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Purpose: Regular aerobic exercise has come to the forefront of non-pharmacological treatment for hypertension. In this line, post-exercise hypotension may have a potential tool for efficient blood pressure management. However, less is known about the influence of acute aerobic exercise on aortic pulse pressure (PP), an important property underlying the pathophysiology of cardiovascular disease. We tested the hypotheses that aortic PP would be attenuated with a single aerobic exercise and that its extent would be associated with the delayed return of reflected wave and the leg vasodilatory capacity. Methods: In 23 apparent healthy men (22 ± 4 years), hemodynamic variables and aortic pulse wave velocity (PWV) were measured before and 20 and 50 min after a 60-min bout of cycling exercise at moderate intensity (corresponding to 65-75 % heart rate reserve). Aortic pressure was estimated from applanation tonometrically measured radial arterial pressure waveform via general transfer function. Peak calf vascular dilatory capacity was measured with the ischemic exercise-induced hyperemia (via venous occlusion plethysmography). Results: Finger, brachial, and aortic PP were significantly attenuated following the exercise. At 20 min after the exercise cessation, individual changes in aortic PWV significantly correlated with corresponding changes in aortic PP ( r = 0.541, P < 0.05), but this correlation was no longer significant at 50 min after the exercise cessation. Peak calf vascular dilatory capacity was not associated with change in aortic PP. Conclusions: We conclude that in young men the aortic PP would be attenuated with the moderate-intensity dynamic exercise partly due to the delayed return of reflection wave from periphery. [ABSTRACT FROM AUTHOR]

Abstract: Background: Regular aerobic exercise improves large artery compliance in middle-aged and older humans. However, the underlying mechanisms are unknown. We tested the hypothesis that the improved central arterial compliance with endurance training is mediated by decreased α-adrenergic tone and/or increased endothelial function. Methods: Seven sedentary healthy adults (60±3 years) underwent systemic α-adrenergic blockade (phentolamine) and nitric oxide synthase (NOS) inhibition using N G-monomethyl-l-arginine in sequence before and after a 3-month moderate endurance training (walk/jog, 4–5 days/week). Phentolamine was given first to isolate the contribution of nitric oxide to arterial compliance by minimizing reflex suppression of sympathetic tone resulting from systemic NOS inhibition as well as to assess the α-adrenergic receptor-mediated modulation of arterial compliance. Results: Baseline arterial compliance (via simultaneous ultrasound and applanation tonometry on the carotid artery) increased 34±12% after exercise training (P <0.01). When α-adrenergic blockade was performed, arterial compliance increased 37±6% (P <0.01) before the exercise training but did not change significantly after the training. Decreases in arterial compliance from the α-adrenergic blockade to the subsequent additional NOS blockade were not different before and after exercise training. Conclusion: Our results suggest that the reduction in α-adrenergic receptor-mediated vascular tone contributes to the improved central arterial compliance with endurance training. [Copyright &y& Elsevier]

Endurance training improves endothelium-dependent vasodilation, yet it does not increase basal blood flow in the legs. We determined the effects of a 3-mo aerobic exercise intervention on basal leg blood flow and α-adrenergic vasoconstriction and nitric oxide (NO) release in seven apparently healthy middle-aged and older adults (60 ± 3 yr). Basal femoral artery blood flow (via Doppler ultrasound) (pretraining: 354 ± 29; posttraining: 335 ± 34 ml/min) and vascular conductance did not change significantly with the exercise training. Before the exercise intervention, femoral artery blood flow increased 32 ± 16% with systemic α-adrenergic blockade (with phentolamine) (P < 0.05), and the addition of nitric oxide synthase (NOS) inhibition using NG-monomethyl-L-arginine (L-NMMA) did not affect femoral artery blood flow. After training was completed, femoral artery blood flow increased 47 ± 7% with α-adrenergic blockade (P < 0.01) and then decreased 18 ± 7% with the subsequent administration of L-NMMA (P < 0.05). Leg vascular conductance showed a greater α-adrenergic blockade-induced vasodilation (+ 1.7 ± 0.5 to +3.0 ± 0.5 units, P < 0.05) as well as NOS inhibition-induced vasoconstriction (-0.8 ± 0.4 to -2.7 ± 0.7 units, P < 0.05) after the exercise intervention. Resting plasma norepinephrine concentration significantly increased after the training. These results suggest that regular aerobic exercise training enhances NO bioavailability in middle-aged and older adults and that basal limb blood flow does not change with exercise training because of the contrasting influences of sympathetic nervous system activity and endothelium-derived vasodilation on the vasculature. [ABSTRACT FROM AUTHOR]

We have reported that baroreflex bradycardia by stimulation of the aortic depressor nerve is blunted at the onset of voluntary static exercise in conscious cats. Central command may contribute to the blunted bradycardia, because the most blunted bradycardia occurs immediately before exercise or when a forelimb is extended before force development. However, it remained unknown whether the blunted bradycardia is due to either reduced sensitivity of the baroreflex stimulus-response curve or resetting of the curve toward a higher blood pressure. To determine this, we examined the stimulus-response relationship between systolic (SAP) or mean arterial pressure (MAP) and heart rate (HR) at the onset of and during the later period of static exercise in seven cats (n = 348 trials) by changing arterial pressure with infusion of nitroprusside and phenylephrine or norepinephrine. The slope of the MAP-HR curve decreased at the onset of exercise to 48% of the preexercise value (2.9 ± 0.4 beats·min-1· mmHg-1); the slope of the MAP-HR curve decreased to 59%. The threshold blood pressures of the stimulus-response curves, at which HR started to fall due to arterial baroreflex, were not affected. In contrast, the slopes of the stimulus-response curves during the later period of exercise returned near the preexercise levels, whereas the threshold blood pressures elevated 6-8 mmHg. The maximal plateau level of HR was not different before and during static exercise, denying an upward shift of the baroreflex stimulus-response curves. Thus central command is likely to attenuate sensitivity of the cardiac component of arterial baroreflex at the onset of voluntary static exercise without shifting the stimulus-response curve. [ABSTRACT FROM AUTHOR]

To examine whether the central characteristics of the aortic baroreflex alter from moment to moment during static exercise, we identified the dynamic changes in the sizes of the bradycardia and depressor response evoked by stimulation of the aortic depressor nerve (ADN). Three conscious cats were trained to voluntarily extend the right forelimb and press a bar for 31 ± 1 s with a peak force of 337 ± 22 g while maintaining a sitting posture. The ADN stimulation-induced bradycardia was attenuated at the initial period of exercise (up to 8 s from the exercise onset) to 62 ± 5% of the preexercise bradycardia and remained blunted until the end of exercise. The most blunted bradycardia was observed immediately before or when the forelimb was extended before force development. The baroreflex-induced bradycardia was suppressed again at cessation of exercise when the forelimb was retracted and recovered within a few seconds. In contrast, static exercise did not affect the ADN stimulation-induced depressor response. The ADN stimulation-induced bradycardia was also blunted at the beginning of naturally occurring body movement such as spontaneous postural change or grooming behavior. Thus it is likely that the central characteristics of the aortic baroreflex dynamically change from moment to moment during voluntary static exercise and during natural body movement and that particularly a central inhibition of the cardiac component of the aortic baroreflex is induced by central command at the onset of static exercise, whereas the central property of the vasomotor component of the baroreflex is preserved. [ABSTRACT FROM AUTHOR]

Cerebral autoregulation is an important factor in prevention of cerebral ischemic events. We tested a traditional but unproven hypothesis that carotid sinus baroafferent signals contribute to dynamic cerebral autoregulation. Middle cerebral artery mean blood velocity (MCA Vmean) responses to thigh‐cuff deflation‐induced acute hypotension were compared between conditions using neck suction soon after cuff deflation, without or with a cushion wrapped around the upper neck, in nine healthy males (aged 25 ± 5 years). Neck suction was applied close to the hypotension. The MCA Vmean response was expected to differ between conditions because the cushion was presumed to prevent the carotid sinus distension by neck suction. The cushion hindered bradycardia and depressor responses during sole neck suction. Thigh‐cuff deflation decreased mean arterial blood pressure (MAP) and MCA Vmean (Ps < 0.05) with an almost unchanged respiratory rate under both conditions. However, in the neck suction + cushion condition, subsequent MCA Vmean restoration was faster and greater (Ps ≤ 0.0131), despite similar changes in MAP in both conditions. Thus, carotid sinus baroafferent signals would accelerate dynamic cerebral autoregulation during rapid hypotension in healthy young males. Elucidating the mechanism underlying cerebral neural autoregulation could provide a new target for preventing cerebral ischemic events. [ABSTRACT FROM AUTHOR]

Vasoconstriction during tachyarrhythmia contributes to maintenance of arterial pressure (AP) by decreasing peripheral blood flow. This cross-sectional observational study aimed to ascertain whether the relationship between peripheral blood flow and AP recovery occurs during both paroxysmal supraventricular (PSVT, n = 19) and ventricular tachycardias (VT, n = 17). Peripheral blood flow was evaluated using forearm tissue oxygen index (TOI), and mean AP (MAP) was measured using a catheter inserted in the brachial or femoral artery during an electrophysiological study. PSVT and VT rapidly decreased MAP with a comparable heart rate (P = 0.194). MAP recovered to the baseline level at 40 s from PSVT onset, but not VT. The forearm TOI decreased during both tachyarrhythmias (P ≤ 0.029). The TOI response was correlated with MAPrecovery (i.e., MAP recovery from the initial rapid decrease) at 20–60 s from PSVT onset (r = -– 0.652 to – 0.814, P ≤ 0.0298); however, this association was not observed during VT. These findings persisted even after excluding patients who had taken vasoactive drugs. Thus, restricting peripheral blood flow was associated with MAP recovery during PSVT, but not VT. This indicates that AP recovery depends on the type of tachyarrhythmia: different cardiac output and/or vasoconstriction ability during tachyarrhythmia. [ABSTRACT FROM AUTHOR]

Purpose: Near-infrared spectroscopy (NIRS) is widely used to investigate cerebral oxygenation and/or neural activation during physiological conditions such as exercise. However, NIRS-determined cerebral oxygenated hemoglobin (OHb) may not necessarily correspond to intracranial blood flow during dynamic exercise. To determine the selectivity of NIRS to assess cerebral oxygenation and neural activation during exercise, we examined the influence of changes in forehead skin blood flow (SkBF) on NIRS signals during dynamic exercise. Methods: In ten healthy men (age: 20 ± 1 years), middle cerebral artery blood flow velocity (MCA V, via transcranial Doppler ultrasonography), SkBF (via laser Doppler flowmetry), and cerebral OHb (via NIRS) were continuously measured. Each subject performed 60 % maximum heart rate moderate-intensity steady-state cycling exercise. To manipulate SkBF, facial cooling using a mist of cold water (~4 °C) was applied for 3 min during steady-state cycling. Results: MCA V significantly increased during exercise and remained unchanged with facial cooling. OHb and SkBF were also significantly increased during exercise; however, both of these signals were lowered with facial cooling and returned to pre-cooling values with the removal of facial cooling. The changes in OHb correlated significantly with the relative percent changes in SkBF in each individual ( r = 0.71-0.99). Conclusions: These findings suggest that during dynamic exercise NIRS-derived OHb signal can be influenced by thermoregulatory changes in SkBF and therefore, may not be completely reflective of cerebral oxygenation or neural activation. [ABSTRACT FROM AUTHOR]

We investigated the effects of cyclic stretch on vascular smooth muscle cell (VSMC) alignment and potential overlap of signaling modalities with stretch-induced proliferation. VSMC were subjected to graded stretch (1 Hz at 100-124% of resting length) for 48 h. Graded stretch resulted in graded VSMC alignment from a minimum of completely random orientation to a maximum of -80-85° to the stretch vector. Alignment was reversible within 48 h of stretch cessation and independent of signaling modalities mediating stretch induced proliferation: modulation of IGF-1, MAPK, phosphatidylinositol 3-kinase, tyrosine kinase, and stretch-activated calcium channels did not affect alignment. Nitric oxide (NO) synthase (NOS) blockade uncoupled alignment. Neither the NO donor, cytokine-induced NOS activity, nor L-citrulline affected alignment, but inhibited VSMC proliferation. Therefore, stretch-induced proliferation and alignment are differentially regulated, with NO a common signaling molecule for both. Targeting NOS in states such as restenosis and hypertension may prove to be beneficial. [ABSTRACT FROM AUTHOR]

• The midbrain is likely to generate spontaneous motor and cardiovascular responses. • We examined which area of the midbrain is crucial for the synchronized activation. • The ventral tegmental area may be crucial to coactivate motor and cardiovascular systems. Central command, a feedforward signal from higher brain centers, regulates the cardiovascular system in association with exercise. Previous evidence suggests that nucleus (or nuclei) around the midbrain may contribute to generating spontaneous motor activity and concomitant cardiovascular responses. To examine which area within the midbrain is important for the spontaneous and synchronized responses, 18 rats were decerebrated at three levels (pre-midbrain, rostroventral midbrain, and caudal midbrain levels) and paralyzed with a neuromuscular blocker. Individual brain sections showed decerebration rostral to the pre-collicular level in the pre-midbrain preparation and, additionally, removal of the periaqueductal gray in the rostroventral midbrain preparation, and decerebration around the midcollicular level in the caudal midbrain preparation. Spontaneous motor activity occurred at frequency of 69 ± 27 times/h and accompanied increases in heart rate (by 15 ± 4 beats/min) and mean arterial blood pressure (by 54 ± 4 mmHg) in the pre-midbrain preparation. Similar motor and cardiovascular responses took place in the rostroventral midbrain preparation, while such responses hardly occurred in the caudal midbrain preparation. We next examined whether injection of a GABAergic receptor agonist (muscimol) in the ventral tegmental area (VTA) inhibits the spontaneous motor and cardiovascular responses in 6 pre-midbrain preparations. The occurrence of spontaneous motor activity and concomitant cardiovascular responses was inhibited clearly (P < 0.05) by injection of muscimol, but not saline. It is concluded that the VTA plays a pivotal role in the spontaneous and synchronized activation of the motor and cardiovascular systems in decerebrate rats. [ABSTRACT FROM AUTHOR]

In order to safely use autonomous vehicle technologies, it is important to understand the state of drivers’ attention as they ride in Level 3 self-driving vehicles, because they might be required to take manual control of the vehicle in certain situations. We assumed that the attentional state of a driver who has perfect confidence in a self-driving system, and as a result, who is unready to take control of the vehicle is similar to that of a passenger riding in a vehicle driven by another person. Therefore, we compared electrophysiological signals from drivers and passengers that were riding a vehicle in real road environments. Results indicated the following differences: (1) The number of small saccadic eye-movements was greater in drivers than in passengers, whereas the number of large saccadic eye-movements was greater in passengers than in drivers, indicating that passengers tended to look at information irrelevant to safe driving. (2) The amplitude of the P1 component of eye-fixation-related brain potentials time-locked to the offset of large saccadic eye-movements was greater in drivers than in passengers, indicating that visual information processing load was lower in passengers. (3) The duration of eye-blinks was longer in passengers than in drivers, indicating that the arousal level of passengers was relatively low. These findings suggest that these electrophysiological indices can be useful measures for evaluating the attention of drivers while riding in Level 3 autonomous vehicles. Possible differences in the attentional state between drivers and passengers are discussed. [ABSTRACT FROM AUTHOR]

In men, regular aerobic exercise increases central arterial elasticity, but it is decreased by resistance training. We determined the relation between the type of exercise training and arterial elasticity in healthy young women: 26 healthy young women who were sedentary (CO, n = 9), endurance-trained (ET, n = 9), and resistance-trained (RT, n = 8) groups. We determined the carotid arterial compliance and distensibility coefficient (simultaneous ultrasound and applanation tonometry), VO(2max), and 1RM (bench press and leg extension). The VO(2max) in the ET groups was higher than in the CO and RT groups. Both 1RM were higher in the RT groups than in the CO and ET groups. No significant difference was found in the carotid artery compliance and distensibility coefficient among the ET, RT, and CO groups. These results underscore the difficulty in detecting a change in arterial elasticity in young female athletes using the type of exercise training by which it is shown in young men. [ABSTRACT FROM AUTHOR]

R1504 --> Functional magnetic resonance imaging (fMRI) based on the blood oxygen level‐dependent (BOLD) signal is widely used for quantification of brain function and network connectivity. The BOLD fMRI signal largely relies on task‐related changes in blood oxygenation, cerebral blood flow, and cerebral blood volume but would be also influenced by changes in blood pressure (BP). Using 3T fMRI combined with BP measurement, we examined the influence of BP on BOLD signal changes during task switching in 23 young subjects (31 ± 7 yr). Changes in BP to the task were obtained during a session outside the MRI scanner and were utilized to the BP estimation inside the scanner. Task switching evoked BOLD signal changes not only in task‐related frontoparietal regions but also in the brainstem. BOLD signal changes in the brainstem correlated with the increase in mean arterial BP during the task (p < 0.05, r = 0.468). Furthermore, task‐induced BOLD signal changes in the brainstem disappeared when adjusting for confounding effect of BP. These results reveal that mean arterial BP changes in response to cognitive task influence BOLD signal changes in the brainstem. [ABSTRACT FROM AUTHOR]