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Hypercapnia-induced increases in cerebral blood flow do not improve lower body negative pressure tolerance during hyperthermia
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health. Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Dallas, TX ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX.
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Dallas, TX ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX ; Cardiff Metropolitan University, Cardiff, Wales.
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Dallas, TX ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX.
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Dallas, TX ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX.
2013 (English)In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 305, no 6, R604-R609 p.Article in journal (Refereed) Published
Abstract [en]

Heat-related decreases in cerebral perfusion are partly the result of ventilatory-related reductions in arterial CO2 tension. Cerebral perfusion likely contributes to an individual's tolerance to a challenge like lower body negative pressure (LBNP). Thus increasing cerebral perfusion may prolong LBNP tolerance. This study tested the hypothesis that a hypercapnia-induced increase in cerebral perfusion improves LBNP tolerance in hyperthermic individuals. Eleven individuals (31 +/- 7 yr; 75 +/- 12 kg) underwent passive heat stress (increased intestinal temperature similar to 1.3 degrees C) followed by a progressive LBNP challenge to tolerance on two separate days (randomized). From 30 mmHg LBNP, subjects inhaled either (blinded) a hypercapnic gas mixture (5% CO2, 21% oxygen, balanced nitrogen) or room air (SHAM). LBNP tolerance was quantified via the cumulative stress index (CSI). Mean middle cerebral artery blood velocity (MCAv(mean),) and end-tidal CO2 (PETCO2) were also measured. CO2 inhalation of 5% increased PETCO2 at similar to 40 mmHg LBNP (by 16 +/- 4 mmHg) and at LBNP tolerance (by 18 +/- 5 mmHg) compared with SHAM (P < 0.01). Subsequently, MCAvmean was higher in the 5% CO2 trial during similar to 40 mmHg LBNP (by 21 +/- 12 cm/s, similar to 31%) and at LBNP tolerance (by 18 +/- 10 cm/s, similar to 25%) relative to the SHAM (P < 0.01). However, hypercapnia-induced increases in MCAvmean did not alter LBNP tolerance (5% CO2 CSI: 339 +/- 155 mmHg X min; SHAM CSI: 273 +/- 158 mmHg X min; P = 0.26). These data indicate that inhaling a hypercapnic gas mixture increases cerebral perfusion during LBNP but does not improve LBNP tolerance when hyperthermic.

Place, publisher, year, edition, pages
2013. Vol. 305, no 6, R604-R609 p.
Keyword [en]
hypercapnia, heat stress, LBNP
National Category
Physiology
Identifiers
URN: urn:nbn:se:umu:diva-81834DOI: 10.1152/ajpregu.00052.2013ISI: 000324753200005OAI: oai:DiVA.org:umu-81834DiVA: diva2:659086
Available from: 2013-10-24 Created: 2013-10-22 Last updated: 2017-12-06Bibliographically approved

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Lucas, Rebekah A. I.

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