High plasma norepinephrine attenuates the dynamic  heart rate response to vagal stimulation

Miyamoto, Tadayoshi; Kawada, Toru; Takaki, Hiroshi; Inagaki, Masumi; Yanagiya, Yusuke; Jin, Yin-Tie; Sugimachi, Masaru; Sunagawa, Kenji

doi:10.1152/ajpheart.00660.2002

Cited by 35 publications

(38 citation statements)

References 24 publications

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“…Buchheit; Laursen and Ahmaidi [6] showed that anaerobic exercise (lactate: 10.9 ± 0.9 mmol.L -1 ) were associated with a low level of parasympathetic modulation reactivation, whereas the moderate intensity exercise (lactate: 3.5 ± 0.2 mmol.L -1 ) induced a more rapid rate of parasympathetic modulation reactivation. Authors like, Kawada et al [20]; Miyamoto et al [27]; Miyamoto et al [28] explain that in the presence of sympathetic activation, vagal stimulation essentially depends on the type and location of the most activated adrenergic receptors. For example, Miyamoto et al [27] showed that the dynamic response of vagal stimulation can be attenuated through activation of postganglionic receptors by high levels of plasma norepinephrine, but not by stimulation of the postganglionic cardiac sympathetic nerve [28].…”

Section: Discussionmentioning

confidence: 99%

“…Authors like, Kawada et al [20]; Miyamoto et al [27]; Miyamoto et al [28] explain that in the presence of sympathetic activation, vagal stimulation essentially depends on the type and location of the most activated adrenergic receptors. For example, Miyamoto et al [27] showed that the dynamic response of vagal stimulation can be attenuated through activation of postganglionic receptors by high levels of plasma norepinephrine, but not by stimulation of the postganglionic cardiac sympathetic nerve [28]. Unfortunately, in this study it was not possible to evaluate the stress of the system (i.e., hormones and muscle metabolites) to verify the level of specific contribution on markers of HRV influencers.…”

Section: Discussionmentioning

confidence: 99%

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Heart Rate Variability Responses in Vertical Jump Performance of Basketball Players

Morales¹,

Filho²,

Sampaio-Jorge³

et al. 2014

sports

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Our objectives were to investigate the acute responses of the heart rate variability (HRV) before, during and after the execution of different Vertical Jump (VJ) protocols and correlate the levels of sympathetic and parasympathetic modulation after the VJ execution with the performance variables in VJ. Eight male athletes (29±4.9 years; 186±8.6 cm; 24.8±2.1 kg.m-2; 12±1.2% body fat) of a team participating in the first division of the National Basketball League (NBL), from Brazil, were evaluated. For the HRV analysis, each subject was instructed to stand in a orthostatic position on the jump platform System Optical (Cefise®, São Paulo) for a period of 10 minutes of rest before (R1) and after the VJ executions (R2). Right after the R1 period, athletes performed 5VJ with five seconds intervals (total time ~ 30 seconds) between VJ (5VJ) and then underwent 60 seconds of maximum continuous VJ (60SVJ). The HRV were automatically transferred and analyzed by the softwares "Polar ProTrainer5™" (version 5.41.002., Kempele, Finland) and HRV analisys (version 2.1., Kuopio, Finland), respectively. The HFnu was used to represent the parasympathetic modulation, whereas LFnu represented the sympathetic modulation. The ratio LF:HF was used to represent the balance between sympathetic and parasympathetic modulations. The one-way Analysis of Variance (ANOVA) with post hoc Tukey test was used to compare differences in HRV during the execution of the experimental protocol. Linear regression and Pearson's correlation coefficient were used between the VJ performance variables (mean of 5VJ and 60SVJ, jumps` number and fatigue index) and the sympathetic and parasympathetic modulation LF:HF R2 (p< 0.05). The following comparisons of the HRV were found between the different protocols: 5VJ (LF 93.9±5.4 nu) versus R1 (LF 64.2±19.9 nu); 5VJ (HF 6.0±5,4 nu) versus R1 (HF 35.6±19,9 nu); 5VJ (LF:HF 40.1±37.4) versus R1 (LF:HF 2.6±1.9 nu) (p < 0.001); 60SVJ (LF:HF 8.3±13.8 ms²) versus 5VJ (LF:HF 40.1±7.7 ms²); R2 (LF:HF 6.5±5.7 ms²) versus 5VJ (LF:HF 40.1±7.7 ms²) (p < 0.001). A significant correlation was found between the average height of 5VJ with the sympathetic and parasympathetic modulation LF:HF R2 (r = 0.7942 , p = 0.01 ) and fatigue index 60SVJ with the sympathetic and parasympathetic modulation LF:HF R2 (r = 0.7206 , p = 0.04). It is concluded that the 5VJ test characterized by intermittent high intensity loads, showed high significant responses of sympathetic modulation (LF; LF:HF) compared to the 60SVJ protocol. The 5 min recovery was not sufficient for the onset of vagal tone (parasympathetic modulation), which was accompanied by higher fatigue index presented by basketball athletes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Heart Rate Variability Responses in Vertical Jump Performance of Basketball Players

Morales¹,

Filho²,

Sampaio-Jorge³

et al. 2014

sports

View full text Add to dashboard Cite

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“…Various investigations have demonstrated complex interactions between the sympathetic and vagal systems with respect to HR regulation (30,32,35,36), resulting in reduced (35) or amplified vagal stimulation (30,32). As recently demonstrated by Sunagawa and coworkers (30,35,36), in the presence of sympathetic activation, HR response to vagal stimulation essentially depends on the type and site of adrenergic receptors most selectively activated under a given condition. For example, Sunagawa et al showed that the dynamic HR response to vagal stimulation can be attenuated via activation of ␣-adrenergic receptors on the preganglionic and/or postganglionic cardiac vagal nerve terminals by high plasma norepinephrine Values are means Ϯ SE.…”

Section: Effect Of Muscular Power Engagement and Anaerobic Process Pamentioning

confidence: 96%

“…levels (35) but not by cardiac postganglionic sympathetic nerve stimulation (36). In contrast, elevated cardiac sympathetic nerve activity can augment the dynamic HR response to vagal nerve stimulation via activation of the postjunctional ␤-adrenergic cascade (30,32).…”

Section: Effect Of Muscular Power Engagement and Anaerobic Process Pamentioning

confidence: 98%

Parasympathetic reactivation after repeated sprint exercise

Buchheit

Laursen²,

Ahmaidi³

2007

American Journal of Physiology-Heart and Circulatory Physiology

237

301

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Buchheit M, Laursen PB, Ahmaidi S. Parasympathetic reactivation after repeated sprint exercise. Am J Physiol Heart Circ Physiol 293: H133-H141, 2007. First published March 2, 2007; doi:10.1152/ajpheart.00062.2007.-The purpose of this study was to examine the effects of muscular power engagement, anaerobic participation, aerobic power level, and energy expenditure on postexercise parasympathetic reactivation. We compared the response of heart rate (HR) after repeated sprinting with that of exercise sessions of comparable net energy expenditure and anaerobic energy contribution. Fifteen moderately trained athletes performed 1) 18 maximal all-out 15-m sprints interspersed with 17 s of passive recovery (RS), 2) a moderate isocaloric continuous exercise session (MC) at a level of mean oxygen uptake similar to that of the RS trial, and 3) a high-intensity intermittent exercise session (HI) conducted at a level of anaerobic energy expenditure similar to that of the RS trial. Subjects were immediately seated after the exercise trials, and beatto-beat HR was recorded for 10 min. Parasympathetic reactivation was evaluated through 1) immediate postexercise HR recovery, 2) the time course of the root mean square for the successive R-R interval difference between successive 30-s segments (RMSSD30s) and 3) HR variability vagal-related indexes calculated for the last 5-min stationary period of recovery. RMSSD30s increased during the 10-min period after the MC trial, whereas RMSSD 30s remained depressed after both the RS and HI trials. Parasympathetic reactivation indexes were similar for the RS and HI trials but lower than for the MC trial (P Ͻ 0.001). When data of the three exercise trials were considered together, only anaerobic contribution was related to HR trial-derived indexes. Parasympathetic reactivation is highly impaired after RS exercise and appears to be mainly related to anaerobic process participation.heart rate recovery; vagal-related indexes; autonomic activity; sprint interval training REPEATED SPRINT (RS) training, characterized by recurring sessions of brief repeated bouts of supramaximal exercise, may be a time-efficient strategy for inducing metabolic adaptations in human skeletal muscle (15). Adaptations shown after a short time course of RS training include increased resting glycogen content (20), increased maximal activities of various enzymes involved in glycolytic (31) and oxidative energy provision (10,20), an increased H ϩ buffer capacity (17,20), and decreased cycling time-trial performance (10,15,20). As a result, RS training has been proposed as a viable alternative to classically prescribed submaximal endurance training (10,17,20).Today, there are growing social and psychological reasons to encourage RS training within clinical populations. First, RS training is remarkably time efficient and more compatible with the Western world's time-poor modern lifestyle. Second, the concept of RS training may also be more attractive than continuous exercise for sedentary individuals who have difficulty han...

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“…The muscle metaboreflex-induced tachycardia occurs primarily via increased sympathetic activity, which may decrease HR gain (19). Indeed, it has been previously shown that high plasma norepinephrine concentration attenuates dynamic HR regulation via the vagus nerve (18), and metaboreflex activation can elicit substantial increases in plasma norepinephrine levels, especially in subjects with heart failure (7).…”

Section: Discussionmentioning

confidence: 99%

Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

Ichinose

Sala‐Mercado

Coutsos

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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.2012.-We tested whether mild and moderate dynamic exercise and muscle metaboreflex activation (MMA) affect dynamic baroreflex control of heart rate (HR) and cardiac output (CO), and the influence of stroke volume (SV) fluctuations on CO regulation in normal (N) and pacing-induced heart failure (HF) dogs by employing transfer function analyses of the relationships between spontaneous changes in left ventricular systolic pressure (LVSP) and HR, LVSP and CO, HR and CO, and SV and CO at low and high frequencies (Lo-F, 0.04 -0.15 Hz; Hi-F, 0.15-0.6 Hz). In N dogs, both workloads significantly decreased the gains for LVSP-HR and LVSP-CO in Hi-F, whereas only moderate exercise also reduced the LVSP-CO gain in Lo-F. MMA during mild exercise further decreased the gains for LVSP-HR in both frequencies and for LVSP-CO in Lo-F. MMA during moderate exercise further reduced LVSP-HR gain in Lo-F. Coherence for HR-CO in Hi-F was decreased by exercise and MMA, whereas that in Lo-F was sustained at a high level (Ͼ0.8) in all settings. HF significantly decreased dynamic HR and CO regulation in all situations. In HF, the coherence for HR-CO in Lo-F decreased significantly in all settings; the coherence for SV-CO in Lo-F was significantly higher. We conclude that dynamic exercise and MMA reduces dynamic baroreflex control of HR and CO, and these are substantially impaired in HF. In N conditions, HR modulation plays a major role in CO regulation. In HF, influence of HR modulation wanes, and fluctuations of SV dominate in CO variations. arterial baroreflex; exercise reflexes; pressor response; impaired cardiac performance BEAT-TO-BEAT CARDIAC OUTPUT (CO) varies considerably across successive heart beats, whereas the average level remains remarkably constant under basal conditions (21, 50). This likely involves control mechanisms operating at markedly different frequencies. Rapid baroreflex control of heart rate (HR) is thought to play a crucial role in dynamic CO regulation. Previous studies suggest that low-frequency (Lo-F: 0.04 -0.15 Hz) blood pressure fluctuations are buffered by the dynamic baroreflex control of HR (25, 28). However, we and others have observed that changes in HR do not necessarily elicit proportional changes in CO because stroke volume (SV) may also vary with the changes in ventricular filling time (17,34,48). Furthermore, transient increases in CO will lower ventricular filling pressure (and decreases in CO will raise filling pressure), thereby providing a self-limiting response (6,30,40). Furthermore, baroreflex control of HR may not functionally buffer high-frequency (Hi-F: above 0.15 Hz) blood pressure fluctuations (4,38,44). In this case, Hi-F variations of CO could facilitate blood pressure variability via a feedforward mechanism rather than buffer arterial pressure. In addition, it has been shown that in anesthetized rats, the blood pressure response to cardiac pacing induced high-frequency oscillation of CO is smaller than that to low-frequency oscillation of CO (41). To our knowledge, however, the dynam...

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High plasma norepinephrine attenuates the dynamic heart rate response to vagal stimulation

Cited by 35 publications

References 24 publications

Heart Rate Variability Responses in Vertical Jump Performance of Basketball Players

Heart Rate Variability Responses in Vertical Jump Performance of Basketball Players

Parasympathetic reactivation after repeated sprint exercise

Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

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