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Although dynamic resistance training (DRT) and isometric handgrip training (IHT) may decrease blood pressure (BP) in hypertensives, the effects of these types of training have not been directly compared, and a possible additive effect of combining IHT to DRT (combined resistance training-CRT), has not been investigated. Thus, this study compared the effects of DRT, IHT and CRT on BP, systemic hemodynamics, vascular function, and cardiovascular autonomic modulation. Sixty-two middle-aged men with treated hypertension were randomly allocated among four groups: DRT (8 exercises, 50% of 1RM, 3 sets until moderate fatigue), IHT (30% of MVC, 4 sets of 2 min), CRT (DRT + IHT) and control (CON - stretching). In all groups, the interventions were administered 3 times/week for 10 weeks. Pre- and post-interventions, BP, systemic hemodynamics, vascular function and cardiovascular autonomic modulation were assessed. ANOVAs and ANCOVAs adjusted for pre-intervention values were employed for analysis. Systolic BP decreased similarly with DRT and CRT (125 ± 11 vs. 119 ± 12 and 128 ± 12 vs. 119 ± 12 mmHg, respectively; P < 0.05), while peak blood flow during reactive hyperaemia (a marker of microvascular function) increased similarly in these groups (774 ± 377 vs. 1067 ± 461 and 654 ± 321 vs. 954 ± 464 mL/min, respectively, P < 0.05). DRT and CRT did not change systemic hemodynamics, flow-mediated dilation, and cardiovascular autonomic modulation. In addition, none of the variables were changed by IHT. In conclusion, DRT, but not IHT, improved BP and microvascular function in treated hypertensive men. CRT did not have any additional effect in comparison with DRT alone.

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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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OBJECTIVES: To summarize existing evidence and quantify the effects of physical activity on vascular function and structure in autoimmune rheumatic diseases (ARDs). METHODS: Databases were searched (through March 2020) for clinical trials evaluating the effects of physical activity interventions on markers of micro- and macrovascular function and macrovascular structure in ARDs. Studies were combined using random effects meta-analysis, which was conducted using Hedges' g. Meta-analyses were performed on each of the following outcomes: microvascular function [i.e. skin blood flow or vascular conductance responses to acetylcholine (ACh) or sodium nitropusside (SNP) administration]; macrovascular function [i.e. brachial flow-mediated dilation (FMD%) or brachial responses to glyceryl trinitrate (GTN%); and macrovascular structure [i.e. aortic pulse wave velocity (PWV)]. RESULTS: Ten studies (11 trials) with a total of 355 participants were included in this review. Physical activity promoted significant improvements in microvascular [skin blood flow responses to ACh, g = 0.92 (95% CI 0.42, 1.42)] and macrovascular function [FMD%, g = 0.94 (95% CI 0.56, 1.02); GTN%, g = 0.53 (95% CI 0.09, 0.98)]. Conversely, there was no evidence for beneficial effects of physical activity on macrovascular structure [PWV, g = -0.41 (95% CI -1.13, 0.32)]. CONCLUSIONS: Overall, the available clinical trials demonstrated a beneficial effect of physical activity on markers of micro- and macrovascular function but not on macrovascular structure in patients with ARDs. The broad beneficial impact of physical activity across the vasculature identified in this review support its role as an effective non-pharmacological management strategy for patients with ARDs.

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This study tested the hypotheses that activation of central command and muscle mechanoreflex during post-exercise recovery delays fast-phase heart rate recovery with little influence on the slow phase. Twenty-five healthy men underwent three submaximal cycling bouts, each followed by a different 5-min recovery protocol: active (cycling generated by the own subject), passive (cycling generated by external force) and inactive (no-cycling). Heart rate recovery was assessed by the heart rate decay from peak exercise to 30 s and 60 s of recovery (HRR30s, HRR60s fast phase) and from 60 s-to-300 s of recovery (HRR60-300s slow phase). The effect of central command was examined by comparing active and passive recoveries (with and without central command activation) and the effect of mechanoreflex was assessed by comparing passive and inactive recoveries (with and without mechanoreflex activation). Heart rate recovery was similar between active and passive recoveries, regardless of the phase. Heart rate recovery was slower in the passive than inactive recovery in the fast phase (HRR60s=20±8vs.27 ±10 bpm, p<0.01), but not in the slow phase (HRR60-300s=13±8vs.10±8 bpm, p=0.11). In conclusion, activation of mechanoreflex, but not central command, during recovery delays fast-phase heart rate recovery. These results elucidate important neural mechanisms behind heart rate recovery regulation.

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This study assessed the additive effects of passive heating and exercise on cardiac baroreflex sensitivity (cBRS) and heart rate variability (HRV). Twelve healthy young men (25 ± 1 yr, 23.8 ± 0.5 kg/m2) randomly underwent two experimental sessions: heat stress (HS; whole body heat stress using a tube-lined suit to increase core temperature by ~1°C) and normothermia (NT). Each session was composed of a preintervention rest (REST1); HS or NT interventions; postintervention rest (REST2); and 14 min of cycling exercise [7 min at 40%HRreserve (EX1) and 7 min at 60%HRreserve (EX2)]. Heart rate and finger blood pressure were continuously recorded. cBRS was assessed using the sequence (cBRSSEQ) and transfer function (cBRSTF) methods. HRV was assessed using the indexes standard deviation of RR intervals (SDNN) and root mean square of successive RR intervals (RMSSD). cBRS and HRV were not different between sessions during EX1 and EX2 (i.e., matched heart rate conditions: EX1 = 116 ± 3 vs. 114 ± 3 and EX2 = 143 ± 4 vs. 142 ± 3 beats/min but different workloads: EX1 = 50 ± 9 vs. 114 ± 8 and EX2 = 106 ± 10 vs. 165 ± 8 W; for HS and NT, respectively; P < 0.01). However, when comparing EX1 of NT with EX2 of HS (i.e., matched workload conditions but with different heart rates), cBRS and HRV were significantly reduced in HS (cBRSSEQ = 1.6 ± 0.3 vs. 0.6 ± 0.1 ms/mmHg, P < 0.01; SDNN = 2.3 ± 0.1 vs. 1.3 ± 0.2 ms, P < 0.01). In conclusion, in conditions matched by HR, the addition of heat stress to exercise does not affect cBRS and HRV. Alternatively, in workload-matched conditions, the addition of heat to exercise results in reduced cBRS and HRV compared with exercise in normothermia. NEW & NOTEWORTHY The present study assessed cardiac baroreflex sensitivity during the combination of heat and exercise stresses. This is the first study to show that prior whole body passive heating reduces cardiac baroreflex sensitivity and autonomic modulation of heart rate during exercise. These findings contribute to the better understanding of the role of thermoregulation on cardiovascular regulation during exercise.

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Post-exercise heart rate (HR) recovery (HRR) presents a biphasic pattern, which is mediated by parasympathetic reactivation and sympathetic withdrawal. Several mechanisms regulate these post-exercise autonomic responses and thermoregulation has been proposed to play an important role. The aim of this study was to test the effects of heat stress on HRR and HR variability (HRV) after aerobic exercise in healthy subjects. Twelve healthy males (25 ± 1 years, 23.8 ± 0.5 kg/m2) performed 14 min of moderate-intensity cycling exercise (40-60% HRreserve) followed by 5 min of loadless active recovery in two conditions: heat stress (HS) and normothermia (NT). In HS, subjects dressed in a whole-body water-perfused tube-lined suit to increase internal temperature (Tc) by ~1°C. In NT, subjects did not wear the suit. HR, core and skin temperatures (Tc and Tsk), mean arterial pressure (MAP) skin blood flow (SKBF), and cutaneous vascular conductance (CVC) were measured throughout and analyzed during post-exercise recovery. HRR was assessed through calculations of HR decay after 60 and 300 s of recovery (HRR60s and HRR300s), and the short- and long-term time constants of HRR (T30 and HRRt). Post-exercise HRV was examined via calculations of RMSSD (root mean square of successive RR intervals) and RMS (root mean square residual of RR intervals). The HS protocol promoted significant thermal stress and hemodynamic adjustments during the recovery (HS-NT differences: Tc = +0.7 ± 0.3°C; Tsk = +3.2 ± 1.5°C; MAP = -12 ± 14 mmHg; SKBF = +90 ± 80 a.u; CVC = +1.5 ± 1.3 a.u./mmHg). HRR and post-exercise HRV were significantly delayed in HS (e.g., HRR60s = 27 ± 9 vs. 44 ± 12 bpm, P < 0.01; HRR300s = 39 ± 12 vs. 59 ± 16 bpm, P < 0.01). The effects of heat stress (e.g., the HS-NT differences) on HRR were associated with its effects on thermal and hemodynamic responses. In conclusion, heat stress delays HRR, and this effect seems to be mediated by an attenuated parasympathetic reactivation and sympathetic withdrawal after exercise. In addition, the impact of heat stress on HRR is related to the magnitude of the heat stress-induced thermal stress and hemodynamic changes.