Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity

The low-frequency component of the heart rate variability spectrum (0.06-0. 10 Hz) is often used as an accurate reflection of sympathetic activity. The refore, interventions that enhance cardiac sympathetic drive, e.g., exercis e and myocardial ischemia, should elicit increases in the low-frequency pow er. Furthermore, because an enhanced sympathetic activation has been linked to an increased propensity for malignant arrhythmias, one might also predi ct a greater low-frequency power in animals that are susceptible to ventric ular fibrillation than in resistant animals. To test these hypotheses, a 2- min coronary occlusion was made during the last minute of exercise in 71 do gs with healed myocardial infarctions: 43 had ventricular fibrillation (sus ceptible) and 28 did not experience arrhythmias (resistant). Exercise or is chemia alone provoked significant heart rate increases in both groups of an imals, with the largest increase in the susceptible animals. These heart ra te increases were attenuated by beta-adrenergic receptor blockade. Despite the sympathetically mediated increases in heart rate, the low-frequency pow er decreased, rather than increased, in both groups, with the largest decre ase again in the susceptible animals: 4.0 +/- 0.2 (susceptible) vs. 4.1 +/- 0.2 In ms(2) (resistant) in preexercise control and 2.2 +/- 0.2 (susceptib le) vs. 2.9 +/- 0.2 In ms(2) (resistant) at highest exercise level. In a si milar manner the parasympathetic antagonist atropine sulfate elicited signi ficant reductions in the low-frequency power. Although sympathetic nerve ac tivity was not directly recorded, these data suggest that the low-frequency component of the heart rate power spectrum probably results from an intera ction of the sympathetic and parasympathetic nervous systems and, as such, does not accurately reflect changes in the sympathetic activity.