Cerebral autoregulation dynamics in endurance-trained individuals

2011 ◽  
Vol 110 (5) ◽  
pp. 1327-1333 ◽  
Author(s):  
Mikkel Lind-Holst ◽  
James D. Cotter ◽  
Jørn W. Helge ◽  
Robert Boushel ◽  
Helene Augustesen ◽  
...  
Keyword(s):  
Low Frequency ◽  
Blood Velocity ◽  
Endurance Athletes ◽  
Cerebral Hypoperfusion ◽  
Trained Subjects ◽  
Delayed Onset ◽  
Transfer Function Gain ◽  
Cerebral Vascular Resistance ◽  
Time Point ◽  
Leg Ischemia

Aerobic fitness may be associated with reduced orthostatic tolerance. To investigate whether trained individuals have less effective regulation of cerebral vascular resistance, we studied the middle cerebral artery (MCA) mean blood velocity ( Vmean) response to a sudden drop in mean arterial pressure (MAP) after 2.5 min of leg ischemia in endurance athletes and untrained subjects (maximal O2 uptake: 69 ± 7 vs. 42 ± 5 ml O2·min−1·kg−1; n = 9 for both, means ± SE). After cuff release when seated, endurance athletes had larger drops in MAP (94 ± 6 to 62 ± 5 mmHg, −39%, vs. 99 ± 5 to 73 ± 4 mmHg, −26%) and MCA Vmean (53 ± 3 to 37 ± 2 cm/s, −30%, vs. 58 ± 3 to 43 ± 2 cm/s, −25%). The athletes also had a slower recovery to baseline of both MAP (25 ± 2 vs. 16 ± 1 s, P < 0.01) and MCA Vmean (15 ± 1 vs. 11 ± 1 s, P < 0.05). The onset of autoregulation, determined by the time point of increase in the cerebrovascular conductance index (CVCi = MCA Vmean/MAP) appeared later in the athletes (3.9 ± 0.4 vs. 2.7 ± 0.4s, P = 0.01). Spectral analysis revealed a normal MAP-to-MCA Vmean phase in both groups but ∼40% higher normalized MAP to MCA Vmean low-frequency transfer function gain in the trained subjects. No significant differences were detected in the rates of recovery of MAP and MCA Vmean and the rate of CVCi regulation (18 ± 4 vs. 24 ± 7%/s, P = 0.2). In highly trained endurance athletes, a drop in blood pressure after the release of resting leg ischemia was more pronounced than in untrained subjects and was associated with parallel changes in indexes of cerebral blood flow. Once initiated, the autoregulatory response was similar between the groups. A delayed onset of autoregulation with a larger normalized transfer gain conforms with a less effective dampening of MAP oscillations, indicating that athletes may be more prone to instances of symptomatic cerebral hypoperfusion when MAP declines.

Tolerance to central hypovolemia: the influence of oscillations in arterial pressure and cerebral blood velocity

2011 ◽  
Vol 111 (4) ◽  
pp. 1048-1058 ◽  
Author(s):  
Caroline A. Rickards ◽  
Kathy L. Ryan ◽  
William H. Cooke ◽  
Victor A. Convertino
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lower Body Negative Pressure ◽  
Low Frequency ◽  
Blood Velocity ◽  
Lower Body ◽  
High Tolerance ◽  
Delayed Onset ◽  
Inspiratory Resistance ◽  
Cerebral Blood Velocity

Higher oscillations of cerebral blood velocity and arterial pressure (AP) induced by breathing with inspiratory resistance are associated with delayed onset of symptoms and increased tolerance to central hypovolemia. We tested the hypothesis that subjects with high tolerance (HT) to central hypovolemia would display higher endogenous oscillations of cerebral blood velocity and AP at presyncope compared with subjects with low tolerance (LT). One-hundred thirty-five subjects were exposed to progressive lower body negative pressure (LBNP) until the presence of presyncopal symptoms. Subjects were classified as HT if they completed at least the −60-mmHg level of LBNP (93 subjects; LBNP time, 1,880 ± 259 s) and LT if they did not complete this level (42 subjects; LBNP time, 1,277 ± 199 s). Middle cerebral artery velocity (MCAv) was measured by transcranial Doppler, and AP was measured at the finger by photoplethysmography. Mean MCAv and mean arterial pressure (MAP) decreased progressively from baseline to presyncope for both LT and HT subjects ( P < 0.001). However, low frequency (0.04–0.15 Hz) oscillations of mean MCAv and MAP were higher at presyncope in HT subjects compared with LT subjects (MCAv: HT, 7.2 ± 0.7 vs. LT, 5.3 ± 0.6 (cm/s)2, P = 0.075; MAP: HT, 15.3 ± 1.4 vs. 7.9 ± 1.2 mmHg2, P < 0.001). Consistent with our previous findings using inspiratory resistance, high oscillations of mean MCAv and MAP are associated with HT to central hypovolemia.

Regulation of middle cerebral artery blood velocity during recovery from dynamic exercise in humans

2007 ◽  
Vol 102 (2) ◽  
pp. 713-721 ◽  
Author(s):  
Shigehiko Ogoh ◽  
James P. Fisher ◽  
Sushmita Purkayastha ◽  
Ellen A. Dawson ◽  
Paul J. Fadel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Transfer Function ◽  
Middle Cerebral Artery ◽  
Diastolic Blood Pressure ◽  
Cerebral Artery ◽  
Low Frequency ◽  
Blood Velocity ◽  
Dynamic Exercise ◽  
Frequency Transfer ◽  
Transfer Function Gain

We sought to examine the regulation of cerebral blood flow during 10 min of recovery from mild, moderate, and heavy cycling exercise by measuring middle cerebral artery blood velocity (MCA V). Transfer function analyses between changes in arterial blood pressure and MCA V were used to assess the frequency components of dynamic cerebral autoregulation (CA). After mild and moderate exercise, the decreases in mean arterial pressure (MAP) and mean MCA V (MCA Vm) were small. However, following heavy exercise, MAP was rapidly and markedly reduced, whereas MCA Vm decreased slowly (−23 ± 4 mmHg and −4 ± 1 cm/s after 1 min for MAP and MCA Vm, respectively; means ± SE). Importantly, for each workload, the normalized low-frequency transfer function gain between MAP and MCA Vm remained unchanged from rest to exercise and during recovery, indicating a maintained dynamic CA. Similar results were found for the systolic blood pressure and systolic MCA V relationship. In contrast, the normalized low-frequency transfer function gain between diastolic blood pressure and diastolic MCA V (MCA Vd) increased from rest to exercise and remained elevated in the recovery period ( P < 0.05). However, MCA Vd was quite stable on the cessation of exercise. These findings suggest that MCA V is well maintained following mild to heavy dynamic exercise. However, the increased transfer function gain between diastolic blood pressure and MCA Vd suggests that dynamic CA becomes less effective in response to rapid decreases in blood pressure during the initial 10 min of recovery from dynamic exercise.

scholarly journals Impact of mild orthostatic stress on aortic-cerebral hemodynamic transmission: insight from the frequency domain

2017 ◽  
Vol 312 (5) ◽  
pp. H1076-H1084 ◽  
Author(s):  
Jun Sugawara ◽  
Tsubasa Tomoto ◽  
Tomoko Imai ◽  
Seiji Maeda ◽  
Shigehiko Ogoh
Keyword(s):  
Transfer Function ◽  
Frequency Domain ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Low Frequency ◽  
Domain Analysis ◽  
Frequency Domain Analysis ◽  
Slow Oscillations ◽  
Transfer Function Gain ◽  
The Brain

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.

Differential effects of acute hypoxia and high altitude on cerebral blood flow velocity and dynamic cerebral autoregulation: alterations with hyperoxia

2008 ◽  
Vol 104 (2) ◽  
pp. 490-498 ◽  
Author(s):  
Philip N. Ainslie ◽  
Shigehiko Ogoh ◽  
Katie Burgess ◽  
Leo Celi ◽  
Ken McGrattan ◽  
...  
Keyword(s):  
Blood Flow ◽  
Transfer Function ◽  
High Altitude ◽  
Blood Flow Velocity ◽  
Cerebral Autoregulation ◽  
Acute Hypoxia ◽  
Low Frequency ◽  
Frequency Range ◽  
Transfer Function Gain ◽  
Dynamic Cerebral Autoregulation

We hypothesized that 1) acute severe hypoxia, but not hyperoxia, at sea level would impair dynamic cerebral autoregulation (CA); 2) impairment in CA at high altitude (HA) would be partly restored with hyperoxia; and 3) hyperoxia at HA and would have more influence on blood pressure (BP) and less influence on middle cerebral artery blood flow velocity (MCAv). In healthy volunteers, BP and MCAv were measured continuously during normoxia and in acute hypoxia (inspired O2 fraction = 0.12 and 0.10, respectively; n = 10) or hyperoxia (inspired O2 fraction, 1.0; n = 12). Dynamic CA was assessed using transfer-function gain, phase, and coherence between mean BP and MCAv. Arterial blood gases were also obtained. In matched volunteers, the same variables were measured during air breathing and hyperoxia at low altitude (LA; 1,400 m) and after 1–2 days after arrival at HA (∼5,400 m, n = 10). In acute hypoxia and hyperoxia, BP was unchanged whereas it was decreased during hyperoxia at HA (−11 ± 4%; P < 0.05 vs. LA). MCAv was unchanged during acute hypoxia and at HA; however, acute hyperoxia caused MCAv to fall to a greater extent than at HA (−12 ± 3 vs. −5 ± 4%, respectively; P < 0.05). Whereas CA was unchanged in hyperoxia, gain in the low-frequency range was reduced during acute hypoxia, indicating improvement in CA. In contrast, HA was associated with elevations in transfer-function gain in the very low- and low-frequency range, indicating CA impairment; hyperoxia lowered these elevations by ∼50% ( P < 0.05). Findings indicate that hyperoxia at HA can partially improve CA and lower BP, with little effect on MCAv.

scholarly journals The Delayed-Onset Mechanical Pain Behavior Induced by Infant Peripheral Nerve Injury Is Accompanied by Sympathetic Sprouting in the Dorsal Root Ganglion

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Pei Liu ◽  
Qing Zhang ◽  
You-shui Gao ◽  
Yi-Gang Huang ◽  
Junjie Gao ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Nerve Injury ◽  
Dorsal Root ◽  
Nerve Lesion ◽  
Adult Rats ◽  
Delayed Onset ◽  
Sympathetic Sprouting ◽  
Heat Hyperalgesia ◽  
Time Point

Background. Sympathetic sprouting in the dorsal root ganglion (DRG) following nerve injuries had been proved to induce adult neuropathic pain. However, it is unclear whether the abnormal sprouting occurs in infant nerve injury. Methods. L5 spinal nerve ligation (SNL) or sham surgery was performed on adult rats and 10-day-old pups, and mechanical thresholds and heat hyperalgesia were analyzed on 3, 7, 14, 28, and 56 postoperative days. Tyrosine hydroxylase-labeled sympathetic fibers were observed at each time point, and 2 neurotrophin receptors (p75NTR and TrkA) were identified to explore the mechanisms of sympathetic sprouting. Results. Adult rats rapidly developed mechanical and heat hyperalgesia from postoperative day 3, with concurrent sympathetic sprouting in DRG. In contrast, the pup rats did not show a significantly lower mechanical threshold until postoperative day 28, at which time the sympathetic sprouting became evident in the DRG. No heat hyperalgesia was presented in pup rats at any time point. There was a late expression of glial p75NTR in DRG of pups from postoperative day 28, which was parallel to the occurrence of sympathetic sprouting. The expression of TrkA did not show such a postoperative syncing change. Conclusion. The delayed-onset mechanical allodynia in the infant nerve lesion was accompanied with parallel sympathetic sprouting in DRG. The late parallel expression of glial p75NTR injury may play an essential role in this process, which provides novel insight into the treatment of delayed adolescent neuropathic pain.

scholarly journals Time-course of changes in indirect markers of muscle damage responses following a 130-km cycling race

2016 ◽  
Vol 18 (3) ◽  
pp. 322 ◽  
Author(s):  
Patrick Rodrigues ◽  
Renata Wassmansdorf ◽  
Fabiano Macedo Salgueirosa ◽  
Sara Gabellone Hernandez ◽  
Vitor Bertoli Nascimento ◽  
...  
Keyword(s):  
Muscle Damage ◽  
Time Course ◽  
Muscle Soreness ◽  
Scientific Literature ◽  
Recovery Period ◽  
Plasma Concentrations ◽  
Endurance Athletes ◽  
Long Distance ◽  
Delayed Onset ◽  
Systematic Training

DOI: http://dx.doi.org/10.5007/1980-0037.2016v18n3p322 The purpose of the present investigation was to identify the effects of a 130-km cycling race on indices of biochemical indirect markers of muscle damage and muscle soreness responses during a 72-hour recovery period. Fifteen endurance-trained male cyclists which were competing for more than 2 years and were involved in systematic training at least of 3 days/wk underwent a collection of indirect biochemical markers of muscle damage (CK, LDH, Myo) and delayed onset of muscle soreness (DOMS), at five different moments of data collection: before (PRE) and immediately after (POST) a 130-km cycling race, and 24, 48, 72 hours following the cycling race. CK and LDH plasma concentrations significantly increased POST-race (p < 0.001) and remained high throughout the 72 hour recover period (CK: p < 0.05; LDH: p < 0.001). Myo increased significantly POST-race (p < 0.001) and returned to the PRE-race values 24 hours thereafter (p < 0.05). DOMS increased significantly POST-race (p < 0.001) and returned to the PRE-race values at 48 hours after (p > 0.05). A 130-km cycling race has a noteworty effect on indices of biochemical indirect markers of muscle damage and muscle soreness responses, indicating that 72 hour recovery period do not seems to be enough for long-distance cyclist, and reinforce the propositions of scientific literature about the need of a sufficient recovery period for cycling endurance athletes. 

Effects of dehydration on cerebrovascular control during standing after heavy resistance exercise

2012 ◽  
Vol 112 (11) ◽  
pp. 1875-1883 ◽  
Author(s):  
Gilbert Moralez ◽  
Steven A. Romero ◽  
Caroline A. Rickards ◽  
Kathy L. Ryan ◽  
Victor A. Convertino ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Resistance Exercise ◽  
Cerebral Perfusion ◽  
Low Frequency ◽  
Blood Velocity ◽  
Fluid Restriction ◽  
Prolonged Standing ◽  
Leg Press ◽  
Heavy Resistance Exercise

We tested the hypothesis that dehydration exacerbates reductions of middle cerebral artery blood velocity (MCAv) and alters cerebrovascular control during standing after heavy resistance exercise. Ten males participated in two trials under 1) euhydration (EUH) and 2) dehydration (DEH; fluid restriction + 40 mg furosemide). We recorded finger photoplethysmographic arterial pressure and MCAv (transcranial Doppler) during 10 min of standing immediately after high-intensity leg press exercise. Symptoms (e.g., lightheadedness) were ranked by subjects during standing (1–5 scale). Low-frequency (LF) oscillations of mean arterial pressure (MAP) and mean MCAv were calculated as indicators of cerebrovascular control. DEH reduced plasma volume by 11% ( P = 0.002; calculated from hemoglobin and hematocrit). During the first 30 s of standing after exercise, subjects reported greater symptoms during DEH vs. EUH ( P = 0.05), but these were mild and resolved at 60 s. While MAP decreased similarly between conditions immediately after standing, MCAv decreased more with DEH than EUH ( P = 0.02). With prolonged standing under DEH, mean MCAv remained below baseline ( P ≤ 0.01), and below EUH values ( P ≤ 0.05). LF oscillations of MAP were higher for DEH at baseline and during the entire 10 min of stand after exercise ( P ≤ 0.057), while LF oscillations in mean MCAv were distinguishable only at baseline and 5 min following stand ( P = 0.05 ). Our results suggest that mean MCAv falls below a “symptomatic threshold” in the acute phase of standing after exercise during DEH, although symptoms were mild and transient. During the prolonged phase of standing, increases in LF MAP and mean MCAv oscillations with DEH may help to maintain cerebral perfusion despite absolute MCAv remaining below the symptomatic threshold.

scholarly journals Chronic physical activity mitigates cerebral hypoperfusion during central hypovolemia in elderly humans

2010 ◽  
Vol 298 (3) ◽  
pp. H1029-H1037 ◽  
Author(s):  
Kevin Formes ◽  
Peizhen Zhang ◽  
Nancy Tierney ◽  
Frederick Schaller ◽  
Xiangrong Shi
Keyword(s):  
Lower Body Negative Pressure ◽  
Arterial Blood Flow ◽  
Cerebral Hypoperfusion ◽  
Active Lifestyle ◽  
Physically Active ◽  
Healthy Elderly ◽  
Arterial Blood ◽  
Intrinsic Mechanism ◽  
Transfer Function Gain ◽  
Elderly Humans

This study sought to test the hypothesis that orthostasis-induced cerebral hypoperfusion would be less severe in physically active elderly humans (ACT group) than in sedentary elderly humans (SED group). The peak O2 uptake of 10 SED (67.1 ± 1.4 yr) and 9 ACT (68.0 ± 1.1 yr) volunteers was determined by a graded cycling exercise test (22.1 ± 1.2 vs 35.8 ± 1.3 ml·min−1·kg−1, P < 0.01). Baseline mean arterial pressure (MAP; tonometry) and middle cerebral arterial blood flow velocity ( VMCA; transcranial Doppler) were similar between the groups (SED vs. ACT group: 91 ± 3 vs. 87 ± 3 mmHg and 54.9 ± 2.3 vs. 57.8 ± 3.2 cm/s, respectively), whereas heart rate was higher and stroke volume (bioimpedance) was smaller in the SED group than in the ACT group. Central hypovolemia during graded lower body negative pressure (LBNP) was larger ( P < 0.01) in the ACT group than in the SED group. However, the slope of VMCA/LBNP was smaller ( P < 0.05) in the ACT group (0.159 ± 0.016 cm/s/Torr) than in the SED group (0.211 ± 0.008 cm/s/Torr). During LBNP, the SED group had a greater augmentation of cerebral vasomotor tone ( P < 0.05) and hypocapnia ( P < 0.001) compared with the ACT group. Baseline MAP variability and VMCA variability were significantly smaller in the SED group than in the ACT group, i.e., 0.49 ± 0.07 vs. 1.04 ± 0.16 (mmHg)2 and 1.06 ± 0.19 vs. 4.24 ± 1.59 (cm/s)2, respectively. However, transfer function gain, coherence, and phase between MAP and VMCA signals (Welch spectral estimator) from 0.08–0.18 Hz were not different between SED (1.41 ± 0.18 cm·s−1·mmHg−1, 0.63 ± 0.06 units, and 38.03 ± 6.57°) and ACT (1.65 ± 0.44 cm·s−1·mmHg−1, 0.56 ± 0.05 units, and 48.55 ± 11.84°) groups. We conclude that a physically active lifestyle improves the intrinsic mechanism of cerebral autoregulation and helps mitigate cerebral hypoperfusion during central hypovolemia in healthy elderly adults.

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