Baroreceptor and chemoreceptor reflexes exert considerable influence on autonomic cardiovascular regulation, although limited information on interactions between these reflexes exists for humans (Somers et al. 1991). During baroreceptor stimulation using a simulated orthostatic challenge to pre-syncope, the influence of hypercapnic acidosis has not been previously studied. Therefore, this study investigated the effect of hypercapnic acidosis on tolerance to orthostatic stress in humans.

With DeMontfort University ethical approval, nine subjects (5 males and 4 females; mean ± S.D., age 21.9 ± 0.9 years, height 172.4 ± 9.7 cm, mass 70.3 ± 7.1 kg) were exposed to lower body negative pressure (LBNP) until the onset of pre-syncope on two occasions, each separated by approximately one week. In a counterbalanced design, investigations were carried out while subjects were breathing either room air (RA), or normoxic air containing 5 % carbon dioxide (CO₂). While breathing the appropriate mixture, a period of 15 min supine rest was followed by LBNP at -20 mmHg for 3 min, and subsequent decreases in pressure of -10 mmHg every 3 min until pre-syncope, at which time the test was terminated. Measurement of cardiovascular variables and continuous expired gas analysis were carried out on both occasions.

For both mixtures, LBNP induced a decrease in forearm blood flow, estimated cardiac output and stroke volume (all P < 0.05, ANOVA with Fisher post hoc). Minute ventilation, end tidal CO₂, and estimated arterial P_CO2 were elevated when breathing CO₂ compared to RA during supine rest and LBNP (P < 0.001, ANOVA with Fisher post hoc). Compared to RA (using Student paired t test, values are mean ± S.D.), CO₂ increased orthostatic tolerance (191.9 ± 20.4 vs. 210.3 ± 20.9 mmHg min), peak heart rate (123.9 ± 23.7 vs. 131.9 ± 24.9 beats min^-1), and time to peak heart rate (16.1 ± 2.1 vs. 18.1 ± 1.8 min) during LBNP. At pre-syncope, estimated stroke volume was 37.3 ± 2.1 ml when breathing RA, and 29.0 ± 6.7 ml when breathing CO₂ (P > 0.05).

These results suggest that the possible protective element of pre-syncope was delayed during hypercapnic acidosis at the expense of further reductions in stroke volume. This delayed pre-syncope response may have been associated with increases in cerebral blood flow induced by the increased arterial P_CO2.