Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans

2005 ◽  
Vol 288 (4) ◽  
pp. H1532-H1538 ◽  
Author(s):  
Masashi Ichinose ◽  
Takeshi Nishiyasu
Keyword(s):  
Dynamic Effect ◽  
Voluntary Contraction ◽  
Dynamic Responses ◽  
Arterial Baroreflex ◽  
Peripheral Vascular ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Neck Pressure

We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflex [as reflected by alterations in the dynamic responses shown by leg blood flow (LBF: by the ultrasound Doppler method), leg vascular conductance (LVC), mean arterial blood pressure (MAP), and heart rate (HR)] in humans. In 12 healthy subjects (10 men and 2 women), who performed sustained 1-min handgrip exercise at 50% maximal voluntary contraction followed immediately by an imposed postexercise muscle ischemia (PEMI), 5-s periods of neck pressure (NP; 50 mmHg) or neck suction (NS; −60 mmHg) were used to evaluate carotid baroreflex function both at rest (Con) and during PEMI. First, the decreases in LVC and LBF and the augmentation of MAP elicited by NP were all greater during PEMI than in Con (ΔLVC, −1.2 ± 0.2 vs. −1.9 ± 0.2 ml·min−1·mmHg−1; ΔLBF, −97.3 ± 11.2 vs. −177.0 ± 21.8 ml/min; ΔMAP, 6.7 ± 1.2 vs. 11.5 ± 1.4 mmHg, Con vs. PEMI; each P < 0.05). Second, in Con, NS significantly increased both LVC and LBF (ΔLVC, 0.9 ± 0.2 ml·min−1·mmHg−1; ΔLBF, 46.6 ± 9.8 ml/min; significant change from baseline: each P < 0.05), and, whereas during PEMI no significant increases in LVC and LBF occurred during NS itself (ΔLVC, 0.2 ± 0.1 ml·min−1·mmHg−1; ΔLBF, 10.8 ± 9.6 ml/min; each P > 0.05), a decrease was evident in each parameters at 5 s after the cessation of NS. Third, during PEMI, the decrease in MAP elicited by NS was smaller (ΔMAP, −8.4 ± 1.0 vs. −5.8 ± 0.4 mmHg, Con vs. PEMI; P < 0.05), and it recovered to its initial level more quickly after NS (vs. Con). Finally, however, the HR responses to NS and NP were not different between PEMI and Con. These results suggest that during muscle metaboreflex activation in humans, the arterial baroreflex dynamic effect on peripheral vascular conductance is modulated, as exemplified by 1) an augmentation of the NP-induced LVC decrease, and 2) a loss of the NS-induced LVC increase.

scholarly journals Transfer function characteristics of the neural and peripheral arterial baroreflex arcs at rest and during postexercise muscle ischemia in humans

2009 ◽  
Vol 296 (5) ◽  
pp. H1416-H1424 ◽  
Author(s):  
Shigehiko Ogoh ◽  
James P. Fisher ◽  
Colin N. Young ◽  
Peter B. Raven ◽  
Paul J. Fadel
Keyword(s):  
Transfer Function ◽  
Muscle Sympathetic Nerve Activity ◽  
Voluntary Contraction ◽  
Arterial Baroreflex ◽  
Isometric Handgrip ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Arterial Blood ◽  
Muscle Ischemia ◽  
Transfer Function Gain

Previous studies have demonstrated an increase in the arterial baroreflex (ABR) control of muscle sympathetic nerve activity (MSNA) during isolated activation of the muscle metaboreflex with postexercise muscle ischemia (PEMI). However, the increased ABR-MSNA control does not appear to manifest in an enhancement in the ABR control of arterial blood pressure (BP), suggesting alterations in the transduction of MSNA into a peripheral vascular response and a subsequent ABR-mediated change in BP. Thus we examined the operating gains of the neural and peripheral arcs of the ABR and their interactive relationship at rest and during muscle metaboreflex activation. In nine healthy subjects, graded isolation of the muscle metaboreflex was achieved by PEMI following isometric handgrip performed at 15% and 30% maximal voluntary contraction (MVC). To obtain the sensitivities of the ABR neural and peripheral arcs, the transfer function gain from BP to MSNA and MSNA to femoral vascular conductance, respectively, was analyzed. No changes from rest were observed in the ABR neural or peripheral arcs during PEMI after 15% MVC handgrip. However, PEMI following 30% MVC handgrip increased the low frequency (LF) transfer function gain between BP and MSNA (ABR neural arc; +58 ± 28%, P = 0.036), whereas the LF gain between MSNA and femoral vascular conductance (ABR peripheral arc) was decreased from rest (−36 ± 8%, P = 0.017). These findings suggest that during high-intensity muscle metaboreflex activation an increased ABR gain of the neural arc appears to offset an attenuation of the peripheral arc gain to help maintain the overall ABR control of systemic BP.

scholarly journals Impaired carotid baroreflex control of arterial blood pressure in multiple sclerosis

2016 ◽  
Vol 116 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Mu Huang ◽  
Dustin R. Allen ◽  
David M. Keller ◽  
Paul J. Fadel ◽  
Elliot M. Frohman ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vascular Conductance ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Relapsing Remitting ◽  
Neck Pressure

Multiple sclerosis (MS), a progressive neurological disease, can lead to impairments in the autonomic control of cardiovascular function. We tested the hypothesis that individuals with relapsing-remitting MS ( n = 10; 7 females, 3 males; 13 ± 4 yr from diagnosis) exhibit impaired carotid baroreflex control of blood pressure and heart rate compared with sex, age, and body weight-matched healthy individuals (CON: n = 10; 7 females, 3 males). At rest, 5-s trials of neck pressure (NP; +40 Torr) and neck suction (NS; −60 Torr) were applied to simulate carotid hypotension and hypertension, respectively, while mean arterial pressure (MAP; finger photoplethysmography), heart rate (HR), cardiac output (CO; Modelflow), and total vascular conductance (TVC) were continuously measured. In response to NP, there was a blunted increase in peak MAP responses (MS: 5 ± 2 mmHg) in individuals with MS compared with healthy controls (CON: 9 ± 3 mmHg; P = 0.005), whereas peak HR responses were not different between groups. At the peak MAP response to NP, individuals with MS demonstrated an attenuated decrease in TVC (MS, −10 ± 4% baseline vs. CON, −15 ± 4% baseline, P = 0.012), whereas changes in CO were similar between groups. Following NS, all cardiovascular responses (i.e., nadir MAP and HR and percent changes in CO and TVC) were not different between MS and CON groups. These data suggest that individuals with MS have impaired carotid baroreflex control of blood pressure via a blunted vascular conductance response resulting in a diminished ability to increase MAP in response to a hypotensive challenge.

Effect of muscle metaboreflex activation on carotid-cardiac baroreflex function in humans

2008 ◽  
Vol 294 (5) ◽  
pp. H2296-H2304 ◽  
Author(s):  
James P. Fisher ◽  
Colin N. Young ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Maximum Voluntary Contraction ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Response Curves ◽  
Baroreflex Control ◽  
Muscle Metaboreflex ◽  
Baroreflex Function ◽  
Carotid Baroreflex ◽  
Neck Pressure

Whether the activation of metabolically sensitive skeletal muscle afferents (i.e., muscle metaboreflex) influences cardiac baroreflex responsiveness remains incompletely understood. A potential explanation for contrasting findings of previous reports may be related to differences in the magnitude of muscle metaboreflex activation utilized. Therefore, the present study was designed to investigate the influence of graded intensities of muscle metaboreflex activation on cardiac baroreflex function. In eight healthy subjects (24 ± 1 yr), the graded isolation of the muscle metaboreflex was achieved by post-exercise ischemia (PEI) following moderate- (PEI-M) and high- (PEI-H) intensity isometric handgrip performed at 35% and 45% maximum voluntary contraction, respectively. Beat-to-beat heart rate (HR) and blood pressure were measured continuously. Rapid pulse trains of neck pressure and neck suction (+40 to −80 Torr) were applied to derive carotid baroreflex stimulus-response curves. Mean blood pressure increased significantly from rest during PEI-M (+13 ± 3 mmHg) and was further augmented during PEI-H (+26 ± 4 mmHg), indicating graded metaboreflex activation. However, the operating point gain and maximal gain (−0.51 ± 0.09, −0.48 ± 0.13, and −0.49 ± 0.12 beats·min−1·mmHg−1 for rest; PEI-M and PEI-H) of the carotid-cardiac baroreflex function curve were unchanged from rest during PEI-M and PEI-H ( P > 0.05 vs. rest). Furthermore, the carotid-cardiac baroreflex function curve was progressively reset rightward from rest to PEI-M to PEI-H, with no upward resetting. These findings suggest that the muscle metaboreflex contributes to the resetting of the carotid baroreflex control of HR; however, it would appear not to influence carotid-cardiac baroreflex responsiveness in humans, even with high-intensity activation during PEI.

scholarly journals Sex differences in carotid baroreflex control of arterial blood pressure in humans: relative contribution of cardiac output and total vascular conductance

2011 ◽  
Vol 301 (6) ◽  
pp. H2454-H2465 ◽  
Author(s):  
Areum Kim ◽  
Shekhar H. Deo ◽  
Lauro C. Vianna ◽  
George M. Balanos ◽  
Doreen Hartwich ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sex Differences ◽  
Cardiac Output ◽  
Young Women ◽  
Vascular Conductance ◽  
Baroreflex Control ◽  
Relative Contribution ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Neck Pressure

It is presently unknown whether there are sex differences in the magnitude of blood pressure (BP) responses to baroreceptor perturbation or if the relative contribution of cardiac output (CO) and total vascular conductance (TVC) to baroreflex-mediated changes in BP differs in young women and men. Since sympathetic vasoconstrictor tone is attenuated in women, we hypothesized that carotid baroreflex-mediated BP responses would be attenuated in women by virtue of a blunted vascular response (i.e., an attenuated TVC response). BP, heart rate (HR), and stroke volume were continuously recorded during the application of 5-s pulses of neck pressure (NP; carotid hypotension) and neck suction (NS; carotid hypertension) ranging from +40 to −80 Torr in women ( n = 20, 21 ± 0.5 yr) and men ( n = 20, 21 ± 0.4 yr). CO and TVC were calculated on a beat-to-beat basis. Women demonstrated greater depressor responses to NS (e.g., −60 Torr, −17 ± 1%baseline in women vs. −11 ± 1%baseline in men, P < 0.05), which were driven by augmented decreases in HR that, in turn, contributed to larger reductions in CO (−60 Torr, −15 ± 2%baseline in women vs. −6 ± 2%baseline in men, P < 0.05). In contrast, pressor responses to NP were similar in women and men (e.g., +40 Torr, +14 ± 2%baseline in women vs. +10 ± 1%baseline in men, P > 0.05), with TVC being the primary mediating factor in both groups. Our findings indicate that sex differences in the baroreflex control of BP are evident during carotid hypertension but not carotid hypotension. Furthermore, in contrast to our hypothesis, young women exhibited greater BP responses to carotid hypertension by virtue of a greater cardiac responsiveness.

scholarly journals The carotid baroreflex modifies the pressor threshold of the muscle metaboreflex in humans

2017 ◽  
Vol 313 (3) ◽  
pp. H650-H657 ◽  
Author(s):  
Masashi Ichinose ◽  
Tomoko Ichinose-Kuwahara ◽  
Kazuhito Watanabe ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu
Keyword(s):  
Circulatory Arrest ◽  
Maximum Voluntary Contraction ◽  
Cardiovascular Responses ◽  
Normal Loading ◽  
Muscle Metaboreflex ◽  
Carotid Baroreceptors ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Neck Pressure ◽  
Metabolic Stimulation

The purpose of the present study was to test our hypothesis that unloading the carotid baroreceptors alters the threshold and gain of the muscle metaboreflex in humans. Ten healthy subjects performed a static handgrip exercise at 50% of maximum voluntary contraction. Contraction was sustained for 15, 30, 45, and 60 s and was followed by 3 min of forearm circulatory arrest, during which forearm muscular pH is known to decrease linearly with increasing contraction time. The carotid baroreceptors were unloaded by applying 0.1-Hz sinusoidal neck pressure (oscillating from +15 to +50 mmHg) during ischemia. We estimated the threshold and gain of the muscle metaboreflex by analyzing the relationship between the cardiovascular responses during ischemia and the amount of work done during the exercise. In the condition with unloading of the carotid baroreceptors, the muscle metaboreflex thresholds for mean arterial blood pressure (MAP) and total vascular resistance (TVR) corresponded to significantly lower work levels than the control condition (threshold for MAP: 795 ± 102 vs. 662 ± 208 mmHg and threshold for TVR: 818 ± 213 vs. 572 ± 292 kg·s, P < 0.05), but the gains did not differ between the two conditions (gain for MAP: 4.9 ± 1.7 vs. 4.4 ± 1.6 mmHg·kg·s−1·100 and gain for TVR: 1.3 ± 0.8 vs. 1.3 ± 0.7 mmHg·l−1·min−1·kg·s−1·100). We conclude that the carotid baroreflex modifies the muscle metaboreflex threshold in humans. Our results suggest the carotid baroreflex brakes the muscle metaboreflex, thereby inhibiting muscle metaboreflex-mediated pressor and vasoconstriction responses. NEW & NOTEWORTHY We found that unloading the carotid baroreceptors shifts the pressor threshold of the muscle metaboreflex toward lower metabolic stimulation levels in humans. This finding indicates that, in the normal loading state, the carotid baroreflex inhibits the muscle metaboreflex pressor response by shifting the reflex threshold to higher metabolic stimulation levels.

scholarly journals Interindividual variability in muscle sympathetic responses to static handgrip in young men: evidence for sympathetic responder types?

2018 ◽  
Vol 314 (1) ◽  
pp. R114-R121 ◽  
Author(s):  
Anthony V. Incognito ◽  
Connor J. Doherty ◽  
Jordan B. Lee ◽  
Matthew J. Burns ◽  
Philip J. Millar
Keyword(s):  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Interindividual Variability ◽  
Muscle Sympathetic Nerve Activity ◽  
Voluntary Contraction ◽  
Response Patterns ◽  
Arterial Baroreflex ◽  
Muscle Metaboreflex ◽  
Time To Peak ◽  
Pressure Time

Negative and positive muscle sympathetic nerve activity (MSNA) responders have been observed during mental stress. We hypothesized that similar MSNA response patterns could be identified during the first minute of static handgrip and contribute to the interindividual variability throughout exercise. Supine measurements of multiunit MSNA (microneurography) and continuous blood pressure (Finometer) were recorded in 29 young healthy men during the first (HG1) and second (HG2) minute of static handgrip (30% maximal voluntary contraction) and subsequent postexercise circulatory occlusion (PECO). Responders were identified on the basis of differences from the typical error of baseline total MSNA: 7 negative, 12 positive, and 10 nonresponse patterns. Positive responders demonstrated larger total MSNA responses during HG1 ( P < 0.01) and HG2 ( P < 0.0001); however, the increases in blood pressure throughout handgrip exercise were similar between all groups, as were the changes in heart rate, stroke volume, cardiac output, total vascular conductance, and respiration (all P > 0.05). Comparing negative and positive responders, total MSNA responses were similar during PECO ( P = 0.17) but opposite from HG2 to PECO (∆40 ± 46 vs. ∆-21 ± 62%, P = 0.04). Negative responders also had a shorter time-to-peak diastolic blood pressure during HG1 (20 ± 20 vs. 44 ± 14 s, P < 0.001). Total MSNA responses during HG1 were associated with responses to PECO ( r = 0.39, P < 0.05), the change from HG2 to PECO ( r = −0.49, P < 0.01), and diastolic blood pressure time to peak ( r = 0.50, P < 0.01). Overall, MSNA response patterns during the first minute of static handgrip contribute to interindividual variability and appear to be influenced by differences in central command, muscle metaboreflex activation, and rate of loading of the arterial baroreflex.

Attenuated arterial baroreflex buffering of muscle metaboreflex in heart failure

2005 ◽  
Vol 289 (6) ◽  
pp. H2416-H2423 ◽  
Author(s):  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Jaime Rodriguez ◽  
Tadeusz J. Scislo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Before And After ◽  
Chronically Instrumented Dogs

Previous studies have shown that heart failure (HF) or sinoaortic denervation (SAD) alters the strength and mechanisms of the muscle metaboreflex during dynamic exercise. However, it is still unknown to what extent SAD may modify the muscle metaboreflex in HF. Therefore, we quantified the contribution of cardiac output (CO) and peripheral vasoconstriction to metaboreflex-mediated increases in mean arterial blood pressure (MAP) in conscious, chronically instrumented dogs before and after induction of HF in both barointact and SAD conditions during mild and moderate exercise. The muscle metaboreflex was activated via partial reductions in hindlimb blood flow. After SAD, the metaboreflex pressor responses were significantly higher with respect to the barointact condition despite lower CO responses. The pressor response was significantly lower in HF after SAD but still higher than that of HF in the barointact condition. During control experiments in the barointact condition, total vascular conductance summed from all beds except the hindlimbs did not change with muscle metaboreflex activation, whereas in the SAD condition both before and after induction of HF significant vasoconstriction occurred. We conclude that SAD substantially increased the contribution of peripheral vasoconstriction to metaboreflex-induced increases in MAP, whereas in HF SAD did not markedly alter the patterns of the reflex responses, likely reflecting that in HF the ability of the arterial baroreflex to buffer metaboreflex responses is impaired.

Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise

2005 ◽  
Vol 288 (3) ◽  
pp. H1374-H1380 ◽  
Author(s):  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Jaime Rodriguez ◽  
Tadeusz J. Scislo ◽  
Donal S. O'Leary
Keyword(s):  
Pressor Response ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Major Mechanism ◽  
Pressor Responses ◽  
Before And After ◽  
Chronically Instrumented Dogs

Previous studies showed that the arterial baroreflex opposes the pressor response mediated by muscle metaboreflex activation during mild dynamic exercise. However, no studies have investigated the mechanisms contributing to metaboreflex-mediated pressor responses during dynamic exercise after arterial baroreceptor denervation. Therefore, we investigated the contribution of cardiac output (CO) and peripheral vasoconstriction in mediating the pressor response to graded reductions in hindlimb perfusion in conscious, chronically instrumented dogs before and after sinoaortic denervation (SAD) during mild and moderate exercise. In control experiments, the metaboreflex pressor responses were mediated via increases in CO. After SAD, the metaboreflex pressor responses were significantly greater and significantly smaller increases in CO occurred. During control experiments, nonischemic vascular conductance (NIVC) did not change with muscle metaboreflex activation, whereas after SAD NIVC significantly decreased with metaboreflex activation; thus SAD shifted the mechanisms of the muscle metaboreflex from mainly increases in CO to combined cardiac and peripheral vasoconstrictor responses. We conclude that the major mechanism by which the arterial baroreflex buffers the muscle metaboreflex is inhibition of metaboreflex-mediated peripheral vasoconstriction.

scholarly journals Cardiovascular effects of the respiratory muscle metaboreflexes in dogs: rest and exercise

2003 ◽  
Vol 95 (3) ◽  
pp. 1159-1169 ◽  
Author(s):  
Joshua R. Rodman ◽  
Kathleen S. Henderson ◽  
Curtis A. Smith ◽  
Jerome A. Dempsey
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Lactic Acid ◽  
Respiratory Muscle ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Vascular Conductance ◽  
Iliac Arteries ◽  
Muscle Metaboreflex ◽  
Arterial Blood

In awake dogs, lactic acid was injected into the phrenic and deep circumflex iliac arteries to elicit the diaphragm and abdominal muscle metaboreflexes, respectively. At rest, injections into the phrenic or deep circumflex iliac arteries significantly increased mean arterial blood pressure 21 ± 7% and reduced cardiac output 6 ± 2% and blood flow to the hindlimbs 20 ± 9%. Simultaneously, total systemic, hindlimb, and abdominal expiratory muscle vascular conductances were reduced. These cardiovascular responses were not accompanied by significant changes in the amplitude or timing of the diaphragm electromyogram. During treadmill exercise that increased cardiac output, hindlimb blood flow, and vascular conductance 159 ± 106, 276 ± 309, and 299 ± 90% above resting values, lactic acid injected into the phrenic or deep circumflex iliac arteries also elicited pressor responses and reduced hindlimb blood flow and vascular conductance. Adrenergic receptor blockade at rest eliminated the cardiovascular effects of the respiratory muscle metaboreflex. We conclude that the cardiovascular effects of respiratory muscle metaboreflex activation are similar to those previously reported for limb muscles. When activated via metabolite production, the respiratory muscle metaboreflex may contribute to the increased sympathetic tone and redistribution of blood flow during exercise.

scholarly journals Carotid baroreflex control of arterial blood pressure at rest and during dynamic exercise in aging humans

2010 ◽  
Vol 299 (5) ◽  
pp. R1241-R1247 ◽  
Author(s):  
James P. Fisher ◽  
Areum Kim ◽  
Colin N. Young ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Response Curve ◽  
Dynamic Exercise ◽  
Baroreflex Control ◽  
Stimulus Response ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Older Subjects ◽  
Maximal Gain ◽  
Neck Pressure

The arterial baroreflex is fundamental for evoking and maintaining appropriate cardiovascular adjustments to exercise. We sought to investigate how aging influences carotid baroreflex regulation of blood pressure (BP) during dynamic exercise. BP and heart rate (HR) were continuously recorded at rest and during leg cycling performed at 50% HR reserve in 15 young (22 ± 1 yr) and 11 older (61 ± 2 yr) healthy subjects. Five-second pulses of neck pressure and neck suction from +40 to −80 Torr were applied to determine the full carotid baroreflex stimulus response curve and examine baroreflex resetting during exercise. Although the maximal gain of the modeled stimulus response curve was similar in both groups at rest and during exercise, in older subjects the operating point (OP) was located further away from the centering point (CP) and toward the reflex threshold, both at rest (OP minus CP; −10 ± 3 older vs. 0 ± 2 young mmHg, P < 0.05) and during exercise (OP minus CP; −10 ± 2 older vs. 1 ± 3 young mmHg, P < 0.05). In agreement, older subjects demonstrated a reduced BP response to neck pressure (simulated carotid hypotension) and a greater BP response to neck suction (simulated carotid hypertension). In addition, the magnitude of the upward and rightward resetting of the carotid baroreflex-BP stimulus response curve with exercise was ∼40% greater in older individuals. These data indicate that despite a maintained maximal gain, the ability of the carotid baroreflex to defend against a hypotensive challenge is reduced, whereas responses to hypertensive stimuli are greater with advanced age, both at rest and during exercise.

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