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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.

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 x min(-1) x mmHg(-1)); the slope of the SAP-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.

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.

The assumption that tachycardia during light to moderate exercise was predominantly controlled by withdrawal of cardiac parasympathetic nerve activity but not by augmentation of cardiac sympathetic nerve activity (CSNA) was challenged by measuring CSNA during treadmill exercise (speed, 10-60 m/min) for 1 min in five conscious cats. As soon as exercise started, CSNA and heart rate (HR) increased and mean arterial pressure (MAP) decreased; their time courses at the initial 12-s period of exercise were irrespective of the running speed. CSNA increased 168-297% at 7.1 +/- 0.4 s from the exercise onset, and MAP decreased 8-13 mmHg at 6.0 +/- 0.3 s, preceding the increase of 40-53 beats/min in HR at 10.5 +/- 0.4 s. CSNA remained elevated during the later period of exercise, whereas HR and MAP gradually increased until the end of exercise. After the cessation of exercise, CSNA returned quickly to the control, whereas HR was slowly restored. In conclusion, cardiac sympathetic outflow augments at the onset of and during dynamic exercise even though the exercise intensity is low to moderate, which may contribute to acceleration of cardiac pacemaker rhythm.