Introduction: Hypercapnia may be encountered in lung disease as well as during situations involving rebreathing of previously expired air (e.g., occupational diving). Inhibitory effects of elevated arterial carbon dioxide partial pressure on the central nervous system may result in impaired thermoregulation. This study tested the hypothesis that in heat-stressed subjects, cutaneous vascular responsiveness [expressed as cutaneous vascular conductance (CVC)] would be reduced during hypercapnic exposure.
Methods: Four men and three women (mean - SD; age: 35 +/- 7 yr) rested supine while wearing a tube-lined suit perfused with 34 degrees C water (normothermia). Following normothermic data collection, 50 degrees C water was perfused through the suit to increase internal temperature approximately 1 degrees C (whole-body heating). In both thermal conditions, a normoxic-hypercapnic (5% CO2, 21% O2, balance N2) gas mixture was inspired while forearm skin blood flux (laser-Doppler flowmetry) was measured continuously and was used for calculation of CVC (skin blood flux/mean arterial pressure).
Results: End-tidal CO2 increased similarly throughout hypercapnic exposure during both normothermic and whole-body heating conditions (7.9 +/- 2.4 and 8.3 +/- 1.9 mmHg, respectively). However, CVC was not different between normocapnia and hypercapnia under either thermal condition (normothermia: 0.42 +/- 0.24 vs. 0.39 +/- 0.21 flux units/mmHg for normocapnia and hypercapnia, respectively; heat stress: 1.89 +/- 0.67 vs. 1.92 +/- 0.63 flux units/ mmHg for normocapnia and hypercapnia, respectively).
Discussion: Based on these findings, mild hypercapnia is unlikely to impair heat dissipation by reducing cutaneous vasodilation.