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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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