We sought to determine the relative contributions of cessation of skeletal muscle pumping and withdrawal of central command to the rapid decrease in arterial pressure during recovery from exercise. Twelve healthy volunteers underwent three exercise sessions, each consisting of a warm-up, 3 min of cycling at 60% of maximal heart rate, and 5 min of one of the following recovery modes: seated (inactive), loadless pedaling (active), and passive cycling. Mean arterial pressure (MAP), cardiac output, thoracic impedance, and heart rate were measured. When measured 15 s after exercise, MAP decreased less (P < 0.05) during the active (-3 +/- 1 mmHg) and passive (-6 +/- 1 mmHg) recovery modes than during inactive (-18 +/- 2 mmHg) recovery. These differences in MAP persisted for the first 4 min of recovery from exercise. Significant maintenance of central blood volume (thoracic impedance), stroke volume, and cardiac output paralleled the maintenance of MAP during active and passive conditions during 5 min of recovery. These data indicate that engaging the skeletal muscle pump by loadless or passive pedaling helps maintain MAP during recovery from submaximal exercise. The lack of differences between loadless and passive pedaling suggests that cessation of central command is not as important.

Background— Although the hemodynamic changes associated with atrial fibrillation (AF) have been extensively studied, the neural changes remain unclear. We hypothesized that AF is associated with an increase in sympathetic nerve activity (SNA) and that the irregular ventricular response contributes to this state of sympathoexcitation. Methods and Results— In 8 patients referred for an electrophysiological study, SNA, blood pressure (BP), central venous pressure (CVP), and heart rate were recorded during 3 minutes of normal sinus rhythm (NSR) and 3 minutes of induced AF. In 5 of 8 patients who converted to NSR, right atrial (RA) pacing was performed for 3 minutes in atrial pacing triggered by ventricular sensing mode triggered by playback of an FM tape previously recorded from the right ventricle during AF (RA-irregular) and atrial pacing inhibited by atrial sensing mode at a rate equal to the mean heart rate obtained during AF (RA-regular). SNA data were expressed as percentage of baseline during NSR. SNA increased in all 8 patients during induced AF compared with NSR (171±40% versus 100%, respectively; P <0.01). This was associated with a trend for a decrease in BP and an increase in CVP ( P =0.02). Similarly, SNA was significantly higher during RA-irregular pacing compared with RA-regular pacing (124±24% versus 91±20%, respectively; P =0.03). BP and CVP were not significantly different between the 2 pacing modes. Conclusions— Induced AF results in a significant increase in SNA, which is in part attributable to the irregular ventricular response. Our findings suggest that restoring NSR or regularity might be beneficial, particularly in patients with heart failure.

The purpose of this manuscript is to review the current literature regarding the role of the autonomic nervous system (ANS) in atrial fibrillation (AF). We will be reviewing its effect on initiation, maintenance, and termination of AF, with emphasis on the role of baroreflex gain (BRG) and autonomic reflexes in the maintenance of this arrhythmia. While it is generally accepted that the ANS plays an important role in AF, the extent of that role remains controversial. Much of the controversy could be explained by the time frame during which the autonomic measurements were made, the differences in patient population, and possibly the differential effect of the autonomic changes on the trigger versus the substrate. While vagal stimulation results in shortening of the atrial effective refractory period and increased dispersion of refractoriness, its effect on the "trigger" might be antiarrhythmic. During AF, cardiac filling pressure increases while arterial blood pressure decreases sending conflicting messages to the medulla. The acute effect is an increase in sympathetic activity to ensure adequate hemodynamic stability. On the other hand, the long-term effects might be impairment in the cardiopulmonary BRG and changes that accentuate the presence of AF. While radiofrequency ablation has provided us with a unique insight into the role of possible denervation in AF suppression, the exact mechanisms involved are far from being completely understood. Today, in an era where great technological advances have occurred, our need to understand the role of the ANS in AF is greater than ever.

Physiological responses to mental tasks and physical exercise were studied independently and combined. We hypothesized that combined mental and physical stresses produce a synergistic interaction. We studied cardiovascular responses to 5 min of static handgrip, mental arithmetic, and the combined stimuli in random order in 12 healthy subjects. Muscle sympathetic nerve activity (SNA) and mean arterial blood pressure (MAP) responses to handgrip and the combined stimuli exceeded responses to mental arithmetic, yet no significant difference existed between responses to handgrip and the combined stimuli. Peak changes in SNA (in %) were greatest during handgrip (188 ± 41), followed by the combined stimuli (166 ± 31) and mental arithmetic (51 ± 9). Peak changes in MAP (in mmHg) were also greatest during handgrip (26 ± 4), followed by the combined stimuli (23 ± 3) and then mental arithmetic (8 ± 2). Peak changes in heart rate (in beats/min) followed the same trend: handgrip (15 ± 2), combined (13 ± 2), and mental arithmetic (10 ± 2). Mental stimulation did not synergistically interact with or add to the responses elicited by handgrip exercise; in fact, a trend existed for math during handgrip to reduce responses relative to handgrip alone.

Background-Despite similar degrees of left ventricular dysfunction and similar tachycardia or pacing rate, blood pressure (BP) response and symptoms vary greatly among patients. Sympathetic nerve activity (SNA) increases during sustained ventricular tachycardia (VT), and the magnitude of this sympathoexcitatory response appears to contribute to the net hemodynamic outcome. We hypothesize that the magnitude of sympathoexcitation and thus arterial baroreflex gain is an important determinant of the hemodynamic outcome of VT. Methods and Results-We evaluated the relation between arterial baroreflex sympathetic gain and BP recovery during rapid ventricular pacing (VP) in patients referred for electrophysiological study. Efferent postganglionic muscle SNA, BP, and central venous pressure (CVP) were measured in 14 patients during nitroprusside infusion and during VP at 150 (nϭ12) or 120 (nϭ2) bpm. Arterial baroreflex gain was defined as the slope of the relationship of change in SNA to change in diastolic BP during nitroprusside infusion. Recovery of mean arterial pressure (MAP) during VP was measured as the increase in MAP from the nadir at the onset of pacing to the steady-state value during sustained VP. Arterial baroreflex gain correlated positively with recovery of MAP (rϭ0.57, Pϭ0.034). No significant correlation between ejection fraction and baroreflex gain (rϭ0.48, Pϭ0.08) or BP recovery (rϭ0.41, Pϭ0.15) was found. When patients were separated into high versus low baroreflex gain, the recovery of MAP during simulated VT was significantly greater in patients with high gain. Conclusions-These data strongly suggest that arterial baroreflex gain contributes significantly to hemodynamic stability during simulated VT. Knowledge of baroreflex gain in individual patients may help the clinician tailor therapy directed toward sustained VT. (Circulation. 1999;100:381-386.)