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Acute hyperglycemia does not alter central respiratory CO 2 chemoreflex responsiveness
Author(s) -
Bird Jordan,
Skalk Alexandra,
Thrall Scott,
Strzalkowski Nicholas,
Day Trevor A
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.lb586
Subject(s) - chemoreceptor , ventilation (architecture) , medicine , respiratory system , carbon dioxide , arterial blood , endocrinology , chemistry , respiratory rate , anesthesia , peripheral chemoreceptors , respiration , central chemoreceptors , oxygen , control of respiration , blood pressure , heart rate , anatomy , mechanical engineering , receptor , organic chemistry , engineering
The control of breathing is modulated by two distinct but interacting respiratory chemoreceptor compartments: peripheral chemoreceptors (PCRs; carotid bodies) and central chemoreceptors (CCRs; brainstem). The PCRs respond to variety of chemostimuli, including arterial oxygen, arterial carbon dioxide, glucose, insulin and temperature, and are now thought to act as metabolic sensors. However, CCRs have only been characterized as carbon dioxide/acid sensors (PCO 2 /[H + ]). PCRs respond to chemostimulation faster than CCRs, which may mask CCR responses to stimuli like acute hyperglycemia. The aim of this study was to characterize the relationship between alterations in blood glucose concentration and central respiratory chemoreflex responsiveness via hyperoxic rebreathing in healthy humans. We hypothesized that experimentally‐induced relative hyperglycemia following an oral glucose tolerance test (OGTT; 75g, 300 ml) would (a) increase the rate of CO 2 accumulation during rebreathing and (b) augment central respiratory chemoreflex responsiveness due to a synergistic effect of hyperglycemia on the CO 2 sensitivity of CCR neurons. In 10 healthy participants, we measured minute ventilation (V I ; L/min; pneumotachometer) and end‐tidal carbon dioxide (P ET CO 2 ; Torr; gas analyzer). We used the modified hyperoxic rebreathing test to isolate CCRs and quantify the central chemoreflex responsiveness to increases in metabolically‐derived CO 2 . Blood glucose levels were higher 30‐min following the OGTT beverage (i.e., glucose‐loaded) compared to fasted (7.8±1.1 vs. 4.7±0.4 mmol/L; P<0.0001). During rebreathing, the rate of end‐tidal (P ET )CO 2 accumulation was greater in the glucose loaded trial compared to the fasted trial (0.086±0.007 vs. 0.07±0.008 vs. Torr/sec; P=0.0002). These findings confirm the hyperglycemic stimulation between trials. However, the central respiratory chemoreflex responsiveness during rebreathing was not different between glucose loaded and fasted trials (2.3±1.4 vs. 2.5±1.8 vs. L/min/Torr CO 2 ; P=0.59). These preliminary findings suggest that relative hyperglycemia does not affect the central respiratory chemoreflex responsive to hyperoxic rebreathing. The CCRs may be a more specialized respiratory chemoreceptor, with a phenotype to detect only metabolically‐derived accumulations in CO 2 . Support or Funding Information NSERC Discovery and MRU Faculty of Science and Technology This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .