Modulation of the spontaneous beat-to-beat fluctuations in peripheral vascular resistance during activation of muscle metaboreflex

2007 ◽  
Vol 293 (1) ◽  
pp. H416-H424 ◽  
Author(s):  
Masashi Ichinose ◽  
Shunsaku Koga ◽  
Naoto Fujii ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu

Continuous measurement of leg blood flow (LBF) using Doppler ultrasound with simultaneous noninvasive mean arterial blood pressure (MAP) measurement permits beat-to-beat estimates of leg vascular resistance (LVR) in humans. We tested the hypothesis that the beat-to-beat fluctuations in LVR and the dynamic relationship between MAP and LVR are modulated by the activation of muscle metaboreflex. Twelve healthy subjects performed a 1-min isometric handgrip exercise at 50% maximal voluntary contraction, which was followed by a period of imposed postexercise muscle ischemia (PEMI). We then employed transfer function analysis to examine the dynamic relationships between MAP and LBF and between MAP and LVR, both at rest (control) and during PEMI. We found the following. 1) The spectral power for LBF and LVR in low-frequency (∼0.03–0.15 Hz) range significantly increased from control during PEMI without a significant change in the high-frequency (∼0.15–0.35 Hz) power. 2) During PEMI, the transfer function gains for MAP-LBF and MAP-LVR relationships in the low-frequency (∼0.05–0.15 Hz) range were significantly increased during PEMI (vs. control) but were unchanged in the high-frequency (∼0.2–0.3 Hz) range. 3) The phases for MAP-LBF and MAP-LVR relationships were not different during control and PEMI. The phase for MAP-LVR relationship revealed that changes in MAP were followed by directionally similar changes in LVR, which is consistent with the characteristics of intrinsic vascular regulatory mechanisms such as the myogenic response of the resistance arteries. We suggest that, in humans, modulation of the dynamic MAP-LVR relationship during activation of the muscle metaboreflex reflects complex interactions between intrinsic vascular regulatory mechanisms and sympathetic vascular regulation.

2002 ◽  
Vol 283 (3) ◽  
pp. R653-R662 ◽  
Author(s):  
Michael R. Edwards ◽  
J. Kevin Shoemaker ◽  
Richard L. Hughson

Transfer function analysis of the arterial blood pressure (BP)-mean flow velocity (MFV) relationship describes an aspect of cerebrovascular autoregulation. We hypothesized that the transfer function relating BP to cerebrovascular resistance (CVRi) would be sensitive to low-frequency changes in autoregulation induced by head-up tilt (HUT) and altered arterial Pco 2. Nine subjects were studied in supine and HUT positions with end-tidal Pco 2(Pet CO2 ) kept constant at normal levels: +5 and −5 mmHg. The BP-MFV relationship had low coherence at low frequencies, and there were significant effects of HUT on gain only at high frequencies and of Pco 2 on phase only at low frequencies. BP → CVRi had coherence >0.5 from very low to low frequencies. There was a significant reduction of gain with increased Pco 2 in the very low and low frequencies and with HUT at the low frequency. Phase was affected by Pco 2 in the very low frequencies. Transfer function analysis of BP → CVRi provides direct evidence of altered cerebrovascular autoregulation under HUT and higher levels of Pco 2.


2016 ◽  
Vol 120 (12) ◽  
pp. 1434-1441 ◽  
Author(s):  
Sung-Moon Jeong ◽  
Seon-Ok Kim ◽  
Darren S. DeLorey ◽  
Tony G. Babb ◽  
Benjamin D. Levine ◽  
...  

Cerebral vasomotor reactivity (CVMR) and dynamic cerebral autoregulation (CA) are measured extensively in clinical and research studies. However, the relationship between these measurements of cerebrovascular function is not well understood. In this study, we measured changes in cerebral blood flow velocity (CBFV) and arterial blood pressure (BP) in response to stepwise increases in inspired CO2 concentrations of 3 and 6% to assess CVMR and dynamic CA in 13 healthy young adults [2 women, 32 ± 9 (SD) yr]. CVMR was assessed as percentage changes in CBFV (CVMRCBFV) or cerebrovascular conductance index (CVCi, CVMRCVCi) in response to hypercapnia. Dynamic CA was estimated by performing transfer function analysis between spontaneous oscillations in BP and CBFV. Steady-state CBFV and CVCi both increased exponentially during hypercapnia; CVMRCBFV and CVMRCVCi were greater at 6% (3.85 ± 0.90 and 2.45 ± 0.79%/mmHg) than at 3% CO2 (2.09 ± 1.47 and 0.21 ± 1.56%/mmHg, P = 0.009 and 0.005, respectively). Furthermore, CVMRCBFV was greater than CVMRCVCi during either 3 or 6% CO2 ( P = 0.017 and P < 0.001, respectively). Transfer function gain and coherence increased in the very low frequency range (0.02-0.07 Hz), and phase decreased in the low-frequency range (0.07–0.20 Hz) when breathing 6%, but not 3% CO2. There were no correlations between the measurements of CVMR and dynamic CA. These findings demonstrated influences of inspired CO2 concentrations on assessment of CVMR and dynamic CA. The lack of correlation between CVMR and dynamic CA suggests that cerebrovascular responses to changes in arterial CO2 and BP are mediated by distinct regulatory mechanisms.


2009 ◽  
Vol 296 (5) ◽  
pp. H1416-H1424 ◽  
Author(s):  
Shigehiko Ogoh ◽  
James P. Fisher ◽  
Colin N. Young ◽  
Peter B. Raven ◽  
Paul J. Fadel

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.


2004 ◽  
Vol 287 (3) ◽  
pp. R670-R679 ◽  
Author(s):  
Deborah D. O'Leary ◽  
J. Kevin Shoemaker ◽  
Michael R. Edwards ◽  
Richard L. Hughson

Beat-by-beat estimates of total peripheral resistance (TPR) can be obtained from continuous measurements of cardiac output by using Doppler ultrasound and noninvasive mean arterial blood pressure (MAP). We employed transfer function analysis to study the heart rate (HR) and vascular response to spontaneous changes in blood pressure from the relationships of systolic blood pressure (SBP) to HR (SBP→HR), MAP to total peripheral resistance (TPR) and cerebrovascular resistance index (CVRi) (MAP→TPR and MAP→CVRi), as well as stroke volume (SV) to TPR in nine healthy subjects in supine and 45° head-up tilt positions. The gain of the SBP→HR transfer function was reduced with tilt in both the low- (0.03–0.15 Hz) and high-frequency (0.15–0.35 Hz) regions. In contrast, MAP→TPR transfer function gain was not affected by head-up tilt, but it did increase from low- to high-frequency regions. The phase relationships between MAP→TPR were unaffected by head-up tilt, but, consistent with an autoregulatory system, changes in MAP were followed by directionally similar changes in TPR, just as observed for the MAP→CVRi. The SV→TPR had high coherence with a constant phase of 150–160°. Together, these data that showed changes in MAP preceded changes in TPR, as well as a possible link between SV and TPR, are consistent with complex interactions between the vascular component of the arterial and cardiopulmonary baroreflexes and intrinsic properties such as the myogenic response of the resistance arteries.


2000 ◽  
Vol 279 (5) ◽  
pp. H2486-H2492 ◽  
Author(s):  
C. G. Crandall ◽  
R. Zhang ◽  
B. D. Levine

The purpose of this project was to identify whether dynamic baroreflex regulation of heart rate (HR) is altered during whole body heating. In 14 subjects, dynamic baroreflex regulation of HR was assessed using transfer function analysis. In normothermic and heat-stressed conditions, each subject breathed at a fixed rate (0.25 Hz) while beat-by-beat HR and systolic blood pressure (SBP) were obtained. Whole body heating significantly increased sublingual temperature, HR, and forearm skin blood flow. Spectral analysis of HR and SBP revealed that the heat stress significantly reduced HR and SBP variability within the high-frequency range (0.2–0.3 Hz), reduced SBP variability within the low-frequency range (0.03–0.15 Hz), and increased the ratio of low- to high-frequency HR variability (all P < 0.01). Transfer function gain analysis showed that the heat stress reduced dynamic baroreflex regulation of HR within the high-frequency range (from 1.04 ± 0.06 to 0.54 ± 0.6 beats · min−1 · mmHg−1; P < 0.001) without significantly affecting the gain in the low-frequency range ( P = 0.63). These data suggest that whole body heating reduced high-frequency dynamic baroreflex regulation of HR associated with spontaneous changes in blood pressure. Reduced vagal baroreflex regulation of HR may contribute to reduced orthostatic tolerance known to occur in humans during heat stress.


2000 ◽  
Vol 279 (6) ◽  
pp. R2189-R2199 ◽  
Author(s):  
Ken-Ichi Iwasaki ◽  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
James A. Pawelczyk ◽  
Benjamin D. Levine

Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this “deconditioning response” could primarily be a result of hypovolemia, rather than a unique adaptation of the autonomic nervous system to bed rest. To test this hypothesis, nine healthy subjects underwent 2 wk of −6° head-down bed rest. One year later, five of these same subjects underwent acute hypovolemia with furosemide to produce the same reductions in plasma volume observed after bed rest. We took advantage of power spectral and transfer function analysis to examine the dynamic relationship between blood pressure (BP) and R-R interval. We found that 1) there were no significant differences between these two interventions with respect to changes in numerous cardiovascular indices, including cardiac filling pressures, arterial pressure, cardiac output, or stroke volume; 2) normalized high-frequency (0.15–0.25 Hz) power of R-R interval variability decreased significantly after both conditions, consistent with similar degrees of vagal withdrawal; 3) transfer function gain (BP to R-R interval), used as an index of arterial-cardiac baroreflex sensitivity, decreased significantly to a similar extent after both conditions in the high-frequency range; the gain also decreased similarly when expressed as BP to heart rate × stroke volume, which provides an index of the ability of the baroreflex to alter BP by modifying systemic flow; and 4) however, the low-frequency (0.05–0.15 Hz) power of systolic BP variability decreased after bed rest (−22%) compared with an increase (+155%) after acute hypovolemia, suggesting a differential response for the regulation of vascular resistance (interaction, P < 0.05). The similarity of changes in the reflex control of the circulation under both conditions is consistent with the hypothesis that reductions in plasma volume may be largely responsible for the observed changes in cardiac baroreflex control after bed rest. However, changes in vasomotor function associated with these two conditions may be different and may suggest a cardiovascular remodeling after bed rest.


Author(s):  
Rachel J. Skow ◽  
Andrew R. Steele ◽  
Graham M. Fraser ◽  
Margie H. Davenport ◽  
Craig D. Steinback

Isometric handgrip (IHG) is used to assess sympathetic nervous system responses to exercise and may be useful at predicting hypertension in both pregnant and non-pregnant populations. We have previously observed altered sympathetic nervous system control of blood pressure in late pregnancy. Therefore, we measured muscle sympathetic nerve activity (MSNA) and blood pressure during muscle metaboreflex activation (IHG) in normotensive pregnant women in the third trimester compared to healthy non-pregnant women. Nineteen pregnant (32±3wks gestation) and fourteen non-pregnant women were matched for age, non/pre-pregnant BMI, and parity. MSNA (microneurography), heart rate (ECG), and arterial blood pressure (Finometer) were continuously recorded during ten minutes of rest, and then during two-minutes of IHG at 30% of maximal voluntary contraction, and two-minutes of post-exercise circulatory occlusion (PECO). Baseline SNA was elevated in pregnant (41±11 bursts/min) compared to non-pregnant women (27 ± 9 bursts/minute; p=0.005); however, the sympathetic baroreflex gain and neurovascular transduction were not different between groups (p=0.62 and p=0.32, respectively). During IHG and PECO there was no significant differences in the pressor response (∆MAP) during IHG and PECO was not different between groups (p=0.25, main effect of group) nor the sympathetic response (interaction effect: p=0.16, 0.25, and 0.27 for burst frequency, burst incidence, and total SNA respectively). These data suggest that pregnant women who have maintained sympathetic baroreflex and neurovascular transduction also have similar sympathetic and pressor responses during exercise.


2017 ◽  
Vol 312 (5) ◽  
pp. H1076-H1084 ◽  
Author(s):  
Jun Sugawara ◽  
Tsubasa Tomoto ◽  
Tomoko Imai ◽  
Seiji Maeda ◽  
Shigehiko Ogoh

High cerebral pressure and flow fluctuations could be a risk for future cerebrovascular disease. This study aims to determine whether acute systemic vasoconstriction affects the dynamic pulsatile hemodynamic transmission from the aorta to the brain. We applied a stepwise lower body negative pressure (LBNP) (−10, −20, and −30 mmHg) in 15 young men to induce systemic vasoconstriction. To elucidate the dynamic relationship between the changes in aortic pressure (AoP; estimated from the radial arterial pressure waveforms) and the cerebral blood flow velocity (CBFV) at the middle cerebral artery (via a transcranial Doppler), frequency-domain analysis characterized the beat-to-beat slow oscillation (0.02–0.30 Hz) and the intra-beat rapid change (0.78–9.69 Hz). The systemic vascular resistance gradually and significantly increased throughout the LBNP protocol. In the low-frequency range (LF: 0.07–0.20 Hz) of a slow oscillation, the normalized transfer function gain of the steady-state component (between mean AoP and mean CBFV) remained unchanged, whereas that of the pulsatile component (between pulsatile AoP and pulsatile CBFV) was significantly augmented during −20 and −30 mmHg of LBNP (+28.8% and +32.4% vs. baseline). Furthermore, the relative change in the normalized transfer function gain of the pulsatile component at the LF range correlated with the corresponding change in systemic vascular resistance ( r = 0.41, P = 0.005). Regarding the intra-beat analysis, the normalized transfer function gain from AoP to CBFV was not significantly affected by the LBNP stimulation ( P = 0.77). Our findings suggest that systemic vasoconstriction deteriorates the dampening effect on the pulsatile hemodynamics toward the brain, particularly in slow oscillations (e.g., 0.07–0.20 Hz). NEW & NOTEWORTHY We characterized the pulsatile hemodynamic transmission from the heart to the brain by frequency-domain analysis. The low-frequency transmission was augmented with a mild LBNP stimulation partly due to the elevated systemic vascular resistance. A systemic vasoconstriction deteriorates the dampening effect on slow oscillations of pulsatile hemodynamics toward the brain.


2012 ◽  
Vol 113 (7) ◽  
pp. 1058-1067 ◽  
Author(s):  
P. N. Ainslie ◽  
S. J. E. Lucas ◽  
J.-L. Fan ◽  
K. N. Thomas ◽  
J. D. Cotter ◽  
...  

We sought to determine the influence of sympathoexcitation on dynamic cerebral autoregulation (CA), cerebrovascular reactivity, and ventilatory control in humans at high altitude (HA). At sea level (SL) and following 3–10 days at HA (5,050 m), we measured arterial blood gases, ventilation, arterial pressure, and middle cerebral blood velocity (MCAv) before and after combined α- and β-adrenergic blockade. Dynamic CA was quantified using transfer function analysis. Cerebrovascular reactivity was assessed using hypocapnia and hyperoxic hypercapnia. Ventilatory control was assessed from the hypercapnia and during isocapnic hypoxia. Arterial Pco2 and ventilation and its control were unaltered following blockade at both SL and HA. At HA, mean arterial pressure (MAP) was elevated ( P < 0.01 vs. SL), but MCAv remained unchanged. Blockade reduced MAP more at HA than at SL (26 vs. 15%, P = 0.048). At HA, gain and coherence in the very-low-frequency (VLF) range (0.02–0.07 Hz) increased, and phase lead was reduced (all P < 0.05 vs. SL). Following blockade at SL, coherence was unchanged, whereas VLF phase lead was reduced (−40 ± 23%; P < 0.01). In contrast, blockade at HA reduced low-frequency coherence (−26 ± 20%; P = 0.01 vs. baseline) and elevated VLF phase lead (by 177 ± 238%; P < 0.01 vs. baseline), fully restoring these parameters back to SL values. Irrespective of this elevation in VLF gain at HA ( P < 0.01), blockade increased it comparably at SL and HA (∼43–68%; P < 0.01). Despite elevations in MCAv reactivity to hypercapnia at HA, blockade reduced ( P < 0.05) it comparably at SL and HA, effects we attributed to the hypotension and/or abolition of the hypercapnic-induced increase in MAP. With the exception of dynamic CA, we provide evidence of a redundant role of sympathetic nerve activity as a direct mechanism underlying changes in cerebrovascular reactivity and ventilatory control following partial acclimatization to HA. These findings have implications for our understanding of CBF function in the context of pathologies associated with sympathoexcitation and hypoxemia.


2005 ◽  
Vol 289 (3) ◽  
pp. H1202-H1208 ◽  
Author(s):  
Ronney B. Panerai ◽  
Michelle Moody ◽  
Penelope J. Eames ◽  
John F. Potter

Dynamic cerebral autoregulation (CA) describes the transient response of cerebral blood flow (CBF) to rapid changes in arterial blood pressure (ABP). We tested the hypothesis that the efficiency of dynamic CA is increased by brain activation paradigms designed to induce hemispheric lateralization. CBF velocity [CBFV; bilateral, middle cerebral artery (MCA)], ABP, ECG, and end-tidal Pco2 were continuously recorded in 14 right-handed healthy subjects (21–43 yr of age), in the seated position, at rest and during 10 repeated presentations (30 s on-off) of a word generation test and a constructional puzzle. Nonstationarities were not found during rest or activation. Transfer function analysis of the ABP-CBFV (i.e., input-output) relation was performed for the 10 separate 51.2-s segments of data during activation and compared with baseline data. During activation, the coherence function below 0.05 Hz was significantly increased for the right MCA recordings for the puzzle tasks compared with baseline values (0.36 ± 0.16 vs. 0.26 ± 0.13, P < 0.05) and for the left MCA recordings for the word paradigm (0.48 ± 0.23 vs. 0.29 ± 0.16, P < 0.05). In the same frequency range, significant increases in gain were observed during the puzzle paradigm for the right (0.69 ± 0.37 vs. 0.46 ± 0.32 cm·s−1·mmHg−1, P < 0.05) and left (0.61 ± 0.29 vs. 0.45 ± 0.24 cm·s−1·mmHg−1, P < 0.05) hemispheres and during the word tasks for the left hemisphere (0.66 ± 0.31 vs. 0.39 ± 0.15 cm·s−1·mmHg−1, P < 0.01). Significant reductions in phase were observed during activation with the puzzle task for the right (−0.04 ± 1.01 vs. 0.80 ± 0.86 rad, P < 0.01) and left (0.11 ± 0.81 vs. 0.57 ± 0.51 rad, P < 0.05) hemispheres and with the word paradigm for the right hemisphere (0.05 ± 0.87 vs. 0.64 ± 0.59 rad, P < 0.05). Brain activation also led to changes in the temporal pattern of the CBFV step response. We conclude that transfer function analysis suggests important changes in dynamic CA during mental activation tasks.


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