Role of parasympathetic (vagal) cardiac control in elevated heart rates of smokers.

Abstract

Smokers may develop chronic increases in cardiac rate and alterations in cardiovascular control. If the increased mean heart rate (HR) in cigarette smokers is due in part to a deficit in vagal cardiac rate control, this should be reflected in a decreased amplitude of respiratory sinus arrhythmia (RSA). To test this hypothesis we studied 36 smokers and 36 non-smokers, matched for age, race, gender and blood pressure. All subjects were studied in the supine and seated positions. Mean heart rate was determined from the ECG during 30 s of quiet breathing; RSA was determined for 10 consecutive deep (>50% vital capacity) slow (5-7/min) breaths. Mean HRs in smokers were significantly higher than in non-smokers, but the increases in mean HRs evoked by a shift from the supine to seated position were lower in smokers than in non-smokers, suggesting that chronic tobacco use may alter the relative contributions of sympathetic and parasympathetic control of cardiac rate. Because neither the RSAs nor the position-dependent increase in RSA were different between smokers and non-smokers, we conclude that the elevated mean HRs in smokers were not the result of decreased respiratory or vasomotor modulation of vagal cardiac control, but instead were the result primarily of sympathetic stimulation.