A closed-loop approach to the study of the baroreflex dynamics during posture changes at rest and at exercise in humans

2021 ◽  
Author(s):  
Anna Taboni ◽  
Nazzareno Fagoni ◽  
Timothée Fontolliet ◽  
Christian Moia ◽  
Giovanni Vinetti ◽  
...  
Keyword(s):  
Steady State ◽  
Baroreflex Sensitivity ◽  
Closed Loop ◽  
Control Mechanism ◽  
Vagal Activity ◽  
Arterial Baroreflex ◽  
Exercise Onset ◽  
Sequence Method ◽  
Exercise In Humans ◽  
Vagal Withdrawal

We hypothesized that during rapid up-tilting at rest, due to vagal withdrawal, arterial baroreflex sensitivity (BRS) may decrease promptly and precede the operating point (OP) resetting, whereas different kinetics are expected during exercise steady state, due to lower vagal activity than at rest. To test this, eleven subjects were rapidly (< 2s) tilted from supine (S) to upright (U) and vice versa every 3 minutes, at rest and during steady state 50W pedaling. Mean arterial pressure (MAP) was measured by finger cuff (Portapres) and R-to-R interval (RRi) by electrocardiography. BRS was computed with the sequence method both during steady and unsteady states. At rest, BRS was 35.1ms∙mmHg-1 (SD17.1) in S and 16.7ms∙mmHg-1 (SD6.4) in U (p<0.01), RRi was 901ms (SD118) in S and 749ms (SD98) in U (p<0.01), and MAP was 76mmHg (SD11) in S and 83mmHg (SD8) in U (p<0.01). During up-tilt, BRS decreased promptly [first BRS sequence was 19.7ms∙mmHg-1 (SD5.0)] and was followed by an OP resetting (MAP increase without changes in RRi). At exercise, BRS and OP did not differ between supine and upright positions [respectively, BRS was 7.7ms∙mmHg-1 (SD3.0) and 7.7ms∙mmHg-1 (SD3.5), MAP was 85mmHg (SD13) and 88mmHg (SD10), and RRi was 622ms (SD61) and 600ms (SD70)]. The results support the tested hypothesis. The prompt BRS decrease during up-tilt at rest may be ascribed to a vagal withdrawal, similarly to what occurs at exercise onset. The OP resetting may be due to a slower control mechanism, possibly an increase in sympathetic activity.

scholarly journals Testing the vagal withdrawal hypothesis during light exercise under autonomic blockade: a heart rate variability study

2018 ◽  
Vol 125 (6) ◽  
pp. 1804-1811 ◽  
Author(s):  
Timothée Fontolliet ◽  
Vincent Pichot ◽  
Aurélien Bringard ◽  
Nazzareno Fagoni ◽  
Alessandra Adami ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Baroreflex Sensitivity ◽  
Total Power ◽  
Vagal Activity ◽  
Arterial Blood ◽  
Exercise Onset ◽  
Autonomic Blockade ◽  
Vagal Withdrawal

We performed the first analysis of heart rate variability (HRV) at rest and during exercise under full autonomic blockade on the same subjects, to test the conjecture that vagal tone withdrawal occurs at exercise onset. We hypothesized that between rest and exercise there would be 1) no differences in total power (PTOT) under parasympathetic blockade, 2) a PTOT fall under β1-sympathetic blockade, and 3) no differences in PTOT under blockade of both autonomic nervous system branches. Seven men [24 (3) yr, mean (SD)] performed 5-min cycling (80 W) supine, preceded by 5-min rest during control and with administration of atropine, metoprolol, and atropine + metoprolol (double blockade). Heart rate and arterial blood pressure were continuously recorded. HRV and blood pressure variability were determined by power spectral analysis, and baroreflex sensitivity was determined by the sequence method. At rest, PTOT and the powers of low- and high-frequency components of HRV (LF and HF, respectively) were dramatically decreased with atropine and double blockade compared with control and metoprolol, with no effects on LF-to-HF ratio and on the normalized LF (LFnu) and HF (HFnu). During exercise, patterns were the same as at rest. Comparing exercise with rest, PTOT varied as hypothesized. For systolic and diastolic blood pressure, resting PTOT was the same in all conditions. During exercise, in all conditions, PTOT was lower than in control. Baroreflex sensitivity decreased under atropine and double blockade at rest and under control and metoprolol during exercise. The results support the hypothesis that vagal suppression determined disappearance of HRV during exercise. NEW & NOTEWORTHY This study provides the first demonstration, by systematic analysis of heart rate variability at rest and during exercise under full autonomic blockade on the same subjects, that suppression of vagal activity is responsible for the disappearance of spontaneous heart rate variability during exercise. This finding supports previous hypotheses on the role of vagal withdrawal in the control of the rapid cardiovascular response at exercise onset.

Applicability of recent methods used to estimate spontaneous baroreflex sensitivity to resting mice

2008 ◽  
Vol 294 (1) ◽  
pp. R142-R150 ◽  
Author(s):  
Dominique Laude ◽  
Véronique Baudrie ◽  
Jean-Luc Elghozi
Keyword(s):  
Baroreflex Sensitivity ◽  
Low Frequency ◽  
Pulse Interval ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Spectral Estimates ◽  
Sequence Method ◽  
Highly Correlated ◽  
Spontaneous Baroreflex ◽  
Sequence Techniques

Short-term blood pressure (BP) variability is limited by the arterial baroreflex. Methods for measuring the spontaneous baroreflex sensitivity (BRS) aim to quantify the gain of the transfer function between BP and pulse interval (PI) or the slope of the linear relationship between parallel BP and PI changes. These frequency-domain (spectral) and time-domain (sequence) techniques were tested in conscious mice equipped with telemetric devices. The autonomic relevance of these indexes was evaluated using pharmacological blockades. The significant changes of the spectral bandwidths resulting from the autonomic blockades were used to identify the low-frequency (LF) and high-frequency (HF) zones of interest. The LF gain was 1.45 ± 0.14 ms/mmHg, with a PI delay of 0.5 s. For the HF gain, the average values were 2.0 ± 0.19 ms/mmHg, with a null phase. LF and HF bands were markedly affected by atropine. On the same 51.2-s segments used for cross-spectral analysis, an average number of 26.4 ± 2.2 slopes were detected, and the average slope in resting mice was 4.4 ± 0.5 ms/mmHg. Atropine significantly reduced the slopes of the sequence method. BRS measurements obtained using the sequence technique were highly correlated to the spectral estimates. This study demonstrates the applicability of the recent methods used to estimate spontaneous BRS in mice. There was a vagal predominance in the baroreflex control of heart rate in conscious mice in the present conditions.

Enhanced open-loop but not closed-loop cardiac baroreflex sensitivity during orthostatic stress in humans

2011 ◽  
Vol 301 (5) ◽  
pp. R1591-R1598 ◽  
Author(s):  
Toshinari Akimoto ◽  
Jun Sugawara ◽  
Daisuke Ichikawa ◽  
Nobuyuki Terada ◽  
Paul J. Fadel ◽  
...  
Keyword(s):  
Heart Rate ◽  
Transfer Function ◽  
White Noise ◽  
Baroreflex Sensitivity ◽  
Closed Loop ◽  
Low Frequency ◽  
Open Loop ◽  
Orthostatic Stress ◽  
Arterial Baroreflex ◽  
Transfer Function Gain

The neural interaction between the cardiopulmonary and arterial baroreflex may be critical for the regulation of blood pressure during orthostatic stress. However, studies have reported conflicting results: some indicate increases and others decreases in cardiac baroreflex sensitivity (i.e., gain) with cardiopulmonary unloading. Thus the effect of orthostatic stress-induced central hypovolemia on regulation of heart rate via the arterial baroreflex remains unclear. We sought to comprehensively assess baroreflex function during orthostatic stress by identifying and comparing open- and closed-loop dynamic cardiac baroreflex gains at supine rest and during 60° head-up tilt (HUT) in 10 healthy men. Closed-loop dynamic “spontaneous” cardiac baroreflex sensitivities were calculated by the sequence technique and transfer function and compared with two open-loop carotid-cardiac baroreflex measures using the neck chamber system: 1) a binary white-noise method and 2) a rapid-pulse neck pressure-neck suction technique. The gain from the sequence technique was decreased from −1.19 ± 0.14 beats·min−1·mmHg−1 at rest to −0.78 ± 0.10 beats·min−1·mmHg−1 during HUT ( P = 0.005). Similarly, closed-loop low-frequency baroreflex transfer function gain was reduced during HUT ( P = 0.033). In contrast, open-loop low-frequency transfer function gain between estimated carotid sinus pressure and heart rate during white-noise stimulation was augmented during HUT ( P = 0.01). This result was consistent with the maximal gain of the carotid-cardiac baroreflex stimulus-response curve (from 0.47 ± 0.15 beats·min−1·mmHg−1 at rest to 0.60 ± 0.20 beats·min−1·mmHg−1 at HUT, P = 0.037). These findings suggest that open-loop cardiac baroreflex gain was enhanced during HUT. Moreover, under closed-loop conditions, spontaneous baroreflex analyses without external stimulation may not represent open-loop cardiac baroreflex characteristics during orthostatic stress.

Arterial baroreflex control of muscle sympathetic nerve activity in the transition from rest to steady-state dynamic exercise in humans

2007 ◽  
Vol 293 (4) ◽  
pp. H2202-H2209 ◽  
Author(s):  
Shigehiko Ogoh ◽  
James P. Fisher ◽  
Peter B. Raven ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
State Dynamic ◽  
Arm Cycling ◽  
Exercise In Humans

We sought to investigate arterial baroreflex (ABR) control of muscle sympathetic nerve activity (MSNA) in the transition from rest to steady-state dynamic exercise. This was accomplished by assessing the relationship between spontaneous variations in diastolic blood pressure (DBP) and MSNA at rest and during the time course of reaching steady-state arm cycling at 50% peak oxygen uptake (V̇o2peak). Specifically, DBP-MSNA relations were examined in eight subjects (25 ± 1 yr) at the start of unloaded arm cycling and then during the initial and a later period of arm cycling once the 50% V̇o2peak work rate was achieved. Heart rate and arterial blood pressure were progressively increased throughout exercise. Although resting MSNA [16 ± 2 burst/min; 181 ± 36 arbitrary units (au) total activity] was unchanged during unloaded cycling, MSNA burst frequency and total activity were significantly elevated during the initial (27 ± 4 burst/min; 367 ± 76 au; P < 0.05) and later (36 ± 7 burst/min; 444 ± 91 au; P < 0.05) periods of exercise. The relationships between DBP and burst incidence, burst strength, and total MSNA were progressively shifted rightward from unloaded to the initial to the later period of 50% V̇o2peak arm cycling without any changes in the slopes of the linear regressions (i.e., ABR sensitivity). Thus a continuous and dynamic resetting of the ABR control of MSNA occurred during the transition from rest to steady-state dynamic exercise. These findings indicate that the ABR control of MSNA was well maintained throughout dynamic exercise in humans, progressively being reset to operate around the exercise-induced elevations in blood pressure and MSNA without any changes in reflex sensitivity.

Dexamethasone attenuates the modulatory effect of the insular cortex on the baroreflex in anesthetized rat

2021 ◽  
Author(s):  
Tatiana Sergeevna Tumanova ◽  
Tatiana Nikolaevna Кokurina ◽  
Galina Ivanovna Rybakova ◽  
Viacheslav G. Aleksandrov
Keyword(s):  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Insular Cortex ◽  
Neural Mechanism ◽  
Arterial Baroreflex ◽  
Inhibitory Effects ◽  
Short Term ◽  
Central Autonomic Network

The arterial baroreflex (BR) is an important neural mechanism for the stabilization of arterial pressure (AP). It is known that the insular cortex (IC) and other parts of the central autonomic network (CAN) are able to modulate the BR arc, altering baroreflex sensitivity (BRS). In addition, the sensitivity of the BR changes under the influence of hormones, in particular glucocorticoids (GC). It has been suggested that GC may influence BRS by altering the ability of the IC to modulate the BR. This hypothesis has been tested in experiments on rats anesthetized with urethane. It was found that microelectrostimulation of the visceral area in the left IC causes a short-term drop in AP, which is accompanied by bradycardia, and impairs BRS. The synthetic GC dexamethasone (DEX) did not significantly affect the magnitude of depressor responses but increased BRS and impaired the effect of IC stimulation on the BR. The results obtained confirm the hypothesis put forward and suggest that GC can attenuate the inhibitory effects of the IC on the BR arc, thereby enhancing the sensitivity of the BR.

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