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The purpose of this study was to evaluate the effect of interruption of the descending supraspinal sympathetic outflow on heart rate control during exposures to chemical stimuli. We investigated the heart rate responses to progressive isocapnic hypoxia and hyperoxic hypercapnia using the rebreathing technique and quantified the relationship between heart rate (HR), oxygen saturation (SaO2), alveolar PCO2 (PACO2), and minute ventilation (VE) in 16 chronic tetraplegic subjects with low cervical spinal cord transection. The HR responses were determined from the linear slopes of HR on SaO2 and HR on PACO2. We found that mean resting heart rate was within normal range; 66 +/- 3 (SEM) beats min-1. HR increased as oxygenation fell or CO2 tension rose. The mean tetraplegic delta HR/delta SaO2 was 0.83 +/- 0.14 beats min-1 per 1% fall in SaO2 and that of delta HR/delta PACO2 was 0.30 +/- 0.13 beats min-1 per mmHG rise in PACO2. The HR and VE responses to either hypoxia or hypercapnia were related in the tetraplegic subjects. We conclude that the stimulatory HR responses to chemical stimuli are not suppressed by cervical spinal cord transection. Thus, the descending sympathetic activity does not underlie the HR acceleration by chemical stimuli.
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