMR) and washout ratio (WR) from planar MIBG myocardial scintigraphy. Tomographic images and polar maps were generated with 20 segments. The standard deviation of percentage uptake of 20 segments (SD-uptake) as an index of heterogeneous MIBG uptake to the ventricular myocardium was calculated. We compared these MIBG-derived variables with the patients' clinical profiles, including ECG findings and hemodynamics. Eight of 24 patients had RVA (RVA group), and the other 16 did not have RVA (non-RVA group). There were no significant differences in the HMR (1.9 ± 0.5 vs. 2.2 ± 0.4) and WR (50 ± 5 vs. 42 ± 10) between the two groups. SD-uptake was significantly higher in the RVA group than in the non-RVA group (15 ± 3 vs. 12 ± 3, p = 0.03). QT dispersion (ms) was also higher in the RVA group than in the non-RVA group (53 ± 23 vs. 44 ± 18, p = 0.04). Multivariate logistic regression showed that SD-uptake and QT dispersion were independent predictors in the RVA group ( p = 0.02, p = 0.03). In addition to greater QT dispersion, heterogeneous SNA is associated with RVA in TOF patients postoperatively. [ABSTRACT FROM AUTHOR]

We have previously shown that sinusoidal galvanic vestibular stimulation (sGVS), delivered bilaterally at frequencies of 0.08-2.00 Hz, causes a pronounced modulation of muscle sympathetic nerve activity (MSNA) and skin sympathetic nerve activity (SSNA), together with robust frequency-dependent illusions of side-to-side motion. At low frequencies of sGVS (≤0.2 Hz), some subjects report nausea, so we tested the hypothesis that vestibular modulation of MSNA and SSNA is augmented in individuals reporting nausea. MSNA was recorded via tungsten microelectrodes inserted into the left common peroneal nerve in 22 awake, seated subjects; SSNA was recorded in 14 subjects. Bipolar binaural sGVS (±2 mA, 100 cycles) was applied to the mastoid processes at 0.08, 0.13, and 0.18 Hz. Nausea was reported by 21 out of 36 subjects (58 %), but across frequencies of sGVS there was no difference in the magnitude of the vestibular modulation of MSNA in subjects who reported nausea (27.1 ± 1.8 %) and those who did not (30.4 ± 2.9 %). This contrasts with the significantly greater vestibular modulation of SSNA with nausea (41.1 ± 2.0 vs. 28.7 ± 3.1 %) and indicates an organ-specific modulation of sympathetic outflow via the vestibular system during motion sickness. [ABSTRACT FROM AUTHOR]

Background: Tendinopathy is a clinical diagnosis of localised tendon pain often confirmed by imaging findings. The pathophysiological cause of the pain is unknown and the sympathetic nervous system (SNS) may be implicated. Objective: To review what is known regarding the role of the SNS in human tendinopathy. Study selection: Published data describing sympathetic innervation or an index of sympathetic activity in human tendons were eligible for inclusion. Data sources : Bibliographical databases (AMED, Biological Abstracts, CINAHL Plus, EMBASE, MEDLINE, Scopus, SPORTDiscus and Web of Science) were searched for relevant articles. Reference lists from included articles were screened for additional articles. Study appraisal: Studies were scored with a quality assessment tool to identify potential sources of bias. Each question had an explicit decision rule to guide assessment. Results: Nine case-control and four cross-sectional studies examined sympathetic innervation of tendons. There was evidence suggesting a lack of difference in sympathetic innervation of tendon proper between tendinopathy biopsies and healthy controls. In contrast, the paratendinous tissue showed evidence of increased sympathetic innervation in painful tendons. The most notable increase in SNS markers was seen in abnormal tenocytes from painful tendons. Data from two studies were suitable for meta-analysis. These heterogeneous studies revealed no difference in sympathetic innervation between painful and pain-free tendons. No studies recorded SNS activity in vivo. Conclusion: Sympathetic innervation in painful tendons depends on tissue type. Abnormal tenocytes may have increased capacity for self-production of sympathetic neurotransmitters. Future insight may be gained by measuring global in vivo sympathetic drive in tendinopathy. [ABSTRACT FROM AUTHOR]

The distributions of norepinephrinergic and nitroxidergic neurons in solitary tract nucleus, locus coeruleus, and in the small-celled and gigantocellular reticular nuclei were examined in sham-operated and experimental Wistar rats with induced renovascular hypertension. In control rats, the greatest population of norepinephrinergic cells was revealed in the projections of locus coeruleus and reticular gigantocellular nuclei, while the larger number of nitroxidergic neurons were observed in the solitary tract and the small-celled nuclei. During renovascular hypertension, the earliest and the most pronounced changes in luminescence intensity and the number of nitroxidergic neurons were observed in the solitary tract nucleus, while the changes in locus coeruleus were minimal. The significant changes in similar parameters of norepinephrinergic neurons were documented only in reticular gigantocellular nucleus and locus coeruleus, but they were delayed and less pronounced in comparison with the changes of nitroxidergic neurons. [ABSTRACT FROM AUTHOR]

Chemoreceptor activation increases phrenic nerve activity (PNA) and sympathetic nerve activity (SNA). The dorsolateral pontine neurons, including the parabrachial nucleus and the Kölliker-Fuse (KF) region project to several brainstem areas involved in autonomic and respiratory regulation. Here the objective was to further test the hypothesis that the KF region could contribute to central and peripheral sympathetic chemoreflex activation. In urethane-anesthetized sino-aortic denervated or intact and vagotomized male Wistar rats ( N = 7-8/group), hypercapnia (end-expiratory CO from 5 to 10 %) or KCN increased mean arterial pressure (MAP), splanchnic SNA, and PNA frequency and amplitude. Bilateral injection of muscimol (GABA-A agonist; 2 mM-50 nl) into the KF region increased resting PNA amplitude and reduced resting PNA frequency, without significant changes in resting MAP and SNA. Bilateral blockade of the KF region reduced the rise in MAP, sSNA, and PNA frequency and amplitude produced by hypercapnia or hypoxia. Our data suggest that the KF neurons could integrate and modulate breathing and sympathetic outflow during chemoreceptor activation. [ABSTRACT FROM AUTHOR]

The effect of peptide Semax on remodeling of cardiac sympathetic innervation was examined in rats with experimental myocardial infarction. In 28 days after ischemia/reperfusion injury, Semax diminished the growth of sympathetic innervation of ventricular septum, although it produced no effect on the density of β and β adrenoceptors. [ABSTRACT FROM AUTHOR]

Heart failure with reduced ejection fraction involves activation of the sympathetic nervous system and chronic hyperactivation of the sympatho-adrenergic receptors (ARs) β-ARs and α1-ARs, which are thought to be cardiotoxic and worsen pathological remodeling and function. Concurrently, the failing heart manifests significant decreases in sympathetic nerve terminal density, decreased cardiac norepinephrine levels, and marked downregulation of β-AR abundance and signaling. Thus, a state of both feast and famine coexist with respect to the adrenergic state in heart failure. For the failing heart, the hyperadrenergic state is toxic. However, the role of hypoadrenergic mechanisms in the pathophysiology of heart failure is less clear. Cardiotoxic effects are known to arise from the β1-AR subtype, and use of β-AR blockers is a cornerstone of current heart failure therapy. However, cardioprotective effects arise from the β2-AR subtype that counteract hyperactive β1-AR signaling, but unfortunately, β2-AR cardioprotective signaling in heart failure is inhibited by β-AR blocker therapy. In contrast to current dogma, recent research shows β1-AR signaling can also be cardioprotective. Moreover, for some forms of heart failure, β2-AR signaling is cardiotoxic. Thus for both β-AR subtypes, there is a balance between cardiotoxic versus cardioprotective effects. In heart failure, stimulation of α1-ARs is widely thought to be cardiotoxic. However, also contrary to current dogma, recent research shows that α1-AR signaling is cardioprotective. Taken together, recent research identifies cardioprotective signaling arising from β1-AR, β2-AR, and α1-ARs. A goal for future therapies will to harness the protective effects of AR signaling while minimizing cardiotoxic effects. The trajectory of heart failure therapy changed radically from the previous and intuitive use of sympathetic agonists, which unfortunately resulted in greater mortality, to the current use of β-AR blockers, which initially seemed counterintuitive. As a cautionary note, if the slow adoption of beta-blocker therapy in heart failure is any guide, then new treatment strategies, especially counterintuitive therapies involving stimulating β-AR and α1-AR signaling, may take considerable time to develop and gain acceptance. [ABSTRACT FROM AUTHOR]

A number of cardiovascular disease have been shown to be characterized by a marked increase in sympathetic drive to the heart and the peripheral circulation. This is the case for essential hypertension, congestive heart failure, cardiac arrhythmias, obesity, metabolic syndrome, obstructive sleep apnea, and chronic renal disease. This review focuses on the most recent findings documenting the role of sympathetic neural factors in the development and progression of the hypertensive state as well as in the pathogenesis of hypertension-related target organ damage. It also reviews the role of sympathetic neural factors in the development of cardiovascular diseases not necessarily strictly related to the hypertensive state, such as congestive heart failure, cardiac arrhythmias, obesity, metabolic syndrome and renal failure. The paper will finally review the pharmacological and non-pharmacological interventions acting on the sympathetic drive. Emphasis will be given to the new approaches, such as renal nerves ablation and carotid baroreceptor stimulation, which have been shown to exert sympathoinhibitory effects. [ABSTRACT FROM AUTHOR]

During high-intensity dynamic exercise, O delivery to active skeletal muscles is enhanced through marked increases in both cardiac output and skeletal muscle blood flow. When the musculature is vigorously engaged in exercise, the human heart lacks the pumping capacity to meet the blood flow demands of both the skeletal muscles and other organs such as the brain. Vasoconstriction must therefore be induced through activation of sympathetic nervous activity to maintain blood flow to the brain and to produce the added driving pressure needed to increase flow to the skeletal muscles. In this review, we first briefly summarize the local vascular and neural control mechanisms operating during high-intensity exercise. This is followed by a review of the major neural mechanisms regulating blood pressure during high-intensity exercise, focusing mainly on the integrated activities of the arterial baroreflex and muscle metaboreflex. In high cardiac output situations, such as during high-intensity dynamic exercise, small changes in total peripheral resistance can induce large changes in blood pressure, which means that rapid and fine regulation is necessary to avoid unacceptable drops in blood pressure. To accomplish this rapid regulation, arterial baroreflex function may be modulated in various ways through activation of the muscle metaboreflex and/or other neural mechanisms. Moreover, this modulation of the arterial baroreflex may change over the time course of an exercise bout, or to accommodate changes in exercise intensity. Within this model, integration of arterial baroreflex modulation with other neural mechanisms plays an important role in cardiovascular control during high-intensity exercise. [ABSTRACT FROM AUTHOR]

During weightlessness, blood and fluids are immediately shifted from the lower to the upper body segments, and within the initial 2 weeks of spaceflight, brachial diastolic arterial pressure is reduced by 5 mmHg and even more so by some 10 mmHg from the first to the sixth month of flight. Blood pressure thus adapts in space to a level very similar to that of being supine on the ground. At the same time, stroke volume and cardiac output are increased and systemic vascular resistance decreased, whereas sympathetic nerve activity is kept surprisingly high and similar to when ground-based upright seated. This was not predicted from simulation models and indicates that dilatation of the arteriolar resistance vessels is caused by mechanisms other than a baroreflex-induced decrease in sympathetic nervous activity. Results of baroreflex studies in space indicate that compared to being ground-based supine, the carotid (vagal)-cardiac interaction is reduced and sympathetic nerve activity, heart rate and systemic vascular resistance response more pronounced during baroreflex inhibition by lower body negative pressure. The future challenge is to identify which spaceflight mechanism induces peripheral arteriolar dilatation, which could explain the decrease in blood pressure, the high sympathetic nerve activity and associated cardiovascular changes. It is also a challenge to determine the cardiovascular risk profile of astronauts during future long-duration deep space missions. [ABSTRACT FROM AUTHOR]

Though conventional wisdom suggests that a rise in blood pressure is a reality of advancing age, in fact, it appears that progressive elevation in sympathetic activity, not necessarily accompanied by increased blood pressure, is intrinsic to cardiovascular aging in humans. The mechanism behind this elevation would seem to reside in homeostatic cardiovascular regulation; nonetheless, the balance of factors that result in elevated sympathetic outflow with age remains elusive. Age-related increases in sympathetic nervous outflow cannot be fully explained by increases in body mass, body adiposity, or other metabolic factors; interrelations among cardiac output, peripheral resistance, and blood pressure may not reflect a determinative hemodynamic interrelation but rather parallel phenomena; and there is no simple linear relationship between baroreflex control and resting levels of sympathetic activity. In contrast to systemic relationships, available data suggest that elevated sympathetic outflow may derive from the inter-relationship between centrally driven sympathoexcitation and a decline in the ability of sympathetic outflow to effect peripheral vascular responses. This review aims to integrate the current knowledge of mechanisms underlying elevated sympathetic outflow with age. It seeks to synthesize these data in the context of proposing that an age-related decline in the ability of sympathetic outflow to effect regional vascular responses incites a compensatory elevation in resting sympathetic activity to maintain homeostatic balance, presumably to maintain adequate control of blood pressure. [ABSTRACT FROM AUTHOR]

Introduction: Our study aimed to disclose the relationship of cardiac sympathetic nerve innervation and excitability to myocardial hypertrophy in very old elderly male hypertensive patients with low serum testosterone level. Methods: A total of 80 elderly male hypertensive patients aged from 80 to 95 years were recruited. Heart rate variability is determined by 24 h dynamic electrocardiogram and heart rate variability analysis system. Cardiac function and left ventricular mass index were determined using color Doppler ultrasound. Results: Standard deviation of all normal sinus R-R intervals over 24 h (SDNN) significantly decreased in hypertensive cardiac hypertrophy patients as compared with those without cardiac hypertrophy. SDANN and Standard deviation of the average normal sinus R-R intervals for all 5-min segment index, time-domain index reflecting sympathetic nerve tension, obviously decreased and LFnu and LFnu/HFnu, frequency-domain index representing sympathetic nerve excitability, significantly increased in hypertensive cardiac hypertrophy patients as compared with those without cardiac hypertrophy. Myocardial norepinephrine content significantly increased while tyrosine hydroxylase expression significantly lowered in hypertensive cardiac hypertrophy patients, and a negative correlation between myocardial tyrosine hydroxylase expression and myocardial norepinephrine content was present. Serum total testosterone level decreased in hypertensive cardiac hypertrophy patients and was an independent risk factor for the increase in myocardial norepinephrine content and decrease in tyrosine hydroxylase expression. Conclusions: These data confirm that cardiac sympathetic nerve hypoinnervation and relative increase in cardiac sympathetic nerve excitability are closely related to cardiac hypertrophy in very old hypertensive patients. A lower serum total testosterone level was the independent risk factor of cardiac sympathetic nerve hypoinnervation and relative increase in excitability in very old male hypertensive patients. [ABSTRACT FROM AUTHOR]

The aim of the present work was to perform a comparative study of the magnitudes of spontaneous and evoked (by single afferent stimuli) activity in a sympathetic nerve in animals with arterial hypertension of different causes. Acute experiments on anesthetized Wistar rats with renovascular hypertension and rats of the spontaneously hypertensive strain SHR were performed to record spontaneous and evoked (somatosympathetic reflex) activity in the cervical sympathetic trunk. Tonic electrical activity in the sympathetic nerve in hypertensive rats was greater than that in normotensive individuals. The magnitudes of the somatosympathetic reflex in rats with models of arterial hypertension differed from that of the reflex in control animals. The magnitude of the reflex was decreased in rats with the renovascular model of hypertension, while the reflex was increased in rats with spontaneous hypertension, as compared with normotensive animals. The time characteristics of the reflex in hypertensive rats also showed differences. It is suggested that different components of the brainstem show different changes in their functional activity in rats with different experimental models of hypertension. [ABSTRACT FROM AUTHOR]

Bone remodeling is essential for adult bone homeostasis. The failure of this process often leads to the development of osteoporosis, a present major global health concern. The most important factor that affects normal bone remodeling is the tightly controlled and orchestrated regulation of osteoblasts and osteoclasts. The present review summarized the recent discoveries related to osteoblast regulation from several signals, including transforming growth factor-β, bone morphogenetic proteins, Wnt signal, Notch, Eph-Ephrin interaction, parathyroid hormone/parathyroid hormone-related peptide, and the leptin-serotonin-sympathetic nervous systemic pathway. The awareness of these mechanisms will facilitate further research that explores bone remodeling and osteoporosis. Future investigations on the endogenous regulation of osteoblastogenesis will increase the current knowledge required for the development of potential drug targets in the treatment of osteoporosis. [ABSTRACT FROM AUTHOR]

Objectives: Comparisons of sympathetic nervous system activity (SNA) between young and older women have produced equivocal results, in part due to inadequate control for potential differences in sex hormone concentrations, age, and body composition. The aim of the present study was to determine the effect of a short-term reduction in sex hormones on tonic skeletal muscle sympathetic nerve activity (MSNA), an indirect measure of whole body SNA, using an experimental model of sex hormone deficiency in young women. We also assessed the independent effects of estradiol and progesterone add-back therapy on MSNA. Methods: MSNA was measured in 9 women (30 ± 2 years; mean ± SE) on three separate occasions: during the mid-luteal menstrual cycle phase, on the fifth day of gonadotropin-releasing hormone antagonist (GnRHant) administration, and after 5 days add-back of either estradiol ( n = 4) or progesterone ( n = 3) during continued GnRHant administration. Results: In response to GnRHant, there were significant reductions in serum estradiol and progesterone (both p < 0.01) and MSNA (25.0 ± 1.9 vs. 19.2 ± 2.4 bursts/min, p = 0.04). Continued GnRHant plus add-back estradiol or progesterone resulted in a nonsignificant decrease (19.2 ± 1.7 vs. 12.1 ± 1.9 bursts/min, p = 0.07) or increase (16.2 ± 1.7 vs. 21.0 ± 6.0 bursts/min, p = 0.39), respectively, in MSNA when compared with GnRHant alone. Interpretation: The findings of this preliminary study suggest that short-term ovarian hormone suppression attenuates MSNA and that this may be related to the suppression of progesterone rather than estradiol. [ABSTRACT FROM AUTHOR]

β2-Adrenergic receptor agonists are believed to present with ergogenic properties. However, how combined respiratory, cardiovascular and muscular effects of these drugs might affect exercise capacity remain incompletely understood. The effects of salbutamol were investigated in 23 healthy subjects. The study was randomised, placebo-controlled in double-blind and followed a cross-over design. Salbutamol was given at the dose of 10 μg/min in 11 subjects and 20 μg/min iv in the other 12 subjects. Measurements included muscle sympathetic nerve activity (MSNA), ventilatory responses to hyperoxic hypercapnia (7% CO(2) in O(2,) central chemoreflex), isocapnic hypoxia (10% O(2) in N(2), peripheral chemoreflex) and isometric muscle contraction followed by a local circulatory arrest (metaboreflex), cardiopulmonary exercise test (CPET) variables and isokinetic muscle strength. Salbutamol 10 μg/min increased heart rate and blood pressure, while MSNA burst frequency remained unchanged. Peripheral chemosensitivity increased, as evidenced by an increased ventilatory response to hypoxia, but ventilatory responses to hypercapnia or muscle ischaemia remained unchanged. The effects of salbutamol 20 μg/min were similar. Both doses of salbutamol did not affect CPET. Only the higher dose of salbutamol decreased the anaerobic threshold, but this was not associated with a change in VO(2) max. Salbutamol increased the slopes of ventilation as a function of VO(2) (P < 0.05) and VCO(2) (P < 0.001) during CPET. Maximal isokinetic muscle strength was not affected by salbutamol. In conclusion, the acute administration of either low or high dose salbutamol does not affect exercise capacity in normal subjects, in spite of an earlier anaerobic threshold and increased chemosensitivity. [ABSTRACT FROM AUTHOR]

The study was designed to assess the effects of local heat (LH) application on postganglionic muscle sympathetic nerve activity (MSNA) measured by microneurography in healthy men. In the first protocol, MSNA of the left peroneal nerve, blood pressure (BP), heart rate (HR), and skin temperature of the shin (TSK) were recorded in nine men. In the second protocol, leg blood flow (LBF) was measured in the same subjects by strain-gauge plethysmography. In both protocols, after 10 min of rest in the supine position, a heated hydrocollator pack was applied to the shin and anterior foot for 15 min and recovery was monitored over a period of 20 min. TSK gradually increased from 31.7 ± 0.1 to 41.9 ± 0.5°C (mean ± SEM) during LH. No subject complained of pain, and BP and HR remained constant. The MSNA burst rate (16.1 ± 2.1 beats/min) during the control period decreased significantly (P < 0.05) to 72.0 ± 2.3% during LH. Total MSNA also decreased to 59.2 ± 2.6% (P < 0.05) during LH, but both immediately returned to baseline at recovery. In contrast, LBF in the left leg significantly and immediately increased (P < 0.05) after LH application and remained significantly elevated until the end of the recovery period. These results suggest that: (1) LH application significantly attenuates MSNA without any changes in HR and BP. (2) Other factors in addition to MSNA seem to control regional blood flow in the lower extremity during LH. [ABSTRACT FROM AUTHOR]

We examined a hypothesis that static exercise and activation of sympathetic activation by metabolically sensitive skeletal muscle afferents (metaboreflex) influence the sympathetic nervous activity modulating pupil diameter. Nine subjects performed 2 min isometric handgrip exercise at 30% maximal voluntary contraction, which was followed by either 2 min of postexercise muscle ischemia (PEMI) in the forearm or no PEMI (control trial). The pupil diameter and mean blood pressure (MAP) increased significantly from rest during exercise in PEMI and control trials (5 ± 1 and 7 ± 1% in diameter; 13 ± 2 and 12 ± 2 mmHg in MAP, respectively). These increases in the diameter and MAP were maintained during PEMI (7 ± 2% and 9 ± 2 mmHg) but not during the recovery period in the control trial (3 ± 2% and 1 ± 2 mmHg). These results demonstrate that static handgrip exercise increases the pupil diameter, and this increase is partly due to the activation of metaboreflex in humans. [ABSTRACT FROM AUTHOR]

Study design:Controlled experimental human study.Objectives:To assess insulin resistance (IR) in tetraplegia and paraplegia, and the role of the spinal cord (SC) in glucose regulation.Setting:Laboratory of Spinal Research, Loewenstein Rehabilitation Hospital.Methods:Glucose and insulin levels and the heart rate variation spectral components LF (low frequency), HF (high frequency) and LF/HF were studied at supine rest, head-up tilt and after a standard meal in three groups: 13 healthy subjects, 7 patients with T4-T6 paraplegia and 11 patients with C4-C7 tetraplegia.Results:Glucose and insulin increased significantly after the meal in all groups (P<0.001). Glucose increased significantly more in the tetraplegia than in the other groups (P<0.01). Increases in insulin level tended to accompany increases in LF/HF after the meal in the tetraplegia and control groups but not in the paraplegia group.Conclusion:Post-prandial IR appears in C4-C7 but not in T4-T6 SC injury. The results of the study, combined with previously published findings, are consistent with the hypotheses that IR is related to activation of the sympathetic nervous system, and that below T4 the mid-thoracic SC is involved in the regulation of glucose and insulin levels. [ABSTRACT FROM AUTHOR]

Resting energy expenditure of persons with a spinal cord injury (SCI) is generally lower than that seen in able-bodied (AB) individuals due to the reduced amounts of muscle mass and sympathetic nervous system available. However, outside of clinical studies, much less data is available regarding athletes with an SCI. In order to predict the energy expenditure of persons with SCI, the generation and validation of prediction equations in relation to specific levels of SCI and training status are required. Specific prediction equations for the SCI would enable a quick and accurate estimate of energy requirements. When compared with the equivalent AB individuals, sports energy expenditure is generally reduced in SCI with values representing 30-75% of AB values. The lowest energy expenditure values are observed for sports involving athletes with tetraplegia and where the sport is a static version of that undertaken by the AB, such as fencing. As with AB sports there is a lack of SCI data for true competition situations due to methodological constraints. However, where energy expenditure during field tests are predicted from laboratory-based protocols, wheelchair ergometry is likely to be the most appropriate exercise mode. The physiological and metabolic responses of persons with SCI are similar to those for AB athletes, but at lower absolute levels. However, the underlying mechanisms pertaining to substrate utilization appear to differ between the AB and SCI. Carbohydrate feeding has been shown to improve endurance performance in athletes with generally low levels of SCI, but no data have been reported for mid to high levels of SCI or for sport-specific tests of an intermittent nature. Further research within the areas reviewed may help to bridge the gap between what is known regarding AB athletes and athletes with SCI (and other disabilities) during exercise and also the gap between clinical practice and performance. [ABSTRACT FROM AUTHOR]

During mild cold exposure, elderly are at risk of hypothermia. In humans, glabrous skin at the hands is well adapted as a heat exchanger. Evidence exists that elderly show equal vasoconstriction due to local cooling at the ventral forearm, yet no age effects on vasoconstriction at hand skin have been studied. Here, we tested the hypotheses that at hand sites (a) elderly show equal vasoconstriction due to local cooling and (b) elderly show reduced response to noradrenergic stimuli. Skin perfusion and mean arterial pressure were measured in 16 young adults (Y: 18-28 years) and 16 elderly (E: 68-78 years). To study the effect of local vasoconstriction mechanisms local sympathetic nerve terminals were blocked by bretylium (BR). Baseline local skin temperature was clamped at 33 degrees C. Next, local temperature was reduced to 24 degrees C. After 15 min of local cooling, noradrenaline (NA) was administered to study the effect of neural vasoconstriction mechanisms. No significant age effect was observed in vasoconstriction due to local cooling at BR sites. After NA, vasoconstriction at the forearm showed a significant age effect; however, no significant age effect was found at the hand sites. [Change in CVC (% from baseline): Forearm Y: -76 +/- 3 vs. E: -60 +/- 5 (P < 0.01), dorsal hand Y: -74 +/- 4 vs. E: -72 +/- 4 (n.s.), ventral hand Y: -80 +/- 7 vs. E: -70 +/- 11 (n.s.)]. In conclusion, in contrast to results from the ventral forearm, elderly did not show a blunted response to local cooling and noradrenaline at hand skin sites. This indicates that at hand skin the noradrenergic mechanism of vasoconstriction is maintained with age. [ABSTRACT FROM AUTHOR]

The aim of human temperature regulation is to protect body processes by establishing a relative constancy of deep body temperature (regulated variable), in spite of external and internal influences on it. This is basically achieved by a distributed multi-sensor, multi-processor, multi-effector proportional feedback control system. The paper explains why proportional control implies inherent deviations of the regulated variable from the value in the thermoneutral zone. The concept of feedback of the thermal state of the body, conveniently represented by a high-weighted core temperature (T (c)) and low-weighted peripheral temperatures (T (s)) is equivalent to the control concept of "auxiliary feedback control", using a main (regulated) variable (T (c)), supported by an auxiliary variable (T (s)). This concept implies neither regulation of T (s) nor feedforward control. Steady-states result in the closed control-loop, when the open-loop properties of the (heat transfer) process are compatible with those of the thermoregulatory processors. They are called operating points or balance points and are achieved due to the inherent property of dynamical stability of the thermoregulatory feedback loop. No set-point and no comparison of signals (e.g. actual-set value) are necessary. Metabolic heat production and sweat production, though receiving the same information about the thermal state of the body, are independent effectors with different thresholds and gains. Coordination between one of these effectors and the vasomotor effector is achieved by the fact that changes in the (heat transfer) process evoked by vasomotor control are taken into account by the metabolic/sweat processor. [ABSTRACT FROM AUTHOR]

This review first considers how mammalian body temperature regulation evolved, and how the brain's responses to thermoregulatory challenges are likely to be organised differently from the way an engineer would design them. This is because thermoregulatory effector mechanisms would have evolved one at a time, with each being superimposed on pre-existing mechanisms. There may be no functional need for the final ensemble of control loops to be coordinated by neural cross-connections: appropriate thermal thresholds would solve the problem sufficiently. Investigations first into thermoregulatory behaviours and later into unconscious thermoregulatory mechanisms (autonomic and shivering) have led investigators to the realisation that multiple control loops exist in the brain, with each effector system apparently regulated by its own central temperature sensors. This theme is developed with reference to data on four temperature-regulated neural outflows that have been studied on anaesthetized rats under standard conditions in the authors' laboratory. Direct comparisons were made between the behaviour of sympathetic nerves supplying the tail vasculature, vessels in the proximal hairy skin, interscapular brown adipose tissue (BAT) and fusimotor fibres to hind limb muscle. All four outflows were activated by cooling the skin, and all were silenced by neuronal inhibition in the medullary raphé. Their thermal thresholds were quite different, however, as were their relative responsiveness to core temperature. This was ranked as: tail > back skin > BAT > fusimotor. These and other data indicate that the four thermoeffector outflows are driven by separate neural pathways, each regulated by independent brain temperature sensors. [ABSTRACT FROM AUTHOR]

Increases in core temperature (T (c)) augment stress hormones and neurotransmitters; however, the effect of different T (c) tolerated with varying fitness levels during uncompensable exertional heat stress (EHS) is unclear. The purpose was to examine the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic-adrenomedullary system (SAS) responses during uncompensable EHS in trained (TR) versus untrained (UT) males. Twelve TR and 11 UT (VO(2peak) = 70 +/-2 and 50 +/- 1 mL kg of lean body mass(-1) min(-1)) walked on a treadmill to exhaustion (EXH) in 40 degrees C (dry), dressed in protective clothing. PRE and 0.5 degrees C T (c) increments from 38.0-40.0 degrees C/EXH venous blood was obtained. Cortisol responded to absolute thermal strain, increasing throughout EHS and independent of fitness. Adrenocorticotropic Hormone, Norepinephrine, and Dehydroepiandrosterone-Sulphate responded to relative thermal strain with similar EXH values, despite higher T (c) tolerated for TR (39.7 degrees C) than UT (39.0 degrees C). Epinephrine, Growth Hormone (GH), and Aldosterone increased initially, with a plateau above 38.5 degrees C T (c). Findings demonstrate the complexity of the HPA axis, SAS, and T (c) relationship, with the stress pathways responding largely to relative thermal strain, although some hormones exhibited a clamping response likely as a protective mechanism. For the TR, evidence existed for a reduced pituitary sensitivity to glucocorticoids and the amplified GH may have contributed to their greater T (c) tolerated. [ABSTRACT FROM AUTHOR]

It was already established that exposure to hyperbaric conditions induces vagal-depended bradycardia but field study on autonomic nervous system (ANS) activity during self-contained underwater breathing apparatus (SCUBA) diving is lacking. The aim of the present study was to evaluate ANS modifications during real recreational SCUBA diving using heart rate variability analysis (timedomain, frequency-domain and Poincaré plot) in 10 experienced and volunteers recreational divers. Mean RR, root mean square of successive differences of interval (rMSSD), high frequency of spectral analysis and standard deviation 1 of Poincaré Plot increased (P < 0.05) during dive. Low frequency/high frequency ratio decreased during dive (P < 0.05) but increased after (P < 0.05). Recreational SCUBA diving induced a rise in vagal activity and a decrease in cardiac sympathetic activity. Conversely, sympathetic activity increases (P < 0.05) during the recovery. [ABSTRACT FROM AUTHOR]

Estrogens are involved in the modulation of the cardiovascular system, yet their effects in young women remains largely unknown. Women who undergo ovulation induction treatments attain extremely high estrogen concentrations during a very short time period. The aim of the present study was to evaluate the effects of an acute increase in estrogens on the autonomic nervous system modulation of heart rate variability (HRV). A total of 27 women undergoing ovulation induction and 14 normally menstruating women were prospectively studied. HRV was assessed during nadir and peak estrogen using time domain and power spectral density analyses. A significant increase in high-frequency spectral power (243 +/- 77 vs. 188 +/- 73 ms(2)/Hz, P < 0.01) with a significant decrease in the ratio of low to high-frequency power was observed during estrogen peak in women undergoing induction of ovulation. The acute increase in estrogen in women undergoing ovulation induction was associated with vagal activation and altered sympathovagal balance. [ABSTRACT FROM AUTHOR]