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Carotid baroreflex activation lowers blood pressure and might have potential application for the treatment of resistant hypertension. We did a proof-of-principle trial with a novel endovascular baroreceptor amplification device, MobiusHD (Vascular Dynamics, Mountain View, CA, USA), in patients with resistant hypertension. CALM-FIM_EUR was a prospective, first-in-human, open-label study done at six European centres. Eligible patients were adults with resistant hypertension (office systolic blood pressure ≥160 mm Hg despite taking at least three antihypertensive agents, including a diuretic). MobiusHD devices were implanted unilaterally in the internal carotid artery. The primary endpoint was the incidence of serious adverse events at 6 months. Secondary endpoints included changes in office and 24 h ambulatory blood pressure. This trial is registered with ClinicalTrials.gov, number NCT01911897. Between December, 2013, and February, 2016, 30 patients were enrolled and underwent successful implantation. Mean age was 52 years (SD 12), 15 patients (50%) were men, and mean antihypertensive use was 4·4 drugs (1·4). Mean office blood pressure was 184/109 mm Hg (18/14) at baseline and was reduced by 24/12 mm Hg (13–34/6–18) at 6 months (p=0·0003 for systolic and p=0·0001 diastolic blood pressure). Mean baseline 24 h ambulatory blood pressure was 166/100 mm Hg (17/14) at baseline and was reduced by 21/12 mm Hg (14–29/7–16) at 6 months (p<0·0001 for systolic and diastolic blood pressure). Five serious adverse events had occurred in four patients (13%) at 6 months: hypotension (n=2), worsening hypertension (n=1), intermittent claudication (n=1) and wound infection (n=1). In patients with resistant hypertension, endovascular baroreceptor amplification with the MobiusHD device substantially lowered blood pressure with an acceptable safety profile. Randomised, double-blind, sham-controlled trials are warranted to investigate the use of this treatment further. Vascular Dynamics.

Arterial stiffness and cardiac autonomic function are crucial indicators of cardiovascular health. Acute exercise and age impact these parameters, but research often focuses on specific exercise activities, lacking ecological validity. We examined the acute effects of commercially available group fitness classes (indoor cycling, resistance training, combined exercise) on arterial stiffness and vagal-related heart rate variability (HRV) indices in twelve young and twelve middle-aged adults. Participants attended four sessions, including exercise and control conditions, with measurements taken at rest and during recovery. Middle-aged, but not young adults, showed reductions in central and peripheral systolic blood pressure 20-min into recovery across all exercise modalities (range: -7 to -8 mmHg p < 0.05). However, arterial stiffness remained unchanged. Similarly, vagal-related HRV indices (range: -0.51 to -0.90 ms, p < 0.05) and BRS (-4.03, p < 0.05) were reduced immediately after exercise, with differences persisting 30 min into recovery only after indoor cycling. Resistance and combined exercise elicited similar cardiovagal modulation and delayed baroreflex sensitivity recovery to cycling exercise, despite higher energy expenditure during indoor cycling (+87 to +129 kcal, p < 0.05). Acute group fitness classes induce age-dependent alterations in blood pressure, but not in arterial stiffness or cardiovagal modulation. While the overall cardiovascular effects were generally consistent, differences in autonomic recovery were observed between exercise modes, with prolonged effects seen after indoor cycling. This suggests that exercise prescription should consider both age and exercise modality, as well as recovery time. The findings also emphasize the importance of ecological validity in exercise interventions, highlighting that acute effects on cardiovascular health in real-world settings may differ from those observed in controlled laboratory environments (ID: NCT06616428).

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.

This study evaluated the acute cardiovascular responses to resistance exercise (RE) sessions with different set configurations in normotensive and hypertensive postmenopausal females. 50 physically active postmenopausal females performed a control (CON) and three RE sessions matched for total volume (144 repetitions), load (12-repetition maximum load), and total rest time (360s) but differing in set configuration: 4 sets of 9 repetitions with 120 s rest (9 S); 6 sets of 6 repetitions with 72 s rest (6 S); and 9 sets of 4 repetitions with 45 s rest (4 S). Heart rate (HR) was recorded during exercise, while HR variability, baroreflex sensitivity, arterial stiffness, and blood pressure were assessed before and after each session. Peak and mean HR values were higher during exercise in 9 S ( p  ≤ 0.026). All RE protocols induced cardiac parasympathetic withdrawal, reduction in baroreflex sensitivity, and increased post-exercise arterial stiffness compared to CON. However, in 4 S, cardiac parasympathetic withdrawal and baroreflex impairment were attenuated without a significant increase in arterial stiffness. Additionally, a post-exercise hypotensive response was observed only after 9 S in hypertensive participants ( p  = 0.004). Shorter set configurations attenuate chronotropic response during RE and mitigate impairments in cardiac autonomic and baroreflex control following RE sessions, without affecting arterial stiffness or blood pressure.

Abstract Study Objectives Binge alcohol consumption is associated with increased cardiovascular risk. The effects of evening binge alcohol consumption (i.e. 4–5 beverages within 2 h) on the vagal components of HRV and cardiovagal baroreflex sensitivity (cvBRS) during sleep remain largely equivocal. The present study examined the effects of evening binge alcohol consumption on nocturnal cardiac vagal tone and baroreflex sensitivity during stage N2, slow wave (SWS), and rapid eye movement (REM) sleep. We hypothesized that evening binge drinking would reduce HRV and cvBRS in each sleep stage. Methods Following a familiarization night within the laboratory, twenty-three participants were examined following a night of binge alcohol consumption and a fluid control (randomized, crossover design). A quality nocturnal beat-to-beat blood pressure signal was obtained in both conditions in 16 participants (seven men, nine women; 25 ± 1 years). Results Binge drinking reduced both the high frequency (HF) and time-domain components (i.e. pNN50 and RMSSD) of HRV in stage N2 sleep, SWS, and REM. In addition, cvBRS up-up (vagal activation) was reduced following binge alcohol consumption in stage N2 (21 ± 3 vs. 15 ± 3 ms/mmHg, p = 0.035) and REM (15[11–28] vs. 11[9–18] ms/mmHg, p = 0.009). Binge alcohol consumption reduced cvBRS down-down (vagal withdrawal) in stage N2 (23 ± 2 vs. 14 ± 2 ms/mmHg, p < 0.001), SWS (20[14–30] vs. 14[9–17] ms/mmHg, p = 0.022), and REM (14[11–24] vs. 10[7–15] ms/mmHg, p = 0.006). Conclusions Evening binge alcohol consumption disrupts cardiac vagal tone and baroreflex function during nearly all sleep stages. These findings provide mechanistic insight into the potential role of binge drinking and alcohol abuse on cardiovascular risk. Clinical Trials Details Alcohol and Neural Cardiovascular Control in Binge Drinkers, www.clinicaltrials.gov/ct2/show/NCT03567434, NCT03567434.

Blood pressure regulation following spinal cord injury (SCI) is often compromised due to impaired vascular sympathetic control, leading to increased reliance on cardiovagal baroreflex sensitivity to maintain pressure. Whole-body exercise improves cardiovagal baroreflex sensitivity in uninjured individuals, though has not been explored in those with SCI. Our objective was to determine changes in cardiovagal baroreflex sensitivity following 6 months of high-intensity, whole-body exercise in individuals with SCI compared to lower-intensity, arms only exercise, or waitlist. This randomized controlled trial recruited individuals with SCI aged 18–40 years old. Sixty-one individuals were randomized, with 38 completing at least one cardiovagal baroreflex sensitivity assessment. Whole-body exercise was performed with hybrid functional electrical stimulation rowing prescribed as two to three times per week, for 30–60 minutes with a target heart rate of >75% of maximum. The arms only exercise group performed upper body rowing exercise with the same prescription as whole-body exercise. Waitlist controls were not enrolled in any explicit training regimen. After 6 months, those in arms only exercise or waitlist crossed over to whole-body exercise. Cardiovagal baroreflex sensitivity was assessed via the neck suction technique at baseline and at three-month intervals thereafter. Intention to treat analysis with a structured equation model demonstrated no significant effect of waitlist control or arms only exercise on cardiovagal baroreflex sensitivity. Whole-body exercise significantly improved cardiovagal baroreflex sensitivity at 6 months for those initially randomized (p = 0.03), as well as those who crossed over from arms only exercise or waitlist control (p = 0.03 for each). However, amount of exercise performed and aerobic gains (VO 2max ) each poorly correlated with increases in cardiovagal baroreflex sensitivity (R 2 <0.15). In post-hoc analyses, individuals with paraplegia made significantly greater gains in baroreflex sensitivity compared to those with tetraplegia (p = 0.02), though gains within this group were again poorly correlated to gains in aerobic capacity. Clinicaltrials.gov number NCT02139436.

Study DesignSecondary analysis of a clinical trial.ObjectiveTo assess the impact of 6 months of arm cycle 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).SettingTertiary Rehabilitation Centre, Vancouver, Canada.MethodsSixteen 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 to a SUT before and after 6 months of exercise training. Spontaneous cardiovagal baroreflex sensitivity (cvBRS) was assessed using the sequence method.ResultsNeither 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.ConclusionSix 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.SponsorshipCanadian Institutes of Health Research (CIHR)Clinical Trial RegistrationNCT01718977

While it is well established that slow-wave sleep electroencephalography (EEG) rebounds following sleep deprivation, very little research has investigated autonomic nervous system recovery. We examined heart rate variability (HRV) and cardiovagal baroreflex sensitivity (BRS) during four blocks of repetitive sleep restriction and sequential nights of recovery sleep. Twenty-one healthy participants completed the 22-day in-hospital protocol. Following three nights of 8-hr sleep, they were assigned to a repetitive sleep restriction condition. Participants had two additional 8-hr recovery sleep periods at the end of the protocol. Sleep EEG, HRV, and BRS were compared for the baseline, the four blocks of sleep restriction, and the second (R2) and third (R3) nocturnal recovery sleep periods following the last sleep restriction block. Within the first hour of each sleep period, vagal activation, as indexed by increase in high frequency (HF; HRV spectrum analysis), showed a rapid increase, reaching its 24-hr peak. HF was more pronounced (rebound) in R2 than during baseline (p < 0.001). The BRS increased within the first hour of sleep and was higher across all sleep restriction blocks and recovery nights (p = 0.039). Rebound rapid eye movement sleep was observed during both R2 and R3 (p = 0.004), whereas slow-wave sleep did not differ between baseline and recovery nights (p > 0.05). Our results indicate that the restoration of autonomic homeostasis requires a time course that includes at least three nights, following an exposure to multiple nights of sleep curtailed to about half the normal nightly amount.

Purpose The aim of this paper is to investigate the acute effects of short-term transcutaneous vagus nerve stimulation (tVNS) on cardio-vagal baroreflex gain and heart rate variability in patients with chronic heart failure (CHF). Methods A total of 16 adults with CHF and left ventricular ejection fraction (LVEF) < 50% in sinus rhythm were enrolled (65 ± 8 years, 63% men, LVEF 40 ± 5%, 88% on beta-blockers, 50% on quadruple CHF therapy). Over a single experimental session, after a 10-min baseline recording, each patient underwent two trials of 10-min tVNS (Parasym Device, 200 µs, 30 Hz, 1 mA below discomfort threshold) at either the right or left tragus in a randomized order, separated by a 10-min recovery. Results Compared with baseline, tVNS did not affect heart rate, blood pressure, and respiratory rate ( p  > 0.05), and no patients complained of discomfort or any adverse effect. Right-sided tVNS was associated with a significant increase in cardio-vagal baroreflex gain (from 5.6 ± 3.1 to 7.5 ± 3.8 ms/mmHg, ∆ 1.9 ± 1.6 ms/mmHg, p  < 0.001), while no change was observed with left-sided tVNS (∆ 0.5 ± 2.0 ms/mmHg, p  = 0.914). These findings were independent of stimulation-side order (excluding any carry-over effect) and consistent across sex, LVEF category, and HF etiology subgroups ( p -value for interaction > 0.05). Conclusions Acute right-sided tVNS increases cardio-vagal baroreflex gain in patients with CHF and LVEF < 50%, with no tolerability concerns.

Abstract Context Hypoglycemia attenuates cardiovascular homeostatic autonomic control. This attenuation, known as the cardiovascular component of hypoglycemia-associated autonomic failure (HAAF), is characterized most notably by decreased baroreflex sensitivity (BRS) that begins during hypoglycemia and persists until at least the next day, despite return to euglycemia. Understanding the mechanisms underlying this reduction in BRS is important because BRS attenuation is associated with increased morbidity and mortality. Objective The objective of this work is to investigate the role of the adrenocorticotropin (ACTH)-adrenal axis in decreasing BRS. We tested the hypothesis that infusion of ACTH 1–24 (cosyntropin), as compared to placebo, would acutely suppress BRS, and that this decrease in BRS would be present the next day. Design A double-blind, placebo-controlled, random-order, cross-over study was conducted. Setting This study took place in a clinical research center. Participants Participants included healthy men and women. Interventions Interventions included an intravenous infusion of cosyntropin (70 μg/hour for 2.5 hours in the morning and again in the early afternoon) vs normal saline placebo. Main Outcome Measures Outcome measures included BRS during and 16 hours after cosyntropin vs placebo infusions. Results Cosyntropin infusion attenuated BRS (mm Hg/ms) as compared to placebo (baseline 17.8 ± 1.38 vs 17.0 ± 2.07; during 14.4 ± 1.43 vs 17.3 ± 1.65; and next day 14.8 ± 1.42 vs 18.9 ± 2.04; P < .05, time by treatment, analysis of variance). BRS was decreased during the final 30 minutes of the morning cosyntropin infusion as compared to baseline (P < .01) and remained suppressed the next day (16 hours after afternoon infusion) (P < .025). Placebo infusion did not significantly change BRS. Corrected QT interval was not affected. Conclusions ACTH attenuates BRS, raising the possibility that hypoglycemia-induced increases in ACTH may contribute to the cardiovascular component of HAAF.