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Department of Physiology, The Ohio State University, Columbus, Ohio 43210
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.
Therefore, interventions that enhance cardiac sympathetic drive, e.g.,
exercise and myocardial ischemia, should elicit increases in
the low-frequency power. Furthermore, because an enhanced sympathetic
activation has been linked to an increased propensity for malignant
arrhythmias, one might also predict a greater low-frequency power in
animals that are susceptible to ventricular fibrillation than in
resistant animals. To test these hypotheses, a 2-min coronary occlusion
was made during the last minute of exercise in 71 dogs with healed
myocardial infarctions: 43 had ventricular fibrillation (susceptible)
and 28 did not experience arrhythmias (resistant). Exercise or
ischemia alone provoked significant heart rate increases in
both groups of animals, with the largest increase in the susceptible
animals. These heart rate increases were attenuated by 
-adrenergic
receptor blockade. Despite the sympathetically mediated increases in
heart rate, the low-frequency power decreased, rather than increased,
in both groups, with the largest decrease again in the susceptible
animals: 4.0 ± 0.2 (susceptible) vs. 4.1 ± 0.2 ln
ms2 (resistant) in preexercise
control and 2.2 ± 0.2 (susceptible) vs. 2.9 ± 0.2 ln
ms2 (resistant) at highest
exercise level. In a similar manner the parasympathetic antagonist
atropine sulfate elicited significant reductions in the low-frequency
power. Although sympathetic nerve activity was not directly recorded,
these data suggest that the low-frequency component of the heart rate
power spectrum probably results from an interaction of the sympathetic
and parasympathetic nervous systems and, as such, does not accurately
reflect changes in the sympathetic activity.
cardiac parasympathetic activity; exercise; myocardial infarction; myocardial ischemia
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