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Background: We evaluated the acute cardiovascular and thermoregulatory responses to repeated 70° head-up tilts (HUT) performed following exercise-induced hyperthermia. Methods: Eight male subjects underwent intermittent episodes of 70° HUT in either a non-exercise/non-heat stress state (NH) or an exercise-induced hyperthermic state (EIH). Subjects remained supine for 30 min in a thermoneutral environment (22°C) and were subsequently exposed to three successive 6-min 70° head-up tilts (HUT1, HUT2, HUT3), each separated by 10 min of supine resting. During EIH, subjects were rendered hyperthermic by exercise in the heat (core temperature of ~40.0°C) and were then transferred to an ambient temperature of 22°C. We evaluated the relative change in hemodynamic and thermal responses from the last minute in the supine position preceding the HUT to the final minute in HUT. Results: While we measured a difference in the relative change in heart rate between conditions for all HUTs, no differences were observed in mean arterial pressure (MAP), total peripheral resistance, or cardiac output. A reduced change in baroreceptor sensitivity was measured in EIH for HUT1 only (-2 ± 1 ms · mmHg-1 following EIH compared to -13 ± 3 ms · mmHg-1 during NH). A significant transient reduction in cutaneous vascular conductance (CVC) occurred during HUT1 and HUT2 following EIH (-20 ± 5 %CVCmax and -9 ± 3 %CVCmax, respectively), despite significant elevations in core temperature above resting levels (i.e., 1.4°C and 0.9°C for HUT1 and HUT2). Conclusion: We conclude that the maintenance of MAP following exercise in the heat is mitigated by reductions in skin perfusion despite significant elevations in core temperature. [ABSTRACT FROM AUTHOR]

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°C water (normothermia). Following normothermic data collection, 50°C water was perfused through the suit to increase internal temperature approximately 1°C (whole-body heating). In both thermal conditions, a normoxic-hypercapnic (5% CO[sub2], 21% O[sub2], balance N[sub2]) 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 CO[sub2] 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 disspation by reducing cutaneous vasodilation. [ABSTRACT FROM AUTHOR]