Influence of single bout of aerobic exercise on aortic pulse pressure.

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.

Carotid sinus baroafferent signals contribute to cerebral blood flow regulation during acute hypotension in young males: A randomized crossover study.

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.

Skin blood flow influences cerebral oxygenation measured by near-infrared spectroscopy during dynamic exercise.

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 (O2Hb) 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(head)) on NIRS signals during dynamic exercise. METHODS: In ten healthy men (age: 20 ± 1 years), middle cerebral artery blood flow velocity (MCA V mean, via transcranial Doppler ultrasonography), SkBF(head) (via laser Doppler flowmetry), and cerebral O2Hb (via NIRS) were continuously measured. Each subject performed 60 % maximum heart rate moderate-intensity steady-state cycling exercise. To manipulate SkBF(head), facial cooling using a mist of cold water (~4 °C) was applied for 3 min during steady-state cycling. RESULTS: MCA V mean significantly increased during exercise and remained unchanged with facial cooling. O2Hb and SkBF(head) 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 O2Hb correlated significantly with the relative percent changes in SkBF(head) in each individual (r = 0.71-0.99). CONCLUSIONS: These findings suggest that during dynamic exercise NIRS-derived O2Hb signal can be influenced by thermoregulatory changes in SkBF(head) and therefore, may not be completely reflective of cerebral oxygenation or neural activation.

Differential relationship between decreased muscle oxygenation and blood pressure recovery during supraventricular and ventricular tachycardia.

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.

Non-invasive assessment of arterial stiffness using oscillometric blood pressure measurement.

BACKGROUND: Arterial stiffness is a major contributor to cardiovascular diseases. Because current methods of measuring arterial stiffness are technically demanding, the purpose of this study was to develop a simple method of evaluating arterial stiffness using oscillometric blood pressure measurement. METHODS: Blood pressure was conventionally measured in the left upper arm of 173 individuals using an inflatable cuff. Using the time series of occlusive cuff pressure and the amplitudes of pulse oscillations, we calculated local slopes of the curve between the decreasing cuff pressure and corresponding arterial volume. Whole pressure-volume curve was derived from numerical integration of the local slopes. The curve was fitted using an equation and we identified a numerical coefficient of the equation as an index of arterial stiffness (Arterial Pressure-volume Index, API). We also measured brachial-ankle (baPWV) PWV and carotid-femoral (cfPWV) PWV using a vascular testing device and compared the values with API. Furthermore, we assessed carotid arterial compliance using ultrasound images to compare with API. RESULTS: The slope of the calculated pressure-volume curve was steeper for compliant (low baPWV or cfPWV) than stiff (high baPWV or cfPWV) arteries. API was related to baPWV (r = -0.53, P < 0.05), cfPWV (r = -0.49, P < 0.05), and carotid arterial compliance (r = 0.32, P < 0.05). A stepwise multiple regression analysis demonstrated that baPWV and carotid arterial compliance were the independent determinants of API, and that API was the independent determinant of baPWV and carotid arterial compliance. CONCLUSIONS: These results suggest that our method can simply and simultaneously evaluate arterial stiffness and blood pressure based on oscillometric measurements of blood pressure.

Pivotal role of the ventral tegmental area in spontaneous motor activity and concomitant cardiovascular responses in decerebrate rats.

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.

Regular endurance exercise in young men increases arterial baroreflex sensitivity through neural alteration of baroreflex arc.

Endurance exercise training increases arterial baroreflex sensitivity that corresponds to alteration in vessel wall compliance of the carotid artery in elderly men. Here, we examined whether regular endurance exercise increases arterial baroreflex sensitivity through neural alteration of the baroreflex arc in young men. We assessed arterial baroreflex sensitivity in eight sedentary men (age 24 +/- 1 yr) and nine men trained in endurance exercise (age 23 +/- 1 yr) during phase IV of the Valsalva maneuver [systolic arterial blood pressure (SAP)-R-R interval relationship]. Arterial baroreflex sensitivity was further analyzed by dividing the mechanical component [SAP-end-systolic carotid lumen diameter relationship (ultrasonography)] and the neural component (end-systolic carotid lumen diameter-R-R interval relationship). Carotid arterial compliance was determined using B-mode ultrasound and arterial applanation tonometry on the common carotid artery. Arterial baroreflex sensitivity and its neural component were greater in the exercise-trained group (P < 0.05). In contrast, carotid arterial compliance and the mechanical component of arterial baroreflex sensitivity did not differ between groups. These results suggest that regular endurance exercise in young men increases arterial baroreflex sensitivity through changes in the neural component of the baroreflex arc and not through alterations in vessel wall compliance of the carotid artery.

Relationship between augmentation index obtained from carotid and radial artery pressure waveforms.

OBJECTIVE: Increased aortic and carotid arterial augmentation index (AI) has been directly linked with cardiovascular disease risk, mortality and morbidity. The aim of this study was to examine whether AI obtained directly from radial artery pressure waveforms (radial AI) can provide information comparable with carotid arterial AI measurements. METHODS: In a cross-sectional study of 204 apparently healthy subjects (88 men and 116 women) aged 19-76 years (51 +/- 15 years, mean +/- SD), carotid AI [(second peak carotid systolic pressure - first peak carotid systolic pressure)/carotid pulse pressure*100] and radial AI [(second peak radial systolic pressure - diastolic pressure)/(first peak radial systolic pressure - diastolic pressure)*100] were measured using applanation tonometry. RESULTS: Radial AI was strongly correlated with carotid AI (r = 0.86, P < 0.0001, SD of difference 10.0%), although radial AI was consistently approximately 66% higher than carotid AI. In 16 apparently healthy young adults (11 men and five women, aged 23 +/- 3 years) handgrip exercise was immediately followed by post-exercise muscle ischaemia (PEMI) to compare changes in carotid and radial AI during increased sympathetic nervous activity. PEMI caused parallel increases in carotid and radial AI (26 and 19%). Accordingly, changes in radial AI with PEMI were strongly correlated with corresponding changes in carotid AI (r = 0.86, P < 0.0001, SD of difference 7.3%). CONCLUSION: These results suggest that AI obtained directly from radial arterial pressure waveforms could provide equivalent information to carotid arterial AI, and has potential as a surrogate marker of cardiovascular disease.

Effect of systemic nitric oxide synthase inhibition on arterial stiffness in humans.

Stiffening of large elastic arteries impairs the buffering function of the arterial system and contributes to cardiovascular disease. The aim of this study was to determine whether endothelium-derived nitric oxide (NO) modulates the stiffness of large elastic arteries in humans. Seven apparently healthy adults (60+/-3 years, 2 males and 5 females) underwent systemic alpha-adrenergic blockade (phentolamine) and systemic NO synthase inhibition using NG-monomethyl-L-arginine (L-NMMA) in sequence. Phentolamine was given first to isolate contribution of NO to arterial stiffness by preventing reflex changes in sympathetic tone that result from systemic NO synthase inhibition, and also to compare arterial stiffness at a similar mean arterial pressure. Mean arterial blood pressure decreased (p<0.05) after phentolamine infusion but returned to baseline levels after L-NMMA infusion. The carotid beta-stiffness index (via simultaneous ultrasound and applanation tonometry on the common carotid artery) did not change after the restraint of systemic alpha-adrenergic nerve activity (9.8+/-1.2 vs. 9.1+/-1.1 U) but increased (p<0.05) after NO synthase inhibition (12.6+/-2.0 U). These results suggest that NO appears to modulate central arterial stiffness in humans.

Beat-to-beat modulation of atrioventricular conduction during dynamic exercise in humans.

A complex balance between extrinsic neural and intrinsic mechanisms is responsible for regulating atrioventricular (AV) conduction. We hypothesized that atrial excitation interval is shortened during dynamic exercise by extrinsic cardiac autonomic activity and that if AV conduction time responds inversely to fluctuation in atrial rhythm, ventricular excitation interval will be maintained at the predetermined cardiac cycle length. To examine such inverse relationship between PP interval and the subsequent change in PR interval (DeltaPR), we analyzed the beat-to-beat changes in PP, PR, and RR intervals during stair-stepping exercise for 10 min in 11 sedentary and 9 trained subjects. In the sedentary group, the average PR interval significantly shortened during exercise, in parallel with the reduction in the average PP and RR intervals. The variance of PP and RR intervals was also significantly decreased during exercise. The reduction in the variance of RR interval was, however, much greater than that of PP interval, implying that AV conduction time changes inversely to fluctuation in atrial excitation rhythm. Indeed, the variance of PR interval was augmented during exercise and there was a clear inverse relationship between PP and DeltaPR intervals. Although trained subjects were characterized by their lower heart rate response during dynamic exercise, the responses in the variability of PP, PR, and RR intervals were fundamentally identical with those in sedentary subjects. We conclude that the AV nodal mechanism that operates at a higher level of heart rate during dynamic exercise may cancel fluctuation in atrial excitation interval and keep ventricular excitation rhythm at the predetermined cardiac cycle length.

Effects of aerobic exercise training on the stiffness of central and peripheral arteries in middle-aged sedentary men.

Aortic pulse wave velocity (PWV) significantly decreased after 16 weeks of moderate-intensity exercise training (walking/jogging) in 17 sedentary middle-aged men, whereas leg PWV did not. These results suggest that in contrast with central arterial stiffness, peripheral arterial stiffness is difficult to change with aerobic exercise training.

Increased oxygenation of the cerebral prefrontal cortex prior to the onset of voluntary exercise in humans.

To determine whether output from the forebrain (termed central command) may descend early enough to increase cardiac and renal sympathetic outflows at the onset of voluntary exercise, we examined the changes in regional tissue blood flows of bilateral prefrontal cortices with near-infrared spectroscopy, precisely identifying the onset of voluntary ergometer 30-s exercise at 41 ± 2% of the maximal exercise intensity in humans. Prefrontal oxygenated-hemoglobin (Oxy-Hb) concentration was measured as index of regional blood flow unless deoxygenated-hemoglobin concentration remained unchanged. Prefrontal Oxy-Hb concentration increased significantly (P < 0.05) 5 s prior to the onset of exercise with arbitrary start, whereas such increase in prefrontal Oxy-Hb was absent before exercise abruptly started by a verbal cue. Furthermore, the increase in prefrontal Oxy-Hb observed at the initial 15-s period of exercise was greater with arbitrary start than cued start. The prefrontal Oxy-Hb, thereafter, decreased during the later period of exercise, irrespective of either arbitrary or cued start. The reduction in prefrontal Oxy-Hb had the same time course and response magnitude as that during motor-driven passive exercise. Cardiac output increased at the initial period of exercise, whereas arterial blood pressure and total peripheral resistance decreased. The depressor response was more pronounced (P < 0.05) with arbitrary start than cued start. Taken together, it is suggested that the increase in prefrontal Oxy-Hb observed prior to the onset of voluntary exercise may be in association with central command, while the later decrease in the Oxy-Hb during exercise may be in association with feedback stimulated by mechanical limb motion.

Central inhibition of the aortic baroreceptors-heart rate reflex at the onset of spontaneous muscle contraction.

Animals decerebrated at the precollicular-premammillary body level exhibit spontaneous locomotion without any artificial stimulation. Our laboratory reported that the cardiovascular and autonomic responses at the onset of spontaneous locomotor events are evoked by central command, generated from the caudal diencephalon and the brain stem (Matsukawa K, Murata J, and Wada T. Am J Physiol Heart Circ Physiol 275: H1115-H1121, 1998). In this study, we examined whether central command and/or a reflex resulting from muscle afferents modulates arterial baroreflex function using a decerebrate cat model. The baroreflex was evoked by stimulating the aortic depressor nerve (ADN) at the onset of spontaneous muscle contraction (to test the possible influence of central command) and during electrically evoked contraction or passive stretch (to test the possible influence of the muscle reflex). When the ADN was stimulated at rest, heart rate and arterial blood pressure decreased by 40 +/- 2 beats/min and 11 +/- 1 mmHg, respectively. The baroreflex bradycardia was attenuated to 55 +/- 4% at the onset of spontaneous contraction. The attenuating effect on the baroreflex bradycardia was not observed at the onset and middle of electrically evoked contraction or passive stretch. The depressor response to ADN stimulation was identical among resting and any muscle interventions. The inhibition of the baroreflex bradycardia during spontaneous contraction was seen after beta-adrenergic blockade but abolished by muscarinic blockade, suggesting that the bradycardia is mainly evoked through cardiac vagal outflow. We conclude that central command, produced within the caudal diencephalon and the brain stem, selectively inhibits the cardiac component, but not the vasomotor component, of the aortic baroreflex at the onset of spontaneous exercise.

Cardiovascular control during voluntary static exercise in humans with tetraplegia.

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C(6)-C(7)). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.

Forelimb vasodilatation induced by hypothalamic stimulation is greatly mediated with nitric oxide in anesthetized cats.

The aim of this study was to examine whether or not stimulation of the hypothalamic defense area is capable of inducing sympathetic vasodilatation of the forelimb vascular bed in anesthetized cats. When the hypothalamic defense area was electrically stimulated, brachial blood flow velocity (brachial BFV) and vascular conductance were increased as well as femoral BFV and vascular conductance. Brachial BFV and vascular conductance increased by 110-139% during hypothalamic stimulation. These increases were blunted to approximately one-fifth of the control responses following i.v. injection of a synthesis inhibitor of nitric oxide, N(omega)-nitro-L-arginine methyl ester (L-NAME). The attenuating effect of L-NAME on forelimb vasodilatation evoked by hypothalamic stimulation was greater than that on hindlimb vasodilatation. The combined administration of L-NAME and atropine sulfate eliminated nearly all of the increases in brachial BFV and vascular conductance during hypothalamic stimulation. From the present results, we conclude that stimulation of the hypothalamic defense area is able to induce neurogenic vasodilatation of the cat forelimb vascular bed, which is greatly mediated with a nitric oxide mechanism. The contribution of nitric oxide to neurogenic vasodilatation seems to be greater in the forelimbs than hindlimbs.

Implantable microelectrodes with new electro-conductive materials for recording sympathetic neural discharge.

We have developed two new types of bipolar cuff microelectrodes (volume size, 2-3 mm(3)) using electro-conductive rubber or water-absorbent polymer, either of which can be applied to measure sympathetic nerve activity in small animals. A renal nerve bundle of an anesthetized rat was inserted into the center hole of the electrode (diameter, 0.15 mm) through a slit and had good contact with the electrodes. Renal sympathetic nerve activity, which was verified by sympathetic ganglionic blockade, could be recorded using either type of implantable cuff electrode.

Influence of regular exercise training on post-exercise hemodynamic regulation to orthostatic challenge.

To prevent orthostatic hypotension, arterial blood pressure (BP) is neurally and hormonally regulated via increases in heart rate (HR) and peripheral vascular tone. After dynamic exercise, however, the latter arm is blunted because of the increased vasodilators in exercised muscles. Orthostatic tachycardia is likely a more important compensatory mechanism for post-exercise orthostatic intolerance in individuals who have higher leg vasodilator capacity, such as endurance-trained athletes. To test the hypothesis that regular endurance training was associated with the greater augmentation of tachycardia response to post-exercise orthostasis, we compared hemodynamic responses to 5-min 60° head-up tilt (HUT) before and after 60 min of cycling at 70% of HR reserve in the endurance-trained (n = 8) and sedentary men (n = 9). Calf peak vascular conductance was 62% greater in the endurance-trained than the sedentary (P < 0.001). After the exercise, the HUT-induced reduction of SV was significantly augmented in the endurance-trained (from -27.7 ± 6.9 to -33.7 ± 7.7 ml, P = 0.03) but not in their sedentary peers. Nevertheless, MAP was well maintained during post-exercise HUT even in the endurance-trained (from 81 ± 10 to 80 ± 8 mmHg). Tachycardia responses during sustained orthostasis were significantly increased in the sedentary (1.3-fold vs. pre-exercise) and more in the endurance-trained (2.0-fold). The augmented response of HUT-induced tachycardia was greater in the endurance-trained than the sedentary (P = 0.04). Additionally, cardiovagal baroreflex sensitivity (BRS), evaluated by the HR response to the hypotensive perturbation, was improved after the exercise in the endurance-trained (from -0.56 ± 0.32 to -1.03 ± 0.26 bpm/mmHg, P = 0.007) but not in the sedentary. These results suggest that in the endurance-trained men the increased orthostatic tachycardia and augmented cardiovagal BRS may favorably mitigate accumulated risks for orthostatic intolerance in the early phase of post-exercise.

Impact of chronic exercise training on the blood pressure response to orthostatic stimulation.

Exercise training elicits morphological adaptations in the left ventricle (LV) and large-conduit arteries that are specific to the type of training performed (i.e., endurance vs. resistance exercise). We investigated whether the mode of chronic exercise training, and the associated cardiovascular adaptations, influence the blood pressure responses to orthostatic stimulation in 30 young healthy men (10 sedentary, 10 endurance trained, and 10 resistance trained). The endurance-trained group had a significantly larger LV end-diastolic volume normalized by body surface area (vs. sedentary and resistance-trained groups), whereas the resistance-trained group had a significantly higher LV wall thickness and aortic pulse wave velocity (PWV) compared with the endurance-trained group. In response to 60° head-up tilt (HUT), mean arterial pressure (MAP) rose in the resistance-trained group (+6.5 ± 1.6 mmHg, P < 0.05) but did not change significantly in sedentary and the endurance-trained groups. Systolic blood pressure (SBP) decreased in endurance-trained group (-8.3 ± 2.4 mmHg, P < 0.05) but did not significantly change in sedentary and resistance-trained groups. A forward stepwise multiple regression analysis revealed that LV wall thickness and aortic PWV were significantly and independently associated with the MAP response to HUT, explaining ∼41% of its variability (R(2) =0.414, P < 0.001). Likewise, aortic PWV and the corresponding HUT-mediated change in stroke volume were significantly and independently associated with the SBP response to HUT, explaining ∼52% of its variability (R(2) = 0.519, P < 0.0001). Furthermore, the change in stroke volume significantly correlated with LV wall thickness (r = 0.39, P < 0.01). These results indicate that chronic resistance and endurance exercise training differentially affect the BP response to HUT, and that this appears to be associated with training-induced morphological adaptations of the LV and large-conduit arteries.

Racial Differences in Relation Between Carotid and Radial Augmentation Index.

BACKGROUND: Augmented central artery wave reflection is a cardiovascular disease risk factor. Augmentation index (AI) obtained from peripheral artery waveforms provides qualitatively similar information to AI from central artery waveforms. Little information is available, however, regarding the influence of racial difference in association between central and peripheral AI. METHODS: We studied 47 White adults (45+/-17 yr, 20 women) and 94 age-matched Asian adults (45+/-14 yr, 42 women). RESULTS: The White group was significantly taller than the Asian group, whereas there were no significant group differences in blood pressure and heart rate. Carotid and radial AI tended to be lower in White compared with Asian adults (P<0.10 for both). Such tendency disappeared when the difference in height was taken into account using ANCOVA (P=0.84 and P=0.77, respectively). Radial AI was strongly and positively correlated with carotid AI in White adults (r=0.75, P<0.0001) as well as in Asian adults (r=0.82, P<0.0001). The slope and intercept of linear regression line between radial and carotid AI of White adults were highly comparable with those of Asian adults. CONCLUSION: AI in the conveniently located peripheral vasculature may provide a surrogate measure of central AI irrespective of difference in race (e.g., Asian vs. White populations).

Reduction in alpha-adrenergic receptor-mediated vascular tone contributes to improved arterial compliance with endurance training.

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 alpha-adrenergic tone and/or increased endothelial function. METHODS: Seven sedentary healthy adults (60+/-3 years) underwent systemic alpha-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 alpha-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 alpha-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 alpha-adrenergic blockade to the subsequent additional NOS blockade were not different before and after exercise training. CONCLUSION: Our results suggest that the reduction in alpha-adrenergic receptor-mediated vascular tone contributes to the improved central arterial compliance with endurance training.