The Clamping of End-Tidal Carbon Dioxide Does Not Influence Cognitive Function Performance During Moderate Hyperthermia With or Without Skin Temperature Manipulation.

Increases in body temperature from heat stress (i.e., hyperthermia) generally impairs cognitive function across a range of domains and complexities, but the relative contribution from skin versus core temperature changes remains unclear. Hyperthermia also elicits a hyperventilatory response that decreases the partial pressure of end-tidal carbon dioxide (PCO) and subsequently cerebral blood flow that may influence cognitive function. We studied the role of skin and core temperature along with PCO on cognitive function across a range of domains. Eleven males completed a randomized, single-blinded protocol consisting of poikilocapnia (POIKI, no PCO control) or isocapnia (ISO, PCO maintained at baseline levels) during passive heating using a water-perfused suit (water temperature ~ 49°C) while middle cerebral artery velocity (MCA) was measured continuously as an index of cerebral blood flow. Cognitive testing was completed at baseline, neutral core-hot skin (37.0 ± 0.2°C-37.4 ± 0.3°C), hot core-hot skin (38.6 ± 0.3°C-38.7 ± 0.2°C), and hot core-cooled skin (38.5 ± 0.3°C-34.7 ± 0.6°C). The cognitive test battery consisted of a detection task (psychomotor processing), 2-back task (working memory), set-shifting and Groton Maze Learning Task (executive function). At hot core-hot skin, poikilocapnia led to significant (both  < 0.05) decreases in PCO (∆-21%) and MCA (∆-26%) from baseline, while isocapnia clamped PCO (∆ + 4% from baseline) leading to a significantly ( = 0.023) higher MCA (∆-18% from baseline) compared to poikilocapnia. There were no significant differences in errors made on any task (all  > 0.05) irrespective of skin temperature or PCO manipulation. We conclude that neither skin temperature nor PCO maintenance significantly alter cognitive function during passive hyperthermia.