Synergism among reflexes probably contributes to exercise hyperventilation in patients with heart failure with reduced ejection fraction (HFrEF). Thus, we investigated whether the carotid chemoreflex and the muscle metaboreflex interact to the regulation of ventilation (normalV˙E) in HFrEF. Ten patients accomplished 4‐min cycling at 60% peak workload and then recovered for 2 min under either: (a) 21% O2 inhalation (tonic carotid chemoreflex activity) with legs’ circulation free (inactive muscle metaboreflex); (b) 100% O2 inhalation (suppressed carotid chemoreflex activity) with legs’ circulation occluded (muscle metaboreflex activation); (c) 21% O2 inhalation (tonic carotid chemoreflex activity) with legs’ circulation occluded (muscle metaboreflex activation); or (d) 100% O2 inhalation (suppressed carotid chemoreflex activity) with legs’ circulation free (inactive muscle metaboreflex) as control. normalV˙E, tidal volume (VT) and respiratory frequency (fR) were similar between each separated reflex (protocols a and b) and control (protocol d). Calculated sum of separated reflexes effects was similar to control. Oppositely, normalV˙E (mean ± SEM: Δ vs. control = 2.46 ± 1.07 L/min, p = .05) and fR (Δ = 2.47 ± 0.77 cycles/min, p = .02) increased versus control when both reflexes were simultaneously active (protocol c). Therefore, the carotid chemoreflex and the muscle metaboreflex interacted to normalV˙E regulation in a fR‐dependent manner in patients with HFrEF. If this interaction operates during exercise, it can have some contribution to the HFrEF exercise hyperventilation.

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BackgroundPhysical exercise interventions have been extensively advocated for the treatment of obesity; however, clinical trials evaluating the effectiveness of exercise interventions on weight control show controversial results. Compensatory mechanisms through a decrease in energy expenditure and/or an increase in caloric consumption is a possible explanation. Several physiological mechanisms involved in the energy balance could explain compensatory mechanisms, but the influences of physical exercise on these adjustments are still unclear. Therefore, the present trial aims to evaluate the effects of exercise on non-exercise physical activity energy expenditure, energy intake and appetite sensations among active overweight/obese adults, as well as, to investigate hormonal changes associated with physical exercise.MethodsThis study is a randomized controlled trial with parallel, three-group experimental arms. Eighty-one overweight/obese adults will be randomly allocated (1:1:1 ratio) to a vigorous exercise group, moderate exercise group or control group. The trial will be conducted at a military institution and the intervention groups will be submitted to exercise sessions in the evening, three times a week for 65 min, during a 2-week period. The primary outcome will be total spontaneous physical activity energy expenditure during a 2-week period. Secondary outcomes will be caloric intake, appetite sensations and laboratorial biomarkers. Intention-to-treat analysis will be performed using linear mixed-effects models to evaluate the effect of treatment-by-time interaction on primary and secondary outcomes. Data analysis will be performed using SAS 9.3 and statistical significance will be set at p < 0.05.DiscussionThe results of the present study will help to understand the effect of physical exercise training on subsequent non-exercise physical activity, appetite and energy intake as well as understand the physiological mechanisms underlying a possible compensatory phenomenon, supporting the development of more effective interventions for prevention and treatment of obesity.Trial registrationPhysical Exercise and Energy Balance trial registry, trial registration number: NCT 03138187. Registered on 30 April 2017.Electronic supplementary materialThe online version of this article (10.1186/s13063-018-2445-6) contains supplementary material, which is available to authorized users.

The main goal was to determine the impact of mental stress (MS) on blood flow regulation in overweight/obese men. Fourteen overweight/obese men (27 ± 7 years; 29.8 ± 2.6 kg/m2) participated in two randomized experimental sessions with oral administration of the AT1R blocker Olmesartan (40 mg; AT1RB) or placebo (PL). After 2 h, a 5‐min acute MS session (Stroop Color Word Test) was administered. Blood flow was assessed at baseline and during the first 3 min of MS by vascular ultrasound in the brachial artery. Blood was collected before (baseline) and during mental stress (MS) for measurement of nitrite (chemiluminescence) and endothelin‐1 (ELISA kit). The AT1R blocker was able to reverse the MS responses observed in the placebo session for retrograde flow (p < 0.01), retrograde SR (p < 0.01) and oscillatory shear index (p = 0.01). Regarding vasoactive substances, no differences were observed in ET‐1 (p > 0.05) responses to MS between experimental sessions. However, for nitrite responses, the administration of the AT1R blocker was able to increase circulating levels of NO (p = 0.03) Blockade of AT1R appears to prevent the decrease in endothelial function by reducing low shear stress and maintaining the vasoactive substances balance after MS in overweight/obese men.

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Acute exposure to mental stress (MS) leads to endothelial activation, microparticles release and, consequently, transient endothelial dysfunction in overweight/obesity grade 1 men. Considering that angiotensin II generates an oxidative imbalance mediated by angiotensin II type 1 receptors (AT1R), it is unknown whether this process is responsible for transient endothelial dysfunction present in MS in overweight/obesity grade 1. Therefore, the aim of this study was to determine endothelial responses to angiotensin II mediated by AT1R after MS in overweight/obesity grade I men. For this, fourteen overweight/obese men (27±7 years; 30.1±2.9 Kg/m2) participated in two randomized experimental sessions with oral administration of the AT1 receptor blocker (AT1R block) or placebo. Endothelial function was determined by flow‐mediated dilation (FMD) before (baseline), 30 (30MS) and 60 (60MS) minutes after a five minute session of acute MS (Stroop Color Word Test). Blood samples (n=11) were obtained at before (baseline), during (MS) and 60 minutes (60MS) after MS for measurement of: endothelial microparticle (EMP, flow cytometry); endothelial progenitor cells (EPC, flow cytometry); nitrite (chemoluminescence); and oxidative stress [lipid peroxidation (TBARS), protein oxidation (carbonylated proteins) and antioxidant enzyme (catalase) by colorimetry]. During MS, heart rate, systolic, diastolic and mean blood pressure increased similarly in both conditions (p=0.01 vs. baseline). At the placebo session, FMD decreased significantly in 30MS (p=0.04 vs. baseline) and returned to baseline levels in 60MS (p=0.03 vs. 30MS). There was a significant increase in EPC in 60MS (p=0.04 vs. baseline). Carbonylated proteins (p=0.01 vs. baseline) and catalase activity increased during MS (p=0.02 vs. baseline) and returned to baseline in 60MS (p=0.01 vs. MS). No differences were observed in nitrite levels at the placebo session. At AT1R block session, FMD increased in 30MS (p =0.01 vs. baseline) and 60MS (p=0.02 vs. baseline), while EPC levels were different from placebo only 60MS (p=0.04 vs. placebo). There was a significant increase in nitrite (p=0.01 vs. baseline) while no change was observed in carbonylated proteins in 30MS and 60MS. Carbonylated protein concentration was lower during AT1R blockade in MS (p=0.04 vs. placebo). Catalase increased only in 60EM (p=0.02 vs. placebo). There were no differences in the concentrations of EMP and TBARS. In conclusion, AT1R blockade appears to increase flow‐mediated dilatation and nitrite bioavailability in response to MS in addition to preventing the increase of protein oxidation after MS in overweight/obese men.Support or Funding InformationCoordination for the Improvement of Higher Education Personnel (CAPES)Foundation for Research Support of the State of Rio de Janeiro (FAPERJ)National Council for Scientific and Technological Development (CNPq)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Patients with chronic heart failure (CHF) tipically present exacerbated ventilation (VE) response to exercise. This phenomenon is associated with exercise intolerance and worse prognosis, and seems to be mediated, at least in part, by abnormalities in the neural control of VE, such as enhanced VE response to activation of muscle afferents sensitive to metabolites (i.e., enhanced metaboreflex), as well as enhanced VE response to inhalation of hypoxic air at rest (i.e., enhanced peripheral chemoreflex). However, the interaction between these reflexes remains unknown in CHF. Then, we sought to test the hypothesis that the activation of the metaboreflex could enhance the contribution of the peripheral chemoreflex for the regulation of VE in patients with CHF. Six men with CHF under optimal pharmacological treatment (New York Heart Association class II‐III, mean ± SD age of 55 ± 6 years and left ventricular ejection fraction (Simpson) 33.7 ± 2.9%) were submitted to 4 steady‐state cycling sessions at 60% of maximal power output for 4 minutes. Then, they recovered for 2 minutes under either 1) post exercise ischemia (PEI) plus normoxia (21% O2), 2) PEI plus hyperoxia (100% O2), 3) free flow plus normoxia, or 4) free flow plus hyperoxia. PEI was used to trap metabolites in the lower limbs, and, consequently, activate the metaboreflex, while hyperoxia was used to inhibit the peripheral chemoreceptors. Patients were blinded to the O2 concentration in the inhaled air. A rebreathing circuit was used during recovery to match the end tidal partial pressure of CO2 (PetCO2) among conditions. Breath‐by‐breath data recorded at peak and throughout recovery were averaged in 20‐s windows for statistical analyses. Peak VE was similar among conditions. As expected, end tidal partial pressure of O2 was higher during hyperoxia than normoxia throughout the recovery period. VE decayed during recovery in all conditions. Of note, hyperoxia augmented the VE decay versus normoxia at 21–40 s (hyperoxia: 16.7 ± 2.3 L/min vs. normoxia: 22.7 ± 2.9 L/min, P < 0.001) and 41–60 s (hyperoxia: 17.1 ± 1.5 L/min vs. normoxia: 20.5 ± 2.2 L/min, P = 0.01) of recovery during PEI. However, hyperoxia did not change VE decay versus normoxia during free flow recovery. Collectively, our findings indicate that the activation of the metaboreflex enhances the peripheral chemoreflex regulation of VE in patients with CHF, which confirms the interaction between these reflexes. This interaction may, consequently, mediate part of the exaggerated VE response to exercise, which is a hallmark of patients with CHF.Support or Funding InformationSão Paulo Research Foundation (FAPESP), National Counsel of Technological and Scientific Development (CNPq), and Research Support Foundation of the State of Rio de Janeiro (FAPERJ).

Objective We investigated sex differences in blood pressure (BP) response to transcutaneous electrical nerve stimulation (TENS) during orthostatic stress (ORT). Methods Seventeen healthy young adults (males = 9; females = 8) underwent TENS or SHAM stimulus applied in the cervicothoracic region for 30 min in the supine position followed by 10 min in the orthostatic position. Electrocardiogram and BP were continuously recorded at rest and during ORT. Stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) were calculated from the BP signal. Results Orthostatic challenge decreased BP similarly for both sexes during ORT, a deeper drop in CO and a slight increase in heart rate were found in women compared with men (P = 0.03 and 0.05, respectively). TENS evoked a pronounced fall in SBP in men compared with the SHAM condition (P < 0.05). TENS has no effect on SBP in women compared with the SHAM condition. Conclusion This finding suggests a possible modulatory effect by one cervicothoracic TENS session on sympathetic tonus in healthy men.