Heart Rate Reactivity to Acute Mental Stress is Associated With Parasympathetic Withdrawal and Adiposity in Firefighters

Abstract Background Firefighters are regularly exposed to stress and have a high incidence of cardiovascular events. Investigating cardiovascular and autonomic reactivity to acute mental stress (AMS) and its association with adiposity may contribute to explaining the increased cardiovascular risk in these professionals. Objectives To evaluate cardiovascular and autonomic reactivity to AMS in firefighters while considering adiposity parameters. Methods This study recorded the blood pressure and heart rate (HR) of twenty-five firefighters (38±8 years) at rest, while performing the Stroop color-word test to induce AMS, and recovery. Cardiac autonomic modulation (HR variability), baroreflex sensitivity (BRS — sequential method), and adiposity (electrical bioimpedance) were assessed. One-way or two-way analysis of variance followed by Tukey's post hoc test and multiple linear regression were performed. The significance level was P<0.05. Results The AMS increased mean arterial pressure (MAP — Δ16±13 mmHg) and HR (Δ14±7 bpm) ( P <0.05). These responses were associated with parasympathetic modulation withdrawal (RMSSD: baseline: 29.8±18 vs. AMS: 21.5±14 ms; High-frequency: baseline: 5.2±1.4 vs. AMS: 4.5±1.3 Ln ms 2 ; P <0.05) and decreased in the Up gain of the baroreflex (baseline: 8.9±5.1 vs. AMS: 6.3±3.0 mmHg/ms; P <0.05). Groups divided by HR reactivity peak showed parasympathetic modulation withdrawal only in firefighters with lower adiposity (RMSSD: baseline: 27.8±17.6 vs. AMS: 14.4±9.2 ms; High-Frequency: baseline: 5.3±1.2 vs. AMS: 3.8±1.4 Ln ms 2 ; P <0.05). Fat percentage (β = -0.499), BRS (β = 0.486), and sympathetic/parasympathetic balance (β = -0.351) were predictors of HR reactivity ( P <0.05). Conclusion Our results demonstrated that HR reactivity to AMS modulated by cardiac vagal withdrawal seems to be influenced by body composition in this group of firefighters.

The effects of a firefighting simulation on the vascular and autonomic functions and cognitive performance: a randomized crossover study.

Introduction: During firefighting, physical and cognitive demands increase. However, the stress inherent to these events can decrease cognitive performance and increase the risk of cardiovascular events in firefighters. Thus, this crossover study aimed to evaluate the effects of a firefighting Simulation on cognitive performance and vascular and autonomic functions in military firefighters. Methods: Sixteen firefighters (37.8 ± 5.6 years) underwent anthropometry, mental health status, and sleep quality assessments. They randomly performed two interventions, Simulation (Firefighting tasks; 10.0 ± 1.1 min) and Control (rest for 10 min), on different days. After both interventions, cognitive performance was assessed using the Stroop Test, Paced Auditory Serial Addition Test, and Trail Making Test. Then, the vascular function was assessed using ultrasonography through the carotid artery reactivity to the cold pressor test. The arterial pressure, heart rate, and cardiac intervals were recorded before interventions. The cardiac intervals were also measured during the cold pressor test. Student's t-test and Wilcoxon were used for comparisons between Control and Simulation and the analysis of variance for repeated measures was used for comparison over time during the cold pressor test. A significance level of p < 0.05 was adopted. Results: Although the mean and maximum heart rate were higher before the Simulation (p < 0.0001), all the heart rate variability parameters (p > 0.05) and mean arterial pressure (p > 0.3795) were similar before the interventions. After Simulation, the cognitive performance was similar to Control (p > 0.05), except for the improvement in Stroop Test part B (p < 0.0001). After Simulation, carotid artery reactivity was attenuated (p < 0.0010). During the cold pressor test, the high-frequency band of the heart rate variability was lower after the Simulation (p < 0.0104). Discussion: Although firefighting Simulation did not substantially change cognitive performance, the lower carotid artery reactivity and parasympathetic modulation to the heart during the cold pressor test may contribute to greater vulnerability to cardiovascular events in firefighters on duty.

Physiological effects of yerba maté (Ilex paraguariensis): a systematic review.

CONTEXT: Clinical studies have found an association between yerba maté intake and beneficial physiological effects. Nevertheless, no systematic reviews have been conducted to shed light on the data supporting this association. OBJECTIVE: The present systematic review aimed to investigate the physiological effects of yerba maté. DATA SOURCES: Searches were performed in 6 databases (Embase, LILACS, Scopus, PubMed, SciELO, Web of Science) and 3 grey literature databases (OpenGrey, ProQuest, Google Scholar). Relevant publications were identified, and the reference lists of included studies were searched manually for randomized clinical trials, nonrandomized clinical trials, and observational studies investigating the physiological effects of yerba maté. DATA EXTRACTION: Risk of bias was assessed using the Cochrane risk of bias tool for randomized trials and the Cochrane ROBINS-I (Risk Of Bias In Nonrandomized Studies of Interventions) tool. Joanna Briggs Institute critical appraisal tools were used for cross-sectional, case series, cohort, and case-control studies. The overall certainty of the evidence was estimated using the GRADE (Grading of Recommendations, Assessment, Development and Evaluations) working group summary of findings table. DATA ANALYSIS: Of 1096 studies identified, 32 were included. Studies showed consistent effects of yerba maté intake on metabolism improvement and antioxidant and anti-inflammatory activities in different populations. Benefits for body weight and composition, exercise performance, mood, and appetite, in addition cardio- and neuroprotective effects, were also observed. Risk of bias was categorized as high in 22 studies, moderate in 9 studies, and low in 1 study. The certainty of evidence ranged from moderate to very low. CONCLUSION: The available literature indicates that yerba maté can be used within a balanced and healthy diet for prevention and adjuvant treatment of chronic diseases. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration number CRD42020200196.

Effects of Exercise on Vascular Toxicity Associated with Breast Cancer Treatment: A Narrative Review.

Breast cancer is the most common cancer among women worldwide, and its incidence is linearly associated with age. The development of cancer treatments has changed the prognosis of this disease. Despite effective treatments, cardiovascular complications in middle-aged and older women have become challenging. Physical exercise is a powerful tool to prevent senescence symptoms and diseases, besides being an essential component for cardiovascular diseases and cancer prevention and treatment. The present narrative review considers the vascular dysfunction associated with breast cancer treatment, specifically chemotherapy and radiotherapy, and the effects of exercise on vascular toxicity. We also explored the mechanisms involved in these responses. The search strategy involved three databases (Pubmed, Scielo, and Web of Science) with the following descriptors: breast cancer, vascular toxicity, physical exercise, chemotherapy, and radiotherapy. The evidence showed that breast cancer patients, especially those under chemotherapy and over 50 years old, have a potential risk of developing vascular dysfunction, which may persist in the long term. Decreases in nitric oxide bioavailability and increases in oxidative stress and pro-inflammatory cytokines might mediate the chemotherapy and radiotherapy- induced vascular dysfunction. Exercise seems to be a promising strategy for managing this risk. However, there is a need for well-constructed studies evaluating vascular toxicity in breast cancer, especially in middle-aged and elderly patients, to establish whether exercise is beneficial.

Heart rate reactivity to acute mental stress is associated with adiposity, carotid distensibility, sleep efficiency, and autonomic modulation in young men.

Acute mental stress (AMS) increases heart rate (HR) and blood pressure. Since obesity can impair the cardiovascular reactivity to AMS, a better understanding of the mechanisms involved in this response is needed. We aimed to evaluate the cardiovascular reactivity to AMS in young men with normal or excess body fat. We also assessed the association between cardiovascular reactivity to AMS and cardiovascular risk factors, including autonomic modulation, carotid artery distensibility, physical activity levels, and sleep efficiency. Sixty-six young men (26.1 ± 4.1 years old) underwent anthropometric and body fat assessment (dual-energy X-ray absorptiometry) and had right-carotid artery ultrasonography. Accelerometers assessed physical activity levels and sleep efficiency. AMS was induced through the Stroop color-word test while blood pressure, HR, and cardiac interval were measured. Analyses were performed in Normal and Excess fat groups divided by fat mass index (FMI). Continuous data was used for multiple linear regression analyses. An interaction between FMI and time for HR reactivity was observed. Cardiac interval variability analysis showed that only participants with normal fat displayed parasympathetic withdrawal during AMS (P < 0.05). Multiple linear regression analysis supported the role of adiposity and autonomic modulation in the HR reactivity to AMS and showed involvement of carotid distensibility and sleep efficiency (P < 0.05). Carotid distensibility was the only predictor for blood pressure reactivity (P < 0.05). Physical activity was not associated with AMS's cardiovascular reactivity. We conclude that increased adiposity is associated with reduced HR reactivity to AMS, which is possibly linked to an impaired parasympathetic withdrawal. Carotid distension and sleep efficiency seem to contribute to this response.

Effects of Breaking up Deskwork with Physical Activity Combined with Tea Consumption on Cerebrovascular Function, Mood, and Affect

Abstract Background: Prolonged sitting, typical of desk work, decreases cerebral blood flow (CBF), mood and affect. Conversely, short physical activity breaks from sitting may prevent these detrimental effects and provide cardiometabolic benefits. Objective: We evaluated the effect of interrupting prolonged sitting with short breaks of light physical activity combined with tea consumption on CBF, cerebral autoregulation (CA), mood, and affect in desk workers. Methods: Nineteen healthy desk workers (ten male, 27±10 years) performed desk work in a laboratory for six hours on two separate intervention days: tea breaks (TEA-BREAK: short walk combined with ingestion of one cup of tea every hour) and sedentary (SED: ingestion of one cup of water every hour, while seated). Before and after desk work, we assessed mean arterial pressure (MAP), middle cerebral artery blood velocity (MCAv) and CA. Questionnaires were used to assess mood (Bond & Lader, PANAS) and affect (Affect grid) before and after the intervention. Data are expressed as mean ± standard deviation. Two-way ANOVA with repeated measurements followed by Sidak post hoc test was used for data analysis. Paired Student's t-test was also used to compare changes (Δ) between trials. Statistical significance was at p<0.05. Results: Desk work increased MAP (4.6±4.6 Δ mmHg; P<0.05), and decreased MCAv (-5.2±7.0 Δ cm/s; P<0.05), with no difference between interventions in these parameters. TEA-BREAKS, but not SED, decreased gain (-0.08±0.12 Δ cm.s−1.mmHg.−1) and increased phase (5.26±8.84 Δ radians) at very low frequency (P<0.05), but not at low frequency. Small changes in positive affect were found after the six hours of desk work (-5.5±7.3 Δ scale; P<0.05), with no differences between interventions. Conclusion: Changes in MCAv and positive affect induced by prolonged desk work could not be prevented by TEA-BREAKS. However, TEA-BREAKS improved CA, suggesting a higher efficiency in maintaining MCAv in response to blood pressure fluctuations.

Acute exercise-induced changes in cardiac function relates to right ventricular remodeling following 12-wk hypoxic exercise training.

Repeated ventricular exposure to alterations in workload may relate to subsequent cardiac remodeling. We examined whether baseline acute changes in right (RV) and left ventricular (LV) function relate to chronic cardiac adaptation to 12-wk exercise training. Twenty-one healthy individuals performed 12-wk high-intensity endurance running training under hypoxia (fraction of inspired oxygen: 14.5%). Resting transthoracic echocardiography was performed before and after the training program to assess ventricular structure, function, and mechanics (including strain-area/volume loops). In addition, we examined systolic cardiac function during recumbent exercise under hypoxia at baseline (heart rate of 110-120 beats/min, "stress echocardiography"). Fifteen individuals completed training (22.0 ± 2.4 yr, 10 males). Hypoxic exercise training increased RV size, including diameter and area (all P < 0.05). With exception of an increase in RV fractional area change (P = 0.03), RV function did not change post-training (all P > 0.05). Regarding the RV strain-area loop, lower systolic and diastolic slopes were found post-training (P < 0.05). No adaptation in LV structure, function, or mechanics was observed (all P > 0.05). To answer our primary aim, we found that a greater increase in RV fractional area change during baseline stress echocardiography (r = -0.67, P = 0.01) inversely correlated with adaptation in RV basal diameter following 12-wk training. In conclusion, 12-wk high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline increase in RV fractional area change to acute exercise. These data suggest that acute cardiac responses to exercise may relate to subsequent RV remodeling after exercise training in healthy individuals.NEW & NOTEWORTHY During exercise, the right ventricle is exposed to a disproportionally higher wall stress than the left ventricle, which is further exaggerated under hypoxia. In this study, we showed that 12-wk high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline cardiac increase in RV fractional area change to acute exercise. These data suggest that acute RV responses to exercise are related to subsequent right ventricular remodeling in healthy individuals upon hypoxic training.

Exercise-Induced Cardiac Fatigue after a 45-Minute Bout of High-Intensity Running Exercise Is Not Altered under Hypoxia.

BACKGROUND: Acute exercise promotes transient exercise-induced cardiac fatigue, which affects the right ventricle and to a lesser extent the left ventricle. Hypoxic exposure induces an additional increase in right ventricular (RV) afterload. Therefore, exercise in hypoxia may differently affect both ventricles. The aim of this study was to investigate the acute effects of a bout of high-intensity exercise under hypoxia versus normoxia in healthy individuals on right- and left-sided cardiac function and mechanics. METHODS: Twenty-one healthy individuals (mean age, 22.2 ± 0.6 years; 14 men) performed 45-min high-intensity running exercise under hypoxia (fraction of inspired oxygen 14.5%) and normoxia (fraction of inspired oxygen 20.9%) in a randomized order. Pre- and post-exercise echocardiography, at rest and during low-to-moderate intensity recumbent exercise ("stress"), was performed to assess RV and left ventricular (LV) cardiac function and mechanics. RV structure, function, and mechanics were assessed using conventional two-dimensional, Doppler, tissue Doppler, speckle-tracking echocardiographic, and novel strain-area loops. RESULTS: Indices of RV systolic function (RV fractional area change, Tricuspid annular plane systolic excursion, RV s', and RV free wall strain) and LV function (LV ejection fraction and LV global longitudinal strain) were significantly reduced after high-intensity running exercise (P < .01). These exercise-induced changes were more pronounced when echocardiography was examined during stress compared with baseline. These responses in RV and LV indices were not altered under hypoxia (P > .05). CONCLUSIONS: There was no impact of hypoxia on the magnitude of exercise-induced cardiac fatigue in the right and left ventricles after a 45-min bout of high-intensity exercise. This finding suggests that any potential increase in loading conditions does not automatically exacerbate exercise-induced cardiac fatigue in this setting.

The acute and chronic effects of high-intensity exercise in hypoxia on blood pressure and post-exercise hypotension: A randomized cross-over trial.

BACKGROUND: Acute exercise leads to an immediate drop in blood pressure (BP), also called post-exercise hypotension (PEH). Exercise in hypoxia is related to additional vasodilation, potentially contributing to more profound PEH. Therefore, we investigated the impact of hypoxia versus normoxia on the magnitude of PEH. Second, we examined whether these changes in PEH relate to the BP-lowering effects of 12-week exercise training under hypoxia. METHODS: In this prospective study, 21 healthy individuals (age 22.2 ±â€Š3.0 years, 14 male) performed a 45-minute high-intensity running exercise on 2 different days in a random order, under hypoxia (fraction of inspired oxygen 14.5%) and normoxia (fraction of inspired oxygen 20.9%). BP was examined pre-exercise (t = 0) and at t = 15, t = 30, t = 45, and t = 60 minutes post-exercise. Afterward, subjects took part in a 12-week hypoxic running exercise training program. Resting BP was measured before and after the 12-week training program. RESULTS: Acute exercise induced a significant decrease in systolic BP (systolic blood pressure [SBP], P = .001), but not in diastolic BP (diastolic blood pressure [DBP], P = .113). No significant differences were observed in post-exercise BP between hypoxic and normoxic conditions (SBP, P = .324 and DBP, P = .204). Post-exercise changes in SBP, DBP, and mean arterial pressure significantly correlated to the 12-week exercise training-induced changes in SBP (r = 0.557, P = .001), DBP (r = 0.615, P < .001), and mean arterial pressure (r = 0.458, P = .011). CONCLUSION: Our findings show that hypoxia does not alter the magnitude of PEH in healthy individuals, whilst PEH relates to the BP-lowering effects of exercise. These data highlight the strong link between acute and chronic changes in BP.

Behavioral, cardiovascular and endocrine alterations induced by chronic stress in rats fed a high-fat diet.

Chronic stress is a risk factor for cardiovascular diseases (CVD) and anxiety disorders (AD). Obesity also increases the risk of CVD and AD. The modern lifestyle commonly includes high-fat diet (HFD) intake and daily exposure to stressful events. However, it is not completely understood whether chronic stress exacerbates HFD-induced behavioral and physiological changes. Thus, this study aimed to evaluate the effects of the exposure to chronic variable stress (CVS) on behavioral, cardiovascular, and endocrine parameters in rats fed an HFD. Male Wistar rats were divided into four groups: control-standard chow diet (control-SD), control-HFD, CVS-SD, and CVS-HFD. The control-HFD and CVS-HFD groups were fed with HFD for six weeks. The CVS-HFD and CVS-SD groups were exposed to a CVS protocol in the last ten days of the six weeks. The behavioral analysis revealed that CVS decreased the open-arm exploration time during the elevated plus-maze test (p < 0.05). HFD promoted metabolic disorders and increased angiotensin II and leptin blood levels (p < 0.05). CVS or HFD increased blood pressure and the sympathetic nervous system (SNS) modulation of the heart and vessels and decreased baroreflex activity (p < 0.05). Combining CVS and HFD exacerbated the cardiac SNS response and increased basal heart rate (HR) (p < 0.05). CVS or HFD did not affect vascular function and aorta nitrate (p > 0.05). Taken together, these data indicate a synergism between HFD and CVS on the HR and cardiac SNS responses, suggesting an increased cardiovascular risk. Besides, neuroendocrine and anxiogenic disturbers may contribute to the cardiovascular changes induced by HFD and CVS, respectively.

Renovascular hypertension elevates pulmonary ventilation in rats by carotid body-dependent mechanisms.

The two kidney-one clip (2K1C) renovascular hypertension depends on the renin-angiotensin system and sympathetic overactivity. The maintenance of 2K1C hypertension also depends on inputs from the carotid bodies (CB), which when activated stimulate the respiratory activity. In the present study, we investigated the importance of CB afferent activity for the ventilatory responses in 2K1C hypertensive rats and for phrenic and hypoglossal activities in in situ preparations of normotensive rats treated with angiotensin II. Silver clips were implanted around the left renal artery of male Holtzman rats (150 g) to induce renovascular hypertension. Six weeks after clipping, hypertensive 2K1C rats showed, in conscious state, elevated resting tidal volume and minute ventilation compared with the normotensive group. 2K1C rats also presented arterial alkalosis, urinary acidification, and amplified hypoxic ventilatory response. Carotid body removal (CBR), 2 wk before the experiments (4th week after clipping), significantly reduced arterial pressure and pulmonary ventilation in 2K1C rats but not in normotensive rats. Intra-arterial administration of angiotensin II in the in situ preparation of normotensive rats increased phrenic and hypoglossal activities, responses that were also reduced after CBR. Results show that renovascular hypertensive rats exhibit increased resting ventilation that depends on CB inputs. Similarly, angiotensin II increases phrenic and hypoglossal activities in in situ preparations of normotensive rats, responses that also depend on CB inputs. Results suggest that mechanisms that depend on CB inputs in renovascular hypertensive rats or during angiotensin II administration in normotensive animals increase respiratory drive.

Importance of AT1 and AT2 receptors in the nucleus of the solitary tract in cardiovascular responses induced by a high-fat diet.

A high-fat diet (HFD) induces an increase in arterial pressure and a decrease in baroreflex function, which may be associated with increased expression of angiotensin type 1 receptor (AT1R) and pro-inflammatory cytokine genes and reduced expression of the angiotensin type 2 receptor (AT2R) gene within the nucleus of the solitary tract (NTS), a key area of the brainstem involved in cardiovascular control. Thus, in the present study, we evaluated the changes in arterial pressure and gene expression of components of the renin-angiotensin system (RAS) and neuroinflammatory markers in the NTS of rats fed a HFD and treated with either an AT1R blocker or with virus-mediated AT2R overexpression in the NTS. Male Holtzman rats (300-320 g) were fed either a standard rat chow diet (SD) or HFD for 6 weeks before commencing the tests. AT1R blockade in the NTS of HFD-fed rats attenuated the increase in arterial pressure and the impairment of reflex bradycardia, whereas AT2R overexpression in the NTS only improved the baroreflex function. The HFD also increased the hypertensive and decreased the protective axis of the RAS and was associated with neuroinflammation within the NTS. The expression of angiotensin-converting enzyme and neuroinflammatory components, but not AT1R, in the NTS was reduced by AT2R overexpression in this site. Based on these data, AT1R and AT2R in the NTS are differentially involved in the cardiovascular changes induced by a HFD. Chronic inflammation and changes in the RAS in the NTS may also account for the cardiovascular responses observed in HFD-fed rats.

Importance of the commissural nucleus of the solitary tract in renovascular hypertension.

The rodent renovascular hypertension model has been used to investigate the mechanisms promoting hypertension. The importance of the carotid body for renovascular hypertension has been demonstrated. As the commissural NTS (cNTS) is the first synaptic site in the central nervous system that receives information from carotid body chemoreceptors, we evaluated the contribution of cNTS to renovascular hypertension in the present study. Normotensive male Holtzman rats were implanted with a silver clip around the left renal artery to induce two-kidney, one-clip (2K1C) hypertension. Six weeks later, isoguvacine (a GABAA agonist) or losartan (an AT1 antagonist) was injected into the cNTS, and the effects were compared with carotid body removal. Immunohistochemistry for Iba-1 and GFAP to label microglia and astrocytes, respectively, and RT-PCR for components of the renin-angiotensin system and cytokines in the NTS were also performed 6 weeks after renal surgery. The inhibition of cNTS with isoguvacine or the blockade of AT1 receptors with losartan in the cNTS decreased the blood pressure and heart rate of 2K1C rats even more than carotid body removal did. The mRNA expression of NOX2, TNF-α and IL-6, microglia, and astrocytes also increased in the cNTS of 2K1C rats compared to that of normotensive rats. These results indicate that tonically active neurons within the cNTS are essential for the maintenance of hypertension in 2K1C rats. In addition to signals from the carotid body, the present results suggest that angiotensin II directly activates the cNTS and may also induce microgliosis and astrogliosis within the NTS, which, in turn, cause oxidative stress and neuroinflammation.

High-fat diet increases respiratory frequency and abdominal expiratory motor activity during hypercapnia.

Breathing disorders are commonly observed in association with obesity. Here we tested whether high-fat diet (HFD) impairs the chemoreflex ventilatory response. Male Holtzman rats (300-320 g) were fed with standard chow diet (SD) or HFD for 12 weeks. Then, tidal volume (VT), respiratory frequency (fR) and pulmonary ventilation (VE) were determined in conscious rats during basal condition, hypercapnia (7% or 10% CO2) or hypoxia (7% O2). The mean arterial pressure (MAP), heart rate (HR) and baroreflex sensitivity were also evaluated in conscious rats. A group of anesthetized rats was used for the measurements of the activity of inspiratory (diaphragm) and expiratory (abdominal) muscles under the same gas conditions. Baseline fR, VT and VE were similar between SD and HFD rats. During hypercapnia, the increase of fR was exacerbated in conscious HFD rats (60 ± 3, vs. SD: 47 ± 3 Δ breaths.min-1, P < 0.05). In anesthetized rats, hypercapnia strongly increased abdominal muscle activity in HFD group (238 ± 27, vs. basal condition: 100 ± 0.3%; P < 0.05), without significant change in SD group (129 ± 2.1, vs. basal condition: 100 ± 0.8%; P = 0.34). The ventilatory responses to hypoxia were similar between groups. In conscious HFD rats, MAP and HR were elevated and the baroreflex function was impaired (P < 0.05). These data demonstrated that 12 weeks of HFD exaggerate the ventilatory response activated by hypercapnia. The mechanisms involved in these responses need more investigation in future studies.

Cardiovascular and metabolic consequences of the association between chronic stress and high-fat diet in rats.

Obesity and chronic stress are considered independent risk factors for the development of cardiovascular diseases and changes in autonomic system activity. However, the cardiovascular consequences induced by the association between high-fat diet (HFD) and chronic stress are not fully understood. We hypothesized that the association between HFD and exposure to a chronic variable stress (CVS) protocol for four weeks might exacerbate the cardiovascular and metabolic disturbances in rats when compared to these factors singly. To test this hypothesis, male Wistar rats were divided into four groups: control-standard chow diet (SD; n = 8); control-HFD (n = 8); CVS-SD (n = 8); and CVS-HFD (n = 8). The CVS consisted of repeated exposure of the rats to different inescapable and unpredictable stressors (restraint tress; damp sawdust, cold, swim stress and light cycle inversion). We evaluated cardiovascular function, autonomic activity, dietary intake, adiposity and metabolism. The HFD increased body weight, adiposity and blood glucose concentration (∼15%) in both control and CVS rats. The CVS-HFD rats showed decreased insulin sensitivity (25%) compared to CVS-SD rats. The control-HFD and CVS-HFD rats presented increased intrinsic heart rate (HR) values (∼8%). CVS increased cardiac sympathetic activity (∼65%) in both SD- and HFD-fed rats. The HFD increased basal HR (∼10%). Blood pressure and baroreflex analyzes showed no differences among the experimental groups. In conclusion, the present data indicate absence of interaction on autonomic imbalance evoked by either CVS or HFD. Additionally, HFD increased HR and evoked metabolic disruptions which are independent of stress exposure.

Increased Expression of Macrophage Migration Inhibitory Factor in the Nucleus of the Solitary Tract Attenuates Renovascular Hypertension in Rats.

BACKGROUND: Macrophage migration inhibitory factor (MIF) is an intracellular inhibitory regulator of the actions of angiotensin II in the central nervous system. Renovascular hypertensive 2-kidney, 1-clip (2K1C) rats have an increased activity of the renin-angiotensin system and a decrease in baroreflex function compared to normotensive (NT) rats. In the present study, we tested the effects of MIF overexpression within the nucleus of the solitary tract (NTS), a key brainstem region for cardiovascular regulation, on the development of hypertension, on baroreflex function, and on water and food intake in 2K1C rats. METHODS: Holtzman NT rats received a silver clip around the left renal artery to induce 2K1C hypertension. Three weeks later, rats were microinjected in the NTS with AAV2-CBA-MIF, to increase the expression of MIF, or with the control vector AAV2-CBA-enhanced green fluorescent protein. Mean arterial pressure (MAP) and heart rate were recorded by telemetry. Baroreflex function was tested, and water and food intake were also measured. RESULTS: Increasing MIF expression in the NTS of 2K1C rats attenuated the development of hypertension, reversed the impairment of baroreflex function, and reduced the increase in water intake. In contrast to 2K1C rats, similar increases in MIF expression in the NTS of NT rats produced no changes in baseline MAP, baroreflex function, or water intake. CONCLUSIONS: These results indicate that an increased expression of MIF within the NTS attenuates the development of hypertension and restores the baroreflex function in 2K1C rats.

Overexpression of AT2R in the solitary-vagal complex improves baroreflex in the spontaneously hypertensive rat.

The aim of this study was to investigate the physiological effects of increased angiotensin II type 2 receptor (AT2R) expression in the solitary-vagal complex (nucleus of the solitary tract/dorsal motor nucleus of the vagus; NTS/DVM) on baroreflex function in non-anaesthetised normotensive (NT) and spontaneously hypertensive rats (SHR). Ten week old NT Holtzman and SHR were microinjected with either an adeno-associated virus expressing AT2R (AAV2-CBA-AT2R) or enhanced green fluorescent protein (control; AAV2-CBA-eGFP) into the NTS/DVM. Baroreflex and telemetry recordings were performed on four experimental groups: 1) NTeGFP, 2) NTAT2R, 3) SHReGFP and 4) SHRAT2R (n=4-7/group). Following in-vivo experimental procedures, brains were harvested for gene expression analysis. Impaired bradycardia in SHReGFP was restored in SHR rats overexpressing AT2R in the NTS/DMV. mRNA levels of angiotensin converting enzyme decreased and angiotensin converting enzyme 2 increased in the NTS/DMV of SHRAT2R compared to SHReGFP. Increased levels of pro-inflammatory cytokine mRNA levels in the SHReGFP group also decreased in the SHRAT2R group. AT2R overexpression did not elicit any significant change in mean arterial pressure (MAP) in all groups from baseline to 4weeks post viral transfection. Both SHReGFP and SHRAT2R showed a significant elevation in MAP compared to the NTeGFP and NTAT2R groups. Increased AT2R expression within the NTS/DMV of SHR was effective at improving baroreflex function but not MAP. We propose possible mediators involved in improving baroreflex are in the ANG II/ACE2 axis, suggesting a potential beneficial modulatory effect of AT2R overexpression in the NTS/DMV of neurogenic hypertensive rats.

Resistance training prevents the cardiovascular changes caused by high-fat diet.

AIMS: Aerobic exercise is indicated for prevention and treatment of obesity-induced cardiovascular disorders. Although the resistance training (RT) may also produce effects similar to aerobic exercise, this is not completely clear yet. In the present study, we tested if RT in moderate intensity might prevent alterations in blood pressure (BP), sympathetic modulation of systolic blood pressure (SBP), baroreflex function and the changes in renin-angiotensin system (RAS) and cytokines mRNA expression within the nucleus of the tract solitary (NTS) in rats fed with high-fat diet (HFD). MAIN METHODS: Male Holtzman rats (300-320 g) were divided into 4 groups: sedentary with standard chow diet (SED-SD); sedentary with high-fat diet (SED-HFD); RT with standard chow diet (RT-SD); and RT with high-fat diet (RT-HFD). The trained groups performed a total of 10 weeks of moderate intensity RT in a vertical ladder. In the first 3 weeks all experimental groups were fed with SD. In the next 7 weeks, the SED-HFD and RT-HFD groups were fed with HFD. KEY FINDINGS: In SED-HFD, BP and sympathetic modulation of SBP increased, whereas baroreflex bradycardic responses were attenuated. RT prevented the cardiovascular and inflammatory responses (increases in tumoral necrosis factor-α and interleukin-1ß) produced by HFD in SED rats. The anti-inflammatory interleukin-10, angiotensin type 2 receptor, Mas receptor and angiotensin converting enzyme 2 mRNA expressions in the NTS increased in the RT-HFD compared to SED-HFD. SIGNIFICANCE: The data demonstrated that moderate intensity RT prevented obesity-induced cardiovascular disorders simultaneously with reduced inflammatory responses and modifications of RAS in the NTS.

Does aerobic exercise intensity affect health-related parameters in overweight women?

The aim of this study was to compare the effect of a cycling training programme performed at intensity corresponding to the lowest value of the respiratory quotient (RQ) versus at intensity corresponding to the ventilatory threshold (VT), on body composition and health-related parameters in overweight women. Thirty-two sedentary obese women (27-42 years old) were studied in a randomized trial of either RQ (n = 17) or VT (n = 15). RQ and VT training sessions were equalized by time (60 min) and performed in a cycloergometer. Anthropometry, body composition, lipid profile, glucose, basal metabolic rate (BMR) and fitness (maximal oxygen uptake) were evaluated before and after 12 weeks of intervention. Body weight, body mass index, fatness and fitness were improved in both groups (P<0·001). Triglycerides (TG) levels decreased only in response to RQ (P<0·001) and fat-free mass (FFM) to VT (P = 0·002). No differences were observed between groups. Both exercise intensities seem to be effective for improving health in overweight women. However, low-intensity compared with the high-intensity exercise training appears to have additional benefits on TG levels and to maintenance of FFM.