Baroreflex Sensitivity Research Articles

Load-Dependent Mechanisms Contribute to Increased Aortic Stiffness Among Women with a History of Preeclampsia: Relation with Cardiovagal Baroreflex Sensitivity.

Introduction: Preeclampsia, a hypertensive disorder of pregnancy, results in increased lifetime cardiovascular disease (CVD) risk. Total aortic stiffness, a robust risk factor for CVD, is composed of load-dependent (blood pressure load on arterial wall) and structural (intrinsic changes in arterial wall) mechanisms. Total aortic stiffness is also associated with reduced cardiovagal baroreflex sensitivity (BRS). We sought to determine 1) whether elevated total aortic stiffness among women with a history of preeclampsia (hxPE) is attributed to load-dependent or structural stiffness, and 2) whether either mechanism is associated with lower BRS. Methods: Total aortic stiffness (carotid-femoral pulse wave velocity) and spontaneous cardiovagal BRS (sequence technique) were measured among women 1-5 years postpartum (n=115; age 34 ±4yrs; hxPE n=51; controls n=64). Structural aortic stiffness was calculated from participant-specific exponential models, standardizing aortic stiffness to a 'reference' blood pressure. Load-dependent stiffness was calculated as total minus structural stiffness. Results: Total (+0.8 m/sec, 95% CI (-0.99, -0.23), p=0.002) and load-dependent (+0.4 m/sec, 95% CI (-0.56, -0.22), P<0.001), but not structural (95% CI (-0.52, 0.08), p=0.16), aortic stiffness were higher among women with hxPE compared with controls. Women with a hxPE had lower BRS (p=0.042) that was negatively associated with total (B =-3.24 ms/mmHg, 95% CI (-6.35, -0.13), p=0.042) and load-dependent (B =-5.91ms/mmHg, 95% CI (-11.31, -0.51), p=0.033) aortic stiffness. Conclusion: Load-dependent, not structural, aortic stiffness mechanisms contribute to higher total aortic stiffness among women with hxPE and was associated with lower cardiovagal BRS. Postpartum BP monitoring is critical to reduce increased CVD risk in preeclampsia.

The cardiac, vasomotor and myocardial branches of the baroreflex in hypotension: indications of reduced venous return to the heart.

Alterations of autonomic cardiovascular control are implicated in the origin of chronic low blood pressure (BP) (hypotension), but comprehensive analysis of baroreflex function is still lacking. This study explored baroreflex function in its cardiac, vascular and myocardial branches METHODS: Continuous BP was recorded at rest and during a mental arithmetic task in 40 hypotensive and 40 normotensive participants. Assessed cardiovascular variables included stroke volume (SV) (calculated by the Modelflow method), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR) and heart rate variability (HRV). Baroreflex sensitivity (BRS) was calculated using the spontaneous sequence method. Hypotensive participants exhibited greater BRS in the three baroreflex branches, in addition to lower SV, HR and CO and higher HRV and TPR. Reactivity for BP, HRV and CO during the stress task was reduced in hypotensive individuals. The greater cardiac BRS can explain the lower HR and higher HRV observed in hypotension, suggestive of increased vagal cardiac influences. The higher vasomotor BRS may contribute to the greater TPR observed in the hypotensive participants. Abnormal associations between myocardial BRS and SV arose, suggesting aberrant autonomic control of myocardial contractility in hypotension. The results indicate that hemodynamic deficits in hypotension are related to preload factors, probably triggered by hypovolemia and reduced unstressed blood reserves, resulting in lower venous return, ventricular preload and SV. In contrast, afterload mechanisms seem to work appropriately.

The Autonomic Nervous System (ANS)-Immune Network in People Living With HIV.

Pre-clinical studies have demonstrated direct influences of the sympathetic and vagal/parasympathetic branches of the autonomic nervous system (ANS) on the immune system. The relevance of these pathways to the development of inflammatory disorders in humans remains unknown. We hypothesized that a comprehensive examination of the ANS-immune network in patients with HIV, would reveal that the type and severity of autonomic neuropathy (AN) would predict immune phenotypes with distinct clinical and demographic characteristics. This is a cross-sectional study of 79 adult people with a history of well-controlled HIV on stable combination antiretroviral treatment (CART) recruited from a primary care clinic network within the Mount Sinai Health System in New York City. All participants underwent a standardized battery of autonomic function tests summarized as the Composite Autonomic Severity Score (CASS) and vagal and adrenergic baroreflex sensitivity (BRS-V and BRS-A). Immune profiling included: 1) measurement of interleukin-6 (IL-6) as part of the Olink assay Target 96 Inflammation Panel, 2) non-negative matrix factorization (NMF) clustering analyses on Olink immune biomarkers, and 3) mass cytometry (CyTOF) on a subset of participants with and without autonomic neuropathy (N = 10). Reduced activity of caudal vagal circuitry involved in the cholinergic anti-inflammatory pathway (CAP) predicted higher levels of IL-6 (Spearman's rho = -0.352, p=0.002). The comprehensive assessment of the ANS-immune network showed four immunotypes defined by NMF analyses. A pro-inflammatory immunotype defined by elevations in type 1 cytokines (IL-6, IL-17) and increased numbers of CD8+ T-cells was associated with autonomic neuropathy (AN). This association was driven by deficits in the cardiovascular sympathetic nervous system and remained strongly significant after controlling for the older age and greater burden of co-morbid illness among participants with this immunotype (aOR=4.7, p=0.017). Our results provide novel support for the clinical relevance of the CAP in patients with chronic inflammatory AN. These data also provide insight regarding the role of the sympathetic nervous system and aging in the progression and development of co-morbidities in patients with chronic HIV and support future research aimed at developing therapies focused on modulation of the sympathetic and parasympathetic/vagal nervous system.

Acute cardiovascular responses of postmenopausal women to resistance training sessions differing in set configuration: A study protocol for a crossover trial.

Resistance training is hardly recommended for postmenopausal women to counteract negative effects of hormonal changes. However, some concern exists about the marked hemodynamic responses caused by high-load resistance exercises. In this regard, studies on young, healthy, physically active individuals suggest that set configuration can modulate acute cardiovascular, metabolic, and cardiac autonomic responses caused by resistance training sessions, but this has not yet been explored in postmenopausal women. A sample of 60 physically active postmenopausal women (30 normotensive, 30 hypertensive) will participate in this crossover study. After a medical exam, ergometry, familiarization session, and two testing sessions, participants will complete three experimental sessions and one control session in a randomized order. Each experimental session includes 36 repetitions of four exercises (horizontal leg press, bench press, prone leg curl, and lat pull-down) differing in set configuration: 9 sets of 4 repetitions (i.e., 33% intensity of effort) with 45 s of inter-set recovery, 6 sets of 6 repetitions (50% intensity of effort) with 72 s, and 4 sets of 9 repetitions (75% intensity of effort) with 120 s; with 4 min rest between exercises. Before and immediately after each session, arterial stiffness, hemodynamic variables, cardiac autonomic modulation, baroreflex sensitivity, sympathetic vasomotor tone, and resting oxygen uptake will be evaluated. Furthermore, perceived effort, mechanical performance (e.g., power, velocity), heart rate, and lactatemia will be collected throughout sessions. The impact of set configuration on these variables will be analyzed, along with comparisons between normotensive and hypertensive women. Cardiovascular responses to resistance exercise have been scarcely studied in females, particularly postmenopausal women. The results of this study will provide information about the modulating role of set structure on metabolic and cardiovascular responses of normotensive and hypertensive postmenopausal women to resistance training. NCT05544357 on 7 December 2022.

Pre-existing parasympathetic dominance seems to cause persistent heart rate slowing after 6months of fingolimod treatment in patients with multiple sclerosis.

Vagomimetic fingolimod effects cause heart rate (HR) slowing upon treatment initiation but wear off with sphingosine-1-phosphate receptor downregulation. Yet, prolonged HR slowing may persist after months of fingolimod treatment. We evaluated whether cardiovascular autonomic modulation differs before and 6months after fingolimod initiation between patients with RRMS with and without initially prolonged HR slowing upon fingolimod initiation. In 34 patients with RRMS, we monitored RR intervals (RRI) and blood pressure (BP), at rest and upon standing up before fingolimod initiation. Six hours and 6months after fingolimod initiation, we repeated recordings at rest. At the three time points, we calculated autonomic parameters, including RRI standard deviation (RRI-SD), RRI-total-powers, RMSSD, RRI high-frequency [HF] powers, RRI and BP low-frequency (LF) powers, and baroreflex sensitivity (BRS). Between and among patients with and without prolonged HR slowing upon fingolimod initiation, we compared all parameters assessed at the three time points (analysis of variance [ANOVA] with post hoc testing; significance: p < 0.05). Six hours after fingolimod initiation, all patients had decreased HRs but increased RRIs, RRI-SDs, RMSSDs, RRI-HF-powers, RRI-total-powers, and BRS; 11 patients had prolonged HR slowing. Before fingolimod initiation, these 11 patients did not decrease parasympathetic RMSSDs and RRI-HF-powers upon standing up. After 6months, all parameters had reapproached pretreatment values but the 11 patients with prolonged HR slowing had lower HRs while the other 23 patients had lower parasympathetic RMSSDs and RRI-HF-powers, and BRS than before fingolimod initiation. Our patients with prolonged HR slowing upon fingolimod initiation could not downregulate cardiovagal modulation upon standing up even before fingolimod initiation, and 6months after fingolimod initiation still had more parasympathetic effect on HR while cardiovagal modulation and BRS were attenuated in the other 23 patients. Pre-existing parasympathetic predominance may cause prolonged HR slowing upon fingolimod initiation.

Investigating the effects of artificial baroreflex stimulation on pain perception: A comparative study in no-pain and chronic low back pain individuals.

The autonomic nervous system (ANS) and pain exhibit a reciprocal relationship, where acute pain triggers ANS responses, whereas resting ANS activity can influence pain perception. Nociceptive signalling can also be altered by 'top-down' processes occurring in the brain, brainstem and spinal cord, known as 'descending modulation'. By employing the conditioned pain modulation (CPM) paradigm, we previously revealed a connection between reduced low-frequency heart rate variability and CPM. Individuals with chronic pain often experience both ANS dysregulation and impaired CPM. Baroreceptors, which contribute to blood pressure and heart rate variability regulation, may play a significant role in this relationship, although their involvement in pain perception and their functioning in chronic pain have not been sufficiently explored. In the present study, we combined artificial 'baroreceptor stimulation' in both pressure pain and CPM paradigms, seeking to explore the role of baroreceptors in pain perception and descending modulation. In total, 22 individuals with chronic low back pain (CLBP) and 29 individuals with no-pain (NP) took part in the present study. We identified a differential modulation of baroreceptor stimulation on pressure pain between the groups of NP and CLBP participants. Specifically, NP participants perceived less pain in response to baroreflex activation, whereas CLBP participants exhibited increased pain sensitivity. CPM scores were associated with baseline measures of baroreflex sensitivity in both CLBP and NP participants. Our data support the importance of the baroreflex in chronic pain and a possible mechanism of dysregulation involving the interaction between the ANS and descending pain modulation. KEY POINTS: Baroreflex stimulation has different effects on pressure pain in participants with chronic pain compared to matched individuals with no-pain. Baroreceptor activation decreases pain in participants with no-pain but increases pain perception in participants with chronic pain. Baroreflex sensitivity is associated with conditioned pain modulation in both groups of chronic pain and no-pain participants. The reactivity of the baroreflex during autonomic stress demonstrated a positive correlation with Pain Trait scores in participants with chronic back pain.

Hypertension disrupts the vascular clock in both sexes.

Blood pressure (BP) displays a circadian rhythm and disruptions in this pattern elevate cardiovascular risk. Although both central and peripheral clock genes are implicated in these processes, the importance of vascular clock genes is not fully understood. BP, vascular reactivity, and the renin-angiotensin-aldosterone system display overt sex differences, but whether changes in circadian patterns underlie these differences is unknown. Therefore, we hypothesized that circadian rhythms and vascular clock genes would differ across sex and would be blunted by angiotensin II (ANG II)-induced hypertension. ANG II infusion elevated BP and disrupted circadian patterns similarly in both males and females. In females, an impact on heart rate (HR) and locomotor activity was revealed, whereas in males hypertension suppressed baroreflex sensitivity (BRS). A marked disruption in the vascular expression patterns of period circadian regulator 1 (Per1) and brain and muscle aryl hydrocarbon receptor nuclear translocator like protein 1 (Bmal1) was noted in both sexes. Vascular expression of the G protein-coupled estrogen receptor (Gper1) also showed diurnal synchronization in both sexes that was similar to that of Per1 and Per2 and disrupted by hypertension. In contrast, vascular expression of estrogen receptor 1 (Esr1) showed a diurnal rhythm and hypertension-induced disruption only in females. This study shows a strikingly similar impact of hypertension on BP rhythmicity, vascular clock genes, and vascular estrogen receptor expression in both sexes. We identified a greater impact of hypertension on locomotor activity and heart rate in females and on baroreflex sensitivity in males and also revealed a diurnal regulation of vascular estrogen receptors. These insights highlight the intricate ties between circadian biology, sex differences, and cardiovascular regulation.NEW & NOTEWORTHY This study reveals that ANG II-induced hypertension disrupts the circadian rhythm of blood pressure in both male and female mice, with parallel effects on vascular clock gene and estrogen receptor diurnal patterns. Notably, sex-specific responses to hypertension in terms of locomotor activity, heart rate, and baroreflex sensitivity are revealed. These findings pave the way for chronotherapeutic strategies tailored to mitigate cardiovascular risks associated with disrupted circadian rhythms in hypertension.

Spontaneous Cardiovagal Baroreflex Sensitivity Following A Bout Of Subconcussive Head Impacts Is Not Altered

Spontaneous Cardiovagal Baroreflex Sensitivity Following A Bout Of Subconcussive Head Impacts Is Not Altered

Meeting Muscle Strengthening Guidelines Is Associated With Better Cardiovagal Baroreflex Sensitivity In Adults

Meeting Muscle Strengthening Guidelines Is Associated With Better Cardiovagal Baroreflex Sensitivity In Adults

Chronic cannabidiol treatment induces cardiovascular improvement in renovascular hypertensive rats.

Cannabidiol (CBD) is increasingly studied for its therapeutic potential in neurodegenerative diseases. Previous research on acute CBD administration has demonstrated cardiovascular benefits in hypertensive rats, including reduced mean blood pressure and oxidative stress. To investigate the long-term cardiovascular effects of chronic CBD treatment in renovascular hypertension induced by the 2-kidney-1-clip (2K1C) model. Male Wistar rats (180-200 g, 8 weeks old) underwent 2K1C or SHAM surgery. Six weeks later, rats received chronic CBD treatment (20 mg/kg, twice daily for 14 days). A combination of ex vivo, in vitro, and in vivo methods was used to assess CBD's cardiovascular effects in 2K1C hypertensive rats. Chronic CBD treatment significantly reduced blood pressure and the depressor response to hexamethonium (a ganglionic blocker). It also normalized variability in low-frequency (LF) power and LF/high-frequency (HF) ratio. CBD enhanced vasodilation and reduced vasoconstriction in the mesenteric artery of 2K1C rats, accompanied by decreased expression of aortic reactive oxygen species (ROS). Our findings suggest that chronic CBD treatment exerts antihypertensive effects by improving baroreflex sensitivity and vascular function while decreasing arterial ROS levels and sympathetic nerve activity. These results underscore CBD's potential therapeutic role in managing cardiovascular complications associated with renovascular hypertension.

AFTER-CA: Autonomic Function Transformation and Evaluation Following Catheter Ablation in Atrial Fibrillation.

Background: Catheter ablation (CA) is a well-established treatment for atrial fibrillation (AF). However, its effects on autonomic function and underlying mechanisms remain poorly understood. This study investigated autonomic and haemodynamic changes following CA and explored their potential implications for patient outcomes. Methods: Seventy-eight patients with AF underwent CA and were followed up at one, three, and six months. Autonomic function was assessed using a combination of head-up tilt (HUT), handgrip (HG), and deep breathing (DB) manoeuvres along with baroreflex sensitivity (BRS) and baroreflex effectiveness index (BEI) evaluation. Heart rate (HR), blood pressure (BP), and their variability were measured at each time point. Results: Significant autonomic alterations were observed after ablation, particularly at one month, with reductions in parasympathetic tone and baroreflex function. These changes gradually normalised by six months. Both pulmonary vein isolation (PVI) and cryoablation (CryO) had similar effects on autonomic regulation. Improvements in quality of life, measured by the AFEQT scores, were consistent with these physiological changes. Conclusions: CA for AF induces significant time-dependent autonomic and haemodynamic changes with recovery over six months. These findings underscore the need for ongoing monitoring and personalised post-ablation management. Further research is required to explore the mechanisms driving these alterations and their long-term impacts on patient outcomes.

Impact of the Menstrual Cycle on the Cardiovascular and Ventilatory Responses During Exercise in Normoxia and Hypoxia.

Citherlet, Tom, Antoine Raberin, Giorgio Manferdelli, Nicolas Bourdillon, and Grégoire P Millet. Impact of the menstrual cycle (MC) on the cardiovascular and ventilatory responses during exercise in normoxia and hypoxia. High Alt Med Biol. 00:00-00, 2024. Introduction: Ovarian hormones influence several physiological functions in women. This study investigated how the hormonal variations across the menstrual cycle (MC) impact cardiovascular and ventilatory responses during rest and moderate exercise in normobaric hypoxia. Methods: Thirteen eumenorrheic women were tested during the early follicular (Fol1), late follicular (Fol2), and mid-luteal (Lut3) phases with measurement of hormonal levels. Heart rate (HR) variability, blood pressure, and baroreflex sensitivity (BRS) were evaluated at rest in normoxia. Ventilation (VE), peripheral oxygen saturation, and HR were monitored at rest and during moderate-intensity cycling exercise in hypoxia (FiO2 = 14%). Results: Despite expected hormone level variations, no significant changes were observed across the MC in HR variability (root mean square of successive differences; 64 (95% confidence interval [47, 81]) at Fol1, 54 [42, 66] at Fol2, 60 [44, 77] ms at Lut3), blood pressure (mean blood pressure; 85 [79, 90]), 87 [81, 93]), 84 [77, 92] mmHg), BRS (26 [17, 36], 28 [20, 35], 23 [17, 29] ms/mmHg), VE (rest: 8.9 [7.9, 9.8], 9.5 [9.0, 9.9], 9.0 [8.1, 9.9]; exercise: 53 [41, 66], 51.1 [36.4, 65.7], 54.4 [34.0, 74.8] l/min), peripheral oxygen saturation (rest: 89.8 [87.4, 92.1], 91.9 [88.7, 95.0], 90.2 [87.8, 92.6]; exercise: 80.5 [77.4, 83.5], 84.4 [80.4, 88.3], 81.9 [78.3, 85.4] %) HR (rest: 69.7 [60.2, 79.1], 70.8 [63.2, 78.3], 70.5 [64.0, 77.0]; exercise: 148 [136, 160], 146 [132, 161], 146 [132, 160] bpm), and cycling efficiency (0.17 [0.16, 0.18], 0.17 [0.13, 0.21], 0.16 [0.15, 0.18] %) (all p > 0.05). Discussion: From a practical point of view, there is no strong evidence of any usefulness of monitoring hormonal variations and the MC phases for women exercising in hypoxia.

Long-term effects of siponimod on cardiovascular and autonomic nervous system in secondary progressive multiple sclerosis.

Siponimod, a second-generation, selective sphingosine 1-phosphate receptor (S1PR) 1 and 5 modulator, represents an important therapeutic choice for active secondary progressive multiple sclerosis (SPMS). Besides the beneficial immunomodulatory effects, siponimod impacts cardiovascular function through S1PR1 modulation. Short-term vagomimetic effects on cardiac activity have proved to be mitigated by dose titration. However, long-term consequences are less known. This study aimed to investigate the long-term impact of siponimod on cardiac autonomic modulation in people with SPMS (pwSPMS). Heart rate variability (HRV) and vascular hemodynamic parameters were evaluated using Multiple Trigonometric Regressive Spectral analysis in 47 pwSPMS before siponimod therapy and after one, three, six and 12months of treatment. Autonomic activation tests (tilt test for the sympathetic and deep breathing test for the parasympathetic cardiac modulation) were performed at each examination. pwSPMS preserved regular cardiovascular modulation responses during the autonomic tests reflected in the variation of several HRV parameters, such as RMSSD, pNN50, total power of HRV, high-frequency and low-frequency bands of the spectral domain or hemodynamic vascular parameters (Cwk, Zao, TPR, MAP) and baroreflex sensitivity (BRS). In the long-term follow-up, RMSSD, pNN50, total power, BRS and CwK presented a significant decrease, underlining a reduction of the parasympathetic and a shift towards sympathetic predominance in cardiac autonomic modulation that tends to stabilise after 1year of treatment. Due to dose titration, the short-term effects of siponimod on cardiac autonomic modulation are mitigated. The long-term impact on cardiac autonomic modulation is similar to fingolimod. The autonomic activation tests showed normal cardiovascular responses during 1-year follow-up in pwSPMS, confirming the safety profile of siponimod. Further research on autonomic function could reveal whether the observed sympathetic activation is a compensatory response to S1P signaling intervention or a feature of the disease, while also shedding light on the role of S1PR modulation in MS.

Unravelling the interplay between Harmattan wind and baroreflex functions: implications on environmental health and cardiovascular pathophysiology

Harmattan is a season characterized by dust, cold, and sub-humid trade winds in Sub-Saharan countries. It’s similar to meteorological phenomena like Asian dust storms, Santa Ana winds, Australian bushfires, and Saharan dust in the Caribbean. It causes profound changes in the cardiorespiratory system in apparently healthy individuals and increases the risk of hospitalization in susceptible individuals. Exposure to these extreme conditions has been associated with alterations in autonomic function and baroreceptor sensitivity thus resulting in dysregulation of blood pressure control mechanisms. Baroreceptors are critical regulators of hemodynamics and cardiovascular function. They play a vital role in the short-term responses to blood pressure perturbation and are essential for acute restoration of blood pressure following cold exposure. Harmattan wind contains a barrage of chemicals, dust, and particulate matters depending on industrialization, natural and human activities. Particulate matter from Harmattan dust can trigger systemic inflammation and oxidative stress, exacerbating endothelial dysfunction and impairing vascular reactivity thus contributing to the pathogenesis of alterations in baroreceptor insensitivity, and cardiovascular diseases, including hypertension and atherosclerosis. Furthermore, fine particulate matter from dust may penetrate deep into the respiratory tract, activating pulmonary sensory receptors and eliciting reflex responses that influence autonomic tone. The presence of rich acrolein smokes and non-essential heavy metals such as cadmium, lead, and mercury in Harmattan wind also reduces baroreflex sensitivity, culminating in a sustained increase in diastolic and systolic blood pressure. This integrated review aims to provide valuable insights into how changes in each of these environmental constituents alter vital pathophysiologic and immunologic mechanisms of the body leading to baroreceptor instability and ultimately hemodynamic imbalance using available primary studies. Understanding this intricate interplay is crucial for implementing targeted interventions and informed public health strategies to mitigate the adverse effects of extreme environmental exposure and ultimately reduce poor health outcomes in the affected regions.

Abstract P385: Effects Of a High Salt Diet On Glutamatergic Signaling In The Nucleus Of The Solitary Tract And Baroreflex Sensitivity

Hypertension remains a global health concern. Studies have shown a correlation with the loss of normal 24-hour blood pressure patterns and hypertension with a high salt diet. However, the mechanisms behind this are not fully known. The nucleus of the solitary tract (nTS), a key medullary nucleus involved in cardiorespiratory regulation, is known to modulate sympathetic outflow and blood pressure alterations.When blood pressure increases, baroreceptors in peripheral vessels detect these changes and send signals to the nTS through the neurotransmitter glutamate. Increased nTS glutamatergic signaling decreases blood pressure via efferent signals to the heart and blood vessels. The nTS integrates these signals and initiates responses through the baroreflex to counteract changes in blood pressure. Thus, baroreflex sensitivity (BRS), or a measure of how the baroreflex adjusts, serves as an indicator of the regulation of this feedback loop. An increased BRS indicates a more robust ability of the body to respond to blood pressure changes. Conversely, a reduced BRS is associated with hypertension, and autonomic dysfunction. Studies have shown that those with diet-induced hypertension also have a decreased BRS, however, the mechanism is not clear. We hypothesize that dysregulation of the 24-hour circadian glutamatergic signaling within the nTS may cause BRS decrease and hypertension. Salt-sensitive rats were subjected to either a normal salt diet (NSD, 0.4 % NaCl) or high salt diet (HSD, 4% NaCl) for 7 weeks. To determine nTS changes related to HSD, we measured blood pressure using 24/7 telemetry, and activation of glutamatergic neurons via immunohistochemistry (IHC). Antibodies against glutamate (CAMKII) and neuronal activation (cFos) were used to detect neuronal activation 6 hours apart, at the end of the NSD or HSD. Our preliminary findings reveal near significant decreases in glutamate signaling during the active period (at 9pm), suggesting a potential shift in the excitatory signaling in the nTS. Additionally, HSD over 7 weeks caused a significant increase in blood pressure and a decrease in BRS during the active period. Our preliminary data shows a connection between 24-hour regulation of glutamate within the nTS, diet-induced hypertension, and loss of BRS. This dysregulation in the blood pressure regulation underscores the importance of understanding the molecular mechanisms linking diet and development of disease.

Arterial blood pressure regulation during prolonged isometric exercise in artistic gymnastic athletes compared to controls.

The aim of this cross-sectional study was to examine the baroreflex sensitivity alterations in regulating arterial blood pressure during prolonged isometric exercise at different intensities in elite artistic gymnastic athletes compared to non-athletes. Fourteen young males participated in the study; 7 international level artistic gymnastics athletes and 7 physically active students inexperienced to isometric or resistance training. On two occasions, both groups performed 3 minutes of isometric handgrip exercise either at 30% or 50% of maximum voluntary contraction (MVC), in a randomized order. Force production, arterial blood pressure and baroreflex sensitivity through finger plethysmograph were continuously recorded. At rest, arterial blood pressure was normal in both groups (systolic blood pressure [SBP], athletes [A]: 128±9.0 mmHg, non-athletes [NA]: 130±7.2 mmHg, P=0.62; DIA, A: 75.6±5.2, NA: 78.5±4.6, P=0.31) but baroreflex sensitivity (BRS) was higher in athletes than in non-athletes (A: 16.6±7.4, NA: 12.0±7.9, P=0.02). During prolonged isometric exercise at 30% MVC, blood pressure was similar between groups (SBP, A: 176.9±16 mmHg vs. NA: 189.5±15.1 mmHg P=0.9, diastolic blood pressure [DBP], A: 108±11 mmHg vs. NA: 118±11 mmHg, P=0.6) and BRS was still higher in athletes (A: 13.28±5.75 ms/mmHg vs. NA: 6.72±3.83, P=0.04), whereas at 50% MVC, blood pressure was lower in the athletes compared to the control group (SBP, A: 182.5±15 mmHg vs. NA: 222.1±19.3 mmHg, P=0.001; DBP A: 115±14 mmHg vs. NA: 141±20 mmHg, P=0.02,without statistically significant difference in BRS between groups (A: 7.39±5.34 ms/mmHg vs. NA: 3.9±1.73 ms/mmHg, P=0.44). The results of our cross-sectional study revealed that after years of exposure in high amounts of training loads, baroreflex sensitivity is increased in healthy athletes probably in order to prevent excessive increases in blood pressure during exercise.

P098 CARDIAC REMODELING IN MICE TREATED WITH SODIUM OXALATE AND AORTIC STENOSIS

Background: Cardiovascular Diseases are one of the main global public health problems, with increasing mortality due to population aging and Hypertension (HTN). HTN is a risk factor for other diseases, such as aortic stenosis, renal dysfunction, and cardiac hypertrophy (CH). The hemodynamic overload caused by HTN affects the heart and kidneys, but the exact mechanisms of these alterations are not fully understood. Experimental models help study these mechanisms; however, a well-established model of CH with cardiorenal dysfunction does not yet exist. Objective: to evaluate whether the combination of cardiac hypertrophy, induced by transverse aortic constriction (TAC), and renal injury, induced by soluble sodium oxalate (OXA), can be a new model of CH with cardiorenal dysfunction. Methods: Male C57BL mice were randomized as follows: SHAM, receiving saline or OXA solution, and TAC, receiving saline or OXA solution. Echocardiography, direct blood pressure (BP) recording, metabolic cage, histology were performed to evaluate cardiac and renal function, hemodynamics, autonomic modulation, and baroreflex. Results: The TAC+OXA group showed the highest systolic BP(SBP) (SBP: SHAM: 122±5.24 vs. TAC+OXA: 160±5.24 mmHg, p&lt;0.01), increased double product (DP) (DP: SHAM: 64.65±4.76 mmHg/bpm vs. TAC: 89.53±5.85 mmHg/bpm, p=0.02), significant reduction in autonomic modulation (RMSSD: OXA: 12.5±1.8 vs. TAC+OXA: 2.8±0.2 ms, p&lt;0.01) and reflex tachycardia, eccentric hypertrophy, and worse renal function. The TAC group showed eccentric hypertrophy, increased BP variability (SD-SBP: SHAM: 2.97±0.07 mmHg vs. TAC: 5.63±0.57 mmHg, p≤0.01), diastolic dysfunction, and dilated left ventricle in diastole. The OXA group showed increased autonomic modulation and heart rate variability, renal damage characterized by inflammation, proximal tubule damage, and interstitial fibrosis when associated with TAC. All treated groups showed a significant reduction in reflex tachycardia. Conclusion: Transverse aortic constriction combined with OXA gavage is a model of CH with renal dysfunction, as the combination caused more significant renal damage, systemic hypertension, decreased autonomic modulation and baroreflex sensitivity, and eccentric hypertrophy with subsequent LV diastolic dysfunction.

Acustimulation combined with pharmacological prophylaxis versus pharmacological prophylaxis alone in postoperative nausea and vomiting (PONV) prophylaxis among patients undergoing laparoscopy abdominal surgery: a research protocol for a randomised controlled trial

IntroductionThis study evaluates the efficacy of integrating percutaneous electrical nerve stimulation at the pericardium 6 (PC6) acupuncture point through a wearable acustimulation device with standard pharmacological prophylaxis to prevent postoperative...

Effects of exercise on autonomic cardiovascular control in individuals with chronic, motor-complete spinal cord injury: an exploratory randomised clinical trial.

Secondary analysis of a clinical trial. To assess the impact of 6 months of armcycle ergometry training (ACET), or body weight-supported treadmill training (BWSTT), on autonomic cardiovascular responses to a laboratory sit-up test (SUT) in individuals with chronic (≥1-year post-injury) spinal cord injury (SCI). Tertiary Rehabilitation Centre, Vancouver, Canada. Sixteen individuals with motor-complete (American Spinal Injury Association Impairment Scale A-B) SCI between the fourth cervical and sixth thoracic spinal cord segments, aged 39 ± 11 years, were assessed. Participants were randomized to receive 72 sessions of moderate-to-vigorous intensity ACET (n = 8) or passive BWSTT (n = 8). Changes in mean arterial pressure (finger plethysmography), hemodynamics (Modelflow® method), and heart rate/heart rate variability (HR/HRV; electrocardiography) were measured in response toa SUT before and after 6 months of exercise training. Spontaneous cardiovagal baroreflex sensitivity (cvBRS) was assessed using the sequence method. Neither ACET nor BWSTT impacted hemodynamic responses to SUT or the incidence of orthostatic hypotension (all P > 0.36). ACET increased HR (P < 0.01, ηp2 = 0.34) and high frequency (HF) power HRV responses (P < 0.01, ηp2 = 0.42) to SUT following 6 months of training while BWSTT did not. Consistent with this, cvBRS improved (P < 0.05, ηp2 = 0.16) only following ACET. Improvements in cvBRS were correlated with both the HR (r = 0.726, P < 0.0001) and HF power (r = -0.484, P < 0.01) responses to SUT. Six months of ACET, but not BWSTT, improved cardiovagal baroreflex control of HR but had no effect on BP responses to SUT in individuals with chronic, motor-complete SCI. Canadian Institutes of Health Research (CIHR) CLINICAL TRIAL REGISTRATION: NCT01718977.

Body Oxygen Level Test (BOLT) is not associated with exercise performance in highly-trained individuals.

The analysis of chemoreflex and baroreflex sensitivity may contribute to optimizing patient care and athletic performance. Breath-holding tests, such as the Body Oxygen Level Test (BOLT), have gained popularity as a feasible way to evaluate the reflex control over the cardiorespiratory system. According to its proponents, the BOLT score reflects the body's sensitivity to carbon dioxide and homeostasis disturbances, providing feedback on exercise tolerance. However, it has not yet been scientifically validated or linked with exercise performance in highly-trained individuals. Therefore, we investigated the association of BOLT scores with the results of standard performance tests in elite athletes. A group of 49 speedskaters performed BOLT, Wingate Anaerobic Test (WAnT), and cardiopulmonary exercise test (CPET) on a cycle ergometer. Peak power, total work, and power drop were measured during WAnT. Time to exhaustion and maximum oxygen uptake were measured during CPET. Spearman's rank correlation and multiple linear regression were performed to analyze the association of BOLT scores with parameters obtained during the tests, age, somatic indices, and training experience. No significant correlations between BOLT scores and parameters obtained during WAnT and CPET were found, r(47) = -0.172-0.013, p = 0.248-0.984. The parameters obtained during the tests, age, somatic indices, and training experience were not significant in multiple linear regression (p = 0.38-0.85). The preliminary regression model showed an R 2 of 0.08 and RMSE of 9.78sec. Our findings did not demonstrate a significant relationship between BOLT scores and exercise performance. Age, somatic indices, and training experience were not significant in our analysis. It is recommended to interpret BOLT concerning exercise performance in highly-trained populations with a great degree of caution.