Dynamics of the RR-interval versus blood pressure relationship at exercise onset in humans

Bringard, Aurélien; Adami, Alessandra; Fagoni, Nazzareno; Fontolliet, Timothée; Lador, Frédéric; Moia, Christian; Tam, Enrico; Ferretti, Guido

doi:10.1007/s00421-017-3564-6

Cited by 14 publications

(37 citation statements)

References 64 publications

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“…Since the effect of LBNP was more evident on SV than on HR, CO became lower, the higher the LBNP level, in agreement with previous findings [58][59][60]. These results, possibly via a baroreflex inhibition, might have entailed a reduced vagal activity and increased sympathetic activity under LBNP at rest [26,61,62]. Accordingly, TPR was higher under LBNP than in Control (▶Fig.…”

Section: Discussionsupporting

confidence: 90%

Effect of Lower Body Negative Pressure on Phase I Cardiovascular Responses at Exercise Onset

et al. 2020

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We hypothesised that vagal withdrawal and increased venous return interact in determining the rapid cardiac output (CO) response (phase I) at exercise onset. We used lower body negative pressure (LBNP) to increase blood distribution to the heart by muscle pump action and reduce resting vagal activity. We expected a larger increase in stroke volume (SV) and smaller for heart rate (HR) at progressively stronger LBNP levels, therefore CO response would remain unchanged. To this aim ten young, healthy males performed a 50 W exercise in supine position at 0 (Control), −15, −30 and −45 mmHg LBNP exposure. On single beat basis, we measured HR, SV, and CO. Oxygen uptake was measured breath-by-breath. Phase I response amplitudes were obtained applying an exponential model. LBNP increased SV response amplitude threefold from Control to −45 mmHg. HR response amplitude tended to decrease and prevented changes in CO response. The rapid response of CO explained that of oxygen uptake. The rapid SV kinetics at exercise onset is compatible with an increased venous return, whereas the vagal withdrawal conjecture cannot be dismissed for HR. The rapid CO response may indeed be the result of two independent yet parallel mechanisms, one acting on SV, the other on HR.

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Section: Discussionsupporting

confidence: 90%

Effect of Lower Body Negative Pressure on Phase I Cardiovascular Responses at Exercise Onset

et al. 2020

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“…Therefore, φ1 was interpreted as the baroreflex attempt to correct the reduction in MAP (Fagoni et al 2015). Bringard et al (2017) observed similar patterns in the first seconds of light exercise (Bringard et al 2017). They demonstrated that, before the opposite variations of R-to-R interval (RRi) and MAP leading to the arterial baroreflex resetting at exercise, there is an initial progressive consensual decrease of RRi and MAP along a specific baroreflex curve.…”

Section: Introductionmentioning

confidence: 89%

“…In apnoea φ1, which is a dynamic unsteady state condition, only closed-loop method can be employed to analyse baroreflex responses (Bringard et al 2017). Sequences of consecutive beats in which RRi and MAP increase or decrease concurrently can be identified (Sivieri et al 2015;Fagoni et al 2015), defining linear segments of the RRi versus MAP relationship (Taboni et al 2018a).…”

Section: Measurements and Data Treatmentmentioning

confidence: 99%

“…A test of these hypotheses requires an analysis of the characteristics of the cardiac-chronotropic component of arterial baroreflex responses during breath-holding. Since φ1 is an unsteady state condition, only closed-loop methods can conveniently be used for the analysis of arterial baroreflexes (Adami et al 2013;Bringard et al 2017). Therefore, to test these hypotheses, we performed a closed-loop analysis of the arterial baroreflexes during φ1 and φ2 that characterise the cardiovascular time course of a dry apnoea performed at high lung volumes.…”

Section: Introductionmentioning

confidence: 99%

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Baroreflex responses during dry resting and exercise apnoeas in air and pure oxygen

et al. 2020

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Purpose We analysed the characteristics of arterial baroreflexes during the first phase of apnoea (φ1). Methods 12 divers performed rest and exercise (30 W) apnoeas (air and oxygen). We measured beat-by-beat R-to-R interval (RRi) and mean arterial pressure (MAP). Mean RRi and MAP values defined the operating point (OP) before (PRE-ss) and in the second phase (φ2) of apnoea. Baroreflex sensitivity (BRS, ms·mmHg−1) was calculated with the sequence method. Results In PRE-ss, BRS was (median [IQR]): at rest, 20.3 [10.0–28.6] in air and 18.8 [13.8–25.2] in O2; at exercise 9.2[8.4–13.2] in air and 10.1[8.4–13.6] in O2. In φ1, during MAP decrease, BRS was lower than in PRE-ss at rest (6.6 [5.3–11.4] in air and 7.7 [4.9–14.3] in O2, p < 0.05). At exercise, BRS in φ1 was 6.4 [3.9–13.1] in air and 6.7 [4.1–9.5] in O2. After attainment of minimum MAP (MAPmin), baroreflex resetting started. After attainment of minimum RRi, baroreflex sequences reappeared. In φ2, BRS at rest was 12.1 [9.6–16.2] in air, 12.9 [9.2–15.8] in O2. At exercise (no φ2 in air), it was 7.9 [5.4–10.7] in O2. In φ2, OP acts at higher MAP values. Conclusion In apnoea φ1, there is a sudden correction of MAP fall via baroreflex. The lower BRS in the earliest φ1 suggests a possible parasympathetic mechanism underpinning this reduction. After MAPmin, baroreflex resets, displacing its OP at higher MAP level; thus, resetting may not be due to central command. After resetting, restoration of BRS suggests re-establishment of vagal drive.

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“…Different concepts are at stake. In closed-loop context, in which the sequence method is used, different definitions of baroreflex sensitivity provide F I G U R E 1 Graphical representations of: A, Equation (1), constructed using published data; 6 B, Equation (A1), constructed using the same data of panel (A); 6 C, Equation (2), constructed using published data; 5 D, Equation (A3), constructed using the same data of panel (C). 5 Black and grey lines refer to resting and exercising humans, respectively.…”

Section: Discussionmentioning

confidence: 99%

Baroreflex sensitivity: An algebraic dilemma

et al. 2017

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The baroreflex system is a complex mechanism for short-term regulation of arterial blood pressure, involving the heart rate (HR), the heart contractility and the vascular tone in its efferent branches. The study of arterial baroreflexes relies on two different experimental approaches. On the one hand, the closed-loop approach analyses the mutual relationship between HR and arterial blood pressure, both in steady state and in dynamic conditions. The most classical method for the study of arterial baroreflexes with a closed-loop approach is the sequence method.1 The typical representation uses the R-

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Dynamics of the RR-interval versus blood pressure relationship at exercise onset in humans

Cited by 14 publications

References 64 publications

Effect of Lower Body Negative Pressure on Phase I Cardiovascular Responses at Exercise Onset

Effect of Lower Body Negative Pressure on Phase I Cardiovascular Responses at Exercise Onset

Baroreflex responses during dry resting and exercise apnoeas in air and pure oxygen

Baroreflex sensitivity: An algebraic dilemma

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