Smokers may develop chronic increases in cardiac rate and alterations
in cardiovascular control. If the increased mean heart rate (HR) in ci
garette smokers is due in part to a deficit in vagal cardiac rate cont
rol, 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 hea
rt rate was determined from the ECG during 30 s of quiet breathing; RS
A was determined for 10 consecutive deep (> 50% vital capacity) slow (
5-7/min) breaths. Mean HRs in smokers were significantly higher than i
n non-smokers, but the increases in mean HRs evoked by a shift from th
e supine to seated position were lower in smokers than in non-smokers,
suggesting that chronic tobacco use may alter the relative contributi
ons of sympathetic and parasympathetic control of cardiac rate. Becaus
e neither the RSAs nor the position-dependent increase in RSA were dif
ferent between smokers and non-smokers, we conclude that the elevated
mean HRs in smokers were not the result of decreased respiratory or va
somotor modulation of vagal cardiac control, but instead were. the res
ult primarily of sympathetic stimulation.