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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.

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.

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.

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.

To examine a hypothesis of whether static muscle contraction produces a release of catecholamines from the adrenal medulla via reflex stimulation of preganglionic adrenal sympathetic nerve activity induced by receptors in the contracting muscle, we compared the reflex responses in a concentration of epinephrine (Ep) and norepinephrine (NEp) in arterial plasma during static contraction and during a mechanical stretch of the hindlimb triceps surae muscle in anesthetized cats. Static contraction was evoked by electrically stimulating the peripheral ends of the cut L(7) and S(1) ventral roots at 20 or 40 Hz. Mean arterial pressure (MAP) and heart rate (HR) increased 23 +/- 3.1 mmHg and 19 +/- 4.3 beats/min during static contraction. Ep in arterial plasma increased 0.18 +/- 0.072 ng/ml over the control of 0.14 +/- 0.051 ng/ml within 1 min from the onset of static contraction, and NEp increased 0.47 +/- 0.087 ng/ml over the control of 0.71 +/- 0.108 ng/ml. Following a neuromuscular blockade, although the same ventral root stimulation failed to produce the cardiovascular and plasma catecholamine responses, the mechanical stretch of the muscle increased MAP, HR, and plasma Ep, but not plasma NEp. With bilateral adrenalectomy, the baseline Ep became negligible (0.012 +/- 0.001 ng/ml) and the baseline NEp was lowered to 0.52 +/- 0.109 ng/ml. Neither static contraction nor mechanical stretch produced significant responses in plasma Ep and NEp following the adrenalectomy. These results suggest that static muscle contraction augments preganglionic adrenal sympathetic nerve activity, which in turn secretes epinephrine from the adrenal medulla into plasma. A muscle mechanoreflex from the contracting muscle may play a role in stimulation of the adrenal sympathetic nerve activity.