Parasympathetic impairment of baroreflex control of heart rate in Dahl S rats

1990 ◽  
Vol 259 (1) ◽  
pp. R76-R83 ◽  
Author(s):  
S. A. Whitescarver ◽  
C. E. Ott ◽  
T. A. Kotchen
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Sodium Nitroprusside ◽  
Baroreflex Sensitivity ◽  
Parasympathetic Nervous System ◽  
Baroreflex Control ◽  
High Salt Diet ◽  
Salt Diet ◽  
Reflex Bradycardia ◽  
Before And After

To test the hypothesis that impaired baroreflex control of heart rate in Dahl salt-sensitive (S) rats is due to an impairment of the parasympathetic limb of the bradycardic response, baroreflex sensitivity was evaluated in conscious, chronically instrumented Dahl S and salt-resistant (R) animals. Sensitivity was impaired in Dahl S rats when bolus doses of phenylephrine were administered (0.863 +/- 0.042 vs. 1.43 +/- 0.055 ms/mmHg), but it was not different than in R rats when tested with sodium nitroprusside. When the sensitivities before and after blocking the parasympathetic nervous system with atropine were compared, it was revealed that 82% of the reflex bradycardia resulting from bolus doses of phenylephrine was due to the parasympathetic nervous system, whereas the majority (73%) of the bradycardia induced by 5-min infusions of phenylephrine was due to withdrawal of sympathetic tone. Neither baroreflex sensitivity to infusions of phenylephrine (73% sympathetic) or to infusions after atropine (100% sympathetic) were significantly different between S and R rats. Therefore, the impairment of the heart rate reflex in Dahl S rats is due to an impairment of the parasympathetic limb of the response. In addition, a high-salt diet before the development of hypertension did not alter baroreflex sensitivity in either Dahl S or R rats.

Isoflurane Depresses Baroreflex Control of Heart Rate in Decerebrate Rats

2002 ◽  
Vol 96 (5) ◽  
pp. 1214-1222 ◽  
Author(s):  
Jong S. Lee ◽  
Don Morrow ◽  
Michael C. Andresen ◽  
Kyoung S. K. Chang
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Baroreflex Sensitivity ◽  
Baroreflex Control ◽  
Beta Adrenoceptor ◽  
Reflex Bradycardia ◽  
Reflex Tachycardia ◽  
Map Data ◽  
Regulatory Sites

Background Isoflurane inhibits baroreflex control of heart rate (HR) by poorly understood mechanisms. The authors examined whether suprapontine central nervous system cardiovascular regulatory sites are required for anesthetic depression. Methods The effects of isoflurane (1 and 2 rat minimum alveolar concentration [MAC]) on the baroreflex control of HR were determined in sham intact and midcollicular-transected decerebrate rats. Intravenous phenylephrine (0.2-12 microg/kg) and nitroprusside (1-60 microg/kg) were used to measure HR responses to peak changes in mean arterial pressure (MAP). Sigmoidal logistic curve fits to HR-MAP data assessed baroreflex sensitivity (HR/MAP), HR range, lower and upper HR plateau, and MAP at half the HR range (BP50). Four groups (two brain intact and two decerebrate) were studied before, during, and after isoflurane. To assess sympathetic and vagal contributions to HR baroreflex, beta-adrenoceptor (1 mg/kg atenolol) or muscarinic (0.5 mg/kg methyl atropine) antagonists were administered systemically. Results Decerebration did not alter resting MAP and HR or baroreflex parameters. Isoflurane depressed baroreflex slope and HR range in brain-intact and decerebrate rats. In both groups, 1 MAC reduced HR range by depressing peak reflex tachycardia. Maximal reflex bradycardia during increases in blood pressure was relatively preserved. Atenolol during 1 MAC did not alter maximum reflex tachycardia. In contrast, atropine during 1 MAC fully blocked reflex bradycardia. Therefore, 1 MAC predominantly depresses sympathetic components of HR baroreflex. Isoflurane at 2 MAC depressed both HR plateaus and decreased BP50 in both groups. Conclusions Isoflurane depresses HR baroreflex control by actions that do not require suprapontine central nervous system sites. Isoflurane actions seem to inhibit HR baroreflex primarily by the sympathetic nervous system.

Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla

2006 ◽  
Vol 290 (4) ◽  
pp. R1027-R1034 ◽  
Author(s):  
Andréia C. Alzamora ◽  
Robson A. S. Santos ◽  
Maria J. Campagnole-Santos
Keyword(s):  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Opposite Effect ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Differential Modulation ◽  
Baroreflex Control ◽  
Caudal Ventrolateral Medulla ◽  
Angiotensin Peptides ◽  
Reflex Bradycardia

We determined the effect of microinjection of ANG-(1–7) and ANG II into two key regions of the medulla that control the circulation [rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively)] on baroreflex control of heart rate (HR) in anesthetized rats. Reflex bradycardia and tachycardia were induced by increases and decreases in mean arterial pressure produced by intravenous phenylephrine and sodium nitroprusside, respectively. The pressor effects of ANG-(1–7) and ANG II (25 pmol) after RVLM microinjection (11 ± 0.8 and 10 ± 2 mmHg, respectively) were not accompanied by consistent changes in HR. In addition, RVLM microinjection of these angiotensin peptides did not alter the bradycardic or tachycardic component of the baroreflex. CVLM microinjections of ANG-(1–7) and ANG II produced hypotension (−11 ± 1.5 and −11 ± 1.9 mmHg, respectively) that was similarly not accompanied by significant changes in HR. However, CVLM microinjections of angiotensins induced differential changes in the baroreflex control of HR. ANG-(1–7) attenuated the baroreflex bradycardia (0.26 ± 0.06 ms/mmHg vs. 0.42 ± 0.08 ms/mmHg before treatment) and facilitated the baroreflex tachycardia (0.86 ± 0.19 ms/mmHg vs. 0.42 ± 0.10 ms/mmHg before treatment); ANG II produced the opposite effect, attenuating baroreflex tachycardia (0.09 ± 0.06 ms/mmHg vs. 0.31 ± 0.07 ms/mmHg before treatment) and facilitating the baroreflex bradycardia (0.67 ± 0.16 ms/mmHg vs. 0.41 ± 0.05 ms/mmHg before treatment). The modulatory effect of ANG II and ANG-(1–7) on baroreflex sensitivity was completely abolished by peripheral administration of methylatropine. These results suggest that ANG II and ANG-(1–7) at the CVLM produce a differential modulation of the baroreflex control of HR, probably through distinct effects on the parasympathetic drive to the heart.

scholarly journals Identifying physiological origins of baroreflex dysfunction in salt-sensitive hypertension in the Dahl SS rat

2010 ◽  
Vol 42 (1) ◽  
pp. 23-41 ◽  
Author(s):  
Scott M. Bugenhagen ◽  
Allen W. Cowley ◽  
Daniel A. Beard
Keyword(s):  
Heart Rate ◽  
Control System ◽  
Physiological Parameters ◽  
High Salt ◽  
Physiological Mechanisms ◽  
Baroreflex Control ◽  
High Salt Diet ◽  
Salt Diet ◽  
Physiological Variables ◽  
Salt Sensitive Hypertension

Salt-sensitive hypertension is known to be associated with dysfunction of the baroreflex control system in the Dahl salt-sensitive (SS) rat. However, neither the physiological mechanisms nor the genomic regions underlying the baroreflex dysfunction seen in this rat model are definitively known. Here, we have adopted a mathematical modeling approach to investigate the physiological and genetic origins of baroreflex dysfunction in the Dahl SS rat. We have developed a computational model of the overall baroreflex heart rate control system based on known physiological mechanisms to analyze telemetry-based blood pressure and heart rate data from two genetic strains of rat, the SS and consomic SS.13BN, on low- and high-salt diets. With this approach, physiological parameters are estimated, unmeasured physiological variables related to the baroreflex control system are predicted, and differences in these quantities between the two strains of rat on low- and high-salt diets are detected. Specific findings include: a significant selective impairment in sympathetic gain with high-salt diet in SS rats and a protection from this impairment in SS.13BN rats, elevated sympathetic and parasympathetic offsets with high-salt diet in both strains, and an elevated sympathetic tone with high-salt diet in SS but not SS.13BN rats. In conclusion, we have associated several important physiological parameters of the baroreflex control system with chromosome 13 and have begun to identify possible physiological mechanisms underlying baroreflex impairment and hypertension in the Dahl SS rat that may be further explored in future experimental and modeling-based investigation.

Bupivacaine Inhibits Baroreflex Control of Heart Rate in Conscious Rats

2000 ◽  
Vol 92 (1) ◽  
pp. 197-197 ◽  
Author(s):  
Kyoung S. K. Chang ◽  
Don R. Morrow ◽  
Kazuyo Kuzume ◽  
Michael C. Andresen
Keyword(s):  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Cardiovascular Reflexes ◽  
Pulse Interval ◽  
Dependent Manner ◽  
Baroreflex Control ◽  
Conscious Rats ◽  
Reflex Bradycardia ◽  
Adrenergic Antagonist ◽  
Dose Dependent

Background Because exposure to intravenously administered bupivacaine may alter cardiovascular reflexes, the authors examined bupivacaine actions on baroreflex control of heart rate in conscious rats. Methods Baroreflex sensitivity (pulse interval vs. systolic blood pressure in ms/mmHg) was determined before, and 1.5 and 15.0 min after rapid intravenous administration of bupivacaine (0.5, 1.0, and 2.0 mg/kg) using heart rate changes evoked by intravenously administered phenylephrine or nitroprusside. The actions on the sympathetic and parasympathetic autonomic divisions of the baroreflex were tested in the presence of a muscarinic antagonist methyl atropine and a beta-adrenergic antagonist atenolol. Results Within seconds of injection of bupivacaine, mean arterial pressure increased and heart rate decreased in a dose-dependent manner. Baroreflex sensitivity was unaltered after administration of 0.5 mg/kg bupivacaine. In addition, 1 mg/kg bupivacaine at 1.5 min depressed phenylephrine-evoked reflex bradycardia (0.776 +/- 0.325 vs. 0.543 +/- 0.282 ms/mmHg, P < 0.05) but had no effect on nitroprusside-induced tachycardia. Bupivacaine (2 mg/kg), however, depressed reflex bradycardia and tachycardia (phenylephrine, 0.751 +/- 0.318 vs. 0.451 +/- 0.265; nitroprusside, 0.839 +/- 0.256 vs. 0.564 +/- 0.19 ms/mmHg, P < 0.05). Baroreflex sensitivity returned to prebupivacaine levels by 15 min. Bupivacaine (2 mg/kg), in the presence of atenolol, depressed baroreflex sensitivity (phenylephrine, 0.633 +/- 0.204 vs. 0.277 +/- 0.282; nitroprusside, 0.653 +/- 0.142 vs. 0.320 +/- 0.299 ms/mmHg, P < 0.05). In contrast, bupivacaine did not alter baroreflex sensitivity in the presence of methyl atropine. Conclusions Bupivacaine, in clinically relevant concentrations, inhibits baroreflex control of heart rate in conscious rats. This inhibition appears to involve primarily vagal components of the baroreflex-heart rate pathways.

Blockade of AT1 receptors enhances baroreflex control of heart rate in conscious rabbits with heart failure

1996 ◽  
Vol 271 (1) ◽  
pp. R303-R309 ◽  
Author(s):  
H. Murakami ◽  
J. L. Liu ◽  
I. H. Zucker
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Vena Cava ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Baroreflex Control ◽  
At1 Antagonist ◽  
Before And After ◽  
Baroreceptor Activation

Because the renin-angiotensin system is activated in heart failure, we hypothesized that angiotensin II (ANG II) plays a role in altering baroreflex sensitivity in the setting of heart failure. Accordingly, we evaluated the baroreflex control of heart rate (HR) in conscious, chronically instrumented rabbits in the normal state and after the establishment of heart failure. Heart failure was induced by rapid ventricular pacing at a rate of 360-380 beats/min for an average of 14.5 +/- 1.4 days. The data were compared with normal rabbits instrumented in a similar fashion. Baroreflex curves were generated by inflation of implanted hydraulic occluders on the vena cava and aortic arch or by administration of phenylephrine and sodium nitroprusside. Experiments were carried out before and after intravenous administration of the AT1 antagonist L-158,809. Rabbits with heart failure exhibited significantly lower arterial pressure (81 +/- 3 vs. 69 +/- 4 mmHg, P < 0.05), elevated resting HR (230 +/- 5 vs. 260 +/- 10 beats/min, P < 0.05), and elevated left atrial pressure (3.6 +/- 0.7 vs. 13.1 +/- 0.7 mmHg, P < 0.05). ANG II blockade had little effect on resting or baroreflex parameters in normal rabbits. However, in rabbits with heart failure, L-158,809 enhanced baroreflex sensitivity (2.7 +/- 0.5 vs. 4.7 +/- 0.8 beats.min-1.mmHg-1; P < 0.05), primarily by increasing the minimum HR evoked during baroreceptor activation. beta 1-Blockade had no effect on any baroreflex parameter after L-158,809 in rabbits with heart failure. However, L-158,809 significantly reduced the minimum HR after pretreatment with atropine in rabbits with heart failure. These data suggest that ANG II plays a role in modulation of cardiac sympathetic tone in this model of heart failure and may be responsible for the depressed baroreflex sensitivity observed in heart failure.

Effect of vasopressin and phenylephrine on arterial pressure and heart rate in conscious dogs

1986 ◽  
Vol 251 (2) ◽  
pp. H253-H260
Author(s):  
J. L. Robinson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Baroreflex Sensitivity ◽  
Conscious Dogs ◽  
Baroreflex Control ◽  
Pressure Stimulus ◽  
Before And After ◽  
Autonomic Receptors ◽  
The Difference

The effect of arginine vasopressin (AVP) and phenylephrine (PE) infusions on mean arterial pressure (MAP) and heart rate (HR) were compared in conscious dogs with all autonomic receptors intact (I), during muscarinic blockade (MB) and during ganglionic blockade (GB). After either MB or GB, the dose-MAP response curve for AVP and PE was shifted to the left of the I response curve; a greater shift was observed with AVP than with PE. The MAP threshold after GB for AVP and PE occurred at 10 and 50% of the threshold dose observed during the I response, respectively. Not only did the MAP threshold occur at a lower dose after MB and GB, but also the slope of the response curve was steeper than that of the I response. Comparing the amount of drug necessary to increase MAP 25 mmHg above control for PE and AVP before and after GB, the intact PE response required 4.3 +/- 1.0 (P less than 0.01) times more drug than during GB versus the intact AVP required 16.8 +/- 2.8 (P less than 0.01) times more drug than during GB. The baroreflex control of HR when all receptors were intact was 3.4 +/- 0.4 (P = 0.001) times more sensitive during AVP compared with PE; no differences were observed after MB. There were no significant changes in HR to AVP or PE after GB, thus indicating a lack of a direct effect of these agents on the HR. Our results show that MB and GB equally potentiate the pressor effects of AVP and PE, and the augmentation was much greater for AVP than for PE. The difference in the potentiation of these two vasoconstrictors is consistent with the finding that the baroreflex sensitivity during AVP was enhanced compared with PE. We have postulated that, in the resting conscious dog, AVP increases the sensitivity of the baroreflex primarily by producing a greater level of parasympathetic tone to the heart in response to a given pressure stimulus.

scholarly journals Human and Human-Interfaced AI Interactions: Modulation of Human Male Autonomic Nervous System via Pupil Mimicry

Sensors ◽  
2021 ◽  
Vol 21 (4) ◽  
pp. 1028
Author(s):  
Catherine Spicer ◽  
Prashanna Khwaounjoo ◽  
Yusuf Ozgur Cakmak
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Parasympathetic Nervous System ◽  
Pupil Dilation ◽  
Physical Parameters ◽  
Emotional States ◽  
Virtual Humans ◽  
Autonomic Functioning ◽  
Technological Advances ◽  
Pupil Constriction

Pupillary alterations in virtual humans induce neurophysiological responses within an observer. Technological advances have enabled rapid developments in artificial intelligence (AI), from verbal systems, to visual AI interfaces with the ability to express, and respond to emotional states of a user. Visual AI interfaces are able to change their physical parameters, such as pupil diameter. Pupillary changes can alter heart rate, however, effects on heart rate variability (HRV) are unknown. HRV, is an autonomic, non-conscious parameter which monitors sympathetic and parasympathetic nervous system (PNS) activity. N = 34 male participants aged between 19–33 were subjected to a number of conditions such as pupil dilation, constriction and blushing. The present research is the first to investigate the effects of virtual human interactions on human HRV. Outcomes of this study were obtained using eye tracking and HRV measurements. Pupil dilation relative to constriction presented in the female virtual partner induced a significant right pupillary diameter increase (p = 0.041) in human observers. Additionally, female virtual partner pupil constriction relative to dilation induced a significant increase in participants’ PNS HRV response (p = 0.036). These findings indicate the ability of a female virtual interaction partner to modulate parasympathetic autonomic functioning in young healthy male humans. This allows first insights into the effects of interacting with virtual AI interaction partners, on human autonomic functioning, and may aid development of future virtual humans, and their implementation into relevant clinical settings.

scholarly journals Effects of exercise on cardiac autonomic modulation in children: literature update

2015 ◽  
Vol 28 (3) ◽  
pp. 627-636 ◽  
Author(s):  
Gustavo Henrique de Oliveira Mondoni ◽  
Luiz Carlos Marques Vanderlei ◽  
Bruno Saraiva ◽  
Franciele Marques Vanderlei
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Parasympathetic Nervous System ◽  
Healthy Children ◽  
Autonomic Modulation ◽  
Healthy Development ◽  
Autonomic Nervous ◽  
Cardiac Autonomic Modulation

AbstractIntroduction It is known that physical exercise is beneficial and precipitates adjustments to the autonomic nervous system. However, the effect of exercise on cardiac autonomic modulation in children, despite its importance, is poorly investigated.Objective To bring together current information about the effects of exercise on heart rate variability in healthy and obese children.Methods The literature update was performed through a search for articles in the following databases; PubMed, PEDro, SciELO and Lilacs, using the descriptors “exercise” and “child” in conjunction with the descriptors “autonomic nervous system”, “sympathetic nervous system”, “parasympathetic nervous system” and also with no descriptor, but the key word of this study, “heart rate variability”, from January 2005 to December 2012.Results After removal of items that did not fit the subject of the study, a total of 9 articles were selected, 5 with healthy and 4 with obese children.Conclusion The findings suggest that exercise can act in the normalization of existing alterations in the autonomic nervous system of obese children, as well as serve as a preventative factor in healthy children, enabling healthy development of the autonomic nervous system until the child reaches adulthood.

scholarly journals Hemodynamic Patterns and Spectral Analysis of Heart Rate Variability during Dialysis Hypotension

1999 ◽  
Vol 10 (12) ◽  
pp. 2577-2584
Author(s):  
MICHEL G. W. BARNAS ◽  
WALTHER H. BOER ◽  
HEIN A. KOOMANS
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Spectral Analysis ◽  
Parasympathetic Nervous System ◽  
Intradialytic Hypotension ◽  
Intravascular Volume ◽  
Autonomic Nervous System Activity ◽  
System Activity ◽  
Nervous System Activity ◽  
Sympathetic Nervous

Abstract. Intradialytic hypotension, a major source of morbidity during hemodialysis and ultrafiltration, is often accompanied by paradoxical bradycardia. Relatively little is known about the sequential changes in autonomic nervous system activity up to and during the hypotensive episode. Continuous, beat-to-beat measurements of BP and heart rate were made during hemodialysis in patients prone (n = 8) and not prone (n = 11) to develop intradialytic hypotension. Off-line spectral analysis of heart rate variability (HRV) was performed to assess changes in autonomic nervous system activity during dialysis sessions both with and without hypotension. The low frequency (LF) component of HRV is thought to correlate with sympathetic nervous system activity, the high frequency (HF) component with that of the parasympathetic nervous system. In the sessions not complicated by symptomatic hypotension (n = 26), mean arterial BP (MAP) hardly fell, whereas heart rate increased from 77 ± 2 to 89 ± 5 bpm (P < 0.05). The LF component of HRV increased from 45.2 ± 5.0 normalized units (nu) to 59.9 ± 4.9 nu (P < 0.05), whereas the HF component fell from 54.8 ± 5.0 to 40.2 ± 4.4 nu (P < 0.05). These changes agree with compensatory baroreflex-mediated activation of the sympathetic nervous system (and suppressed parasympathetic activity) during ultrafiltration-induced intravascular volume depletion. In the sessions complicated by severe symptomatic hypotension (n = 22), the changes in heart rate and the results of spectral analysis of HRV were similar to those reported above up to the moment of sudden symptomatic (nausea, vomiting, dizziness, cramps) hypotension, whereas MAP had already fallen gradually from 94 ± 3 to 85 ± 3 mmHg (P < 0.05). The sudden further reduction in MAP (to 55 ± 2 mmHg, P < 0.02) was invariably accompanied by bradycardia (heart rate directly before hypotension 90 ± 2 bpm, during hypotension 69 ± 3 bpm, P < 0.002). The LF component of HRV fell from 62.8 ± 4.6 nu directly before to 40.0 ± 3.7 nu (P < 0.05) during hypotension, whereas the HF component increased from 37.9 ± 4.7 to 60.3 ± 3.7 nu (P < 0.05). These findings agree with activation of the cardiodepressor reflex, involving decreased sympathetic and increased parasympathetic nervous system activity, respectively. These findings indicate that activation of the sympatho-inhibitory cardiodepressor reflex (Bezold-Jarisch reflex), which is a physiologic response to a critical reduction in intravascular volume and cardiac filling, is the cause of sudden intradialytic hypotension.

Abstract P161: Tai Chi Movements Bring On Parasympathetic Nerve Output As Indicated By Audible Bowel Sounds

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Desuo Wang
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Tai Chi ◽  
Parasympathetic Nervous System ◽  
Autonomic Nerve ◽  
Parasympathetic Nerve ◽  
Bowel Sounds ◽  
Sympathetic Nervous ◽  
Tai Chi Exercise

Tai Chi movements are unique exercise that can improve cognition, strength somatomotor coordination, and enhance autonomic nerve regulation on internal organ function. The mild increase in heart rate and/or slight sweat during and after practicing Tai Chi indicates the activation of the sympathetic nervous system. There is lack of evidence to show that Tai Chi exercise enhances the activity of parasympathetic nervous system though it has been claimed that practicing Tai Chi could do so. The author tested the hypothesis that Tai Chi exercise brings on an increase in parasympathetic nerve outputs (PNO). The PNO is evaluated by recording the bowel sounds using an audio recorder (Sony digital voice recorder ICD-PX Series) and the data analyses were done using NCH software (WavePad audio editor). The heart rate was simultaneously recorded using a fingertip pulse oximeter (Zacurate Pro Series 500DL) during Tai Chi exercise. All the data was repeatedly collected from a Tai Chi Master in a study period of 6 months. A total of 30 recordings were used to carry out the analysis. The audible bowel sounds occurred when the performer started to do the Ready-Movement of Yang-style Tai Chi. These Tai Chi induced-bowel sounds lasted from the beginning to the end of a set of movements (3-5 min for 24-moves style). The frequency of bowel sounds was in a range of 0.2 to 3.5 Hz. The average number of bowel sounds was approximately 2.5 sounds per Tai Chi Move. The intensity and frequency of the bowel sounds are not related to the change of the performer’s heart rate. In comparison, meditation or deep squat exercise performed by the Tai Chi master did not cause any changes in the bowel sounds. According to the autonomic innervation of the GI tract, increase of bowel movements is mediated by PNO. In conclusion, Tai Chi movements can simultaneously exercise skeletal muscles, sympathetic nervous system and parasympathetic nervous system. The enhancement of parasympathetic nervous system output by Tai Chi exercise is a valuable modality of physical exercise for wellness.

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